Page last updated: 2024-11-02

pioglitazone and Hyperglycemia, Postprandial

pioglitazone has been researched along with Hyperglycemia, Postprandial in 87 studies

Pioglitazone: A thiazolidinedione and PPAR GAMMA agonist that is used in the treatment of TYPE 2 DIABETES MELLITUS.
pioglitazone : A member of the class of thiazolidenediones that is 1,3-thiazolidine-2,4-dione substituted by a benzyl group at position 5 which in turn is substituted by a 2-(5-ethylpyridin-2-yl)ethoxy group at position 4 of the phenyl ring. It exhibits hypoglycemic activity.

Hyperglycemia, Postprandial: Abnormally high BLOOD GLUCOSE level after a meal.

Research Excerpts

ExcerptRelevanceReference
"Maximal-dose pioglitazone had no effects on BMD or bone turnover, while improving glycemic control as expected, in postmenopausal women with impaired fasting glucose or impaired glucose tolerance."9.17Effects of pioglitazone on bone in postmenopausal women with impaired fasting glucose or impaired glucose tolerance: a randomized, double-blind, placebo-controlled study. ( Bone, HG; Lindsay, R; McClung, MR; Perez, AT; Raanan, MG; Spanheimer, RG, 2013)
" Hyperglycemia is an on-target side effect of many inhibitors of PI3K/Akt signaling including the specific PI3K inhibitor PX-866."7.75Peroxisome proliferator-activated receptor gamma agonist pioglitazone prevents the hyperglycemia caused by phosphatidylinositol 3-kinase pathway inhibition by PX-866 without affecting antitumor activity. ( Halter, RJ; Ihle, NT; Kirkpatrick, L; Lemos, R; Oh, J; Powis, G; Schwartz, D; Wipf, P, 2009)
"Here we demonstrate 2 patients who showed marked hyperglycemia after androgen-deprivation therapy for prostate cancer and the efficacy of the thiazolidinedione pioglitazone on their glycemic control."7.73Marked hyperglycemia after androgen-deprivation therapy for prostate cancer and usefulness of pioglitazone for its treatment. ( Azuma, J; Inaba, M; Kasayama, S; Kawase, I; Koga, M; Nishimura, K; Okuyama, A; Otani, Y; Takaha, N, 2005)
"Effects of pioglitazone (5-[4-[2-(5-etyl-2-pyridyl)ethoxy] benzyl]-2,4-thiazolidinedione, AD-4833, also known as U-72, 107E) on peripheral and hepatic insulin resistance were examined using genetically obese-hyperglycemic rats, Wistar fatty."7.68Effects of pioglitazone on hepatic and peripheral insulin resistance in Wistar fatty rats. ( Ikeda, H; Shimura, Y; Sugiyama, Y, 1990)
"A total of 288 type 2 diabetes patients completed this double-blind parallel study (187 men, 101 women; age [mean ± SD], 59 ± 10 years; body mass index, 32."6.76PIOfix-study: effects of pioglitazone/metformin fixed combination in comparison with a combination of metformin with glimepiride on diabetic dyslipidemia. ( Forst, T; Fuchs, W; Lehmann, U; Lobmann, R; Merke, J; Müller, J; Pfützner, A; Schöndorf, T; Tschöpe, D, 2011)
"Metformin treatment also improved hyperleptinemia, whereas pioglitazone was ineffective."5.36Metformin reduces body weight gain and improves glucose intolerance in high-fat diet-fed C57BL/6J mice. ( Hirasawa, Y; Ito, M; Kyuki, K; Matsui, Y; Sugiura, T; Toyoshi, T, 2010)
"Treatment with pioglitazone and rosiglitazone significantly decreased the AT(1)R specific binding in HFD fed rats."5.34PPAR gamma agonists partially restores hyperglycemia induced aggravation of vascular dysfunction to angiotensin II in thoracic aorta isolated from rats with insulin resistance. ( Gaikwad, AB; Ramarao, P; Viswanad, B, 2007)
"Pioglitazone treatment for 8 weeks affected GSH-Px activity in diabetic liver (261."5.33Effects of pioglitazone on hyperglycemia-induced alterations in antioxidative system in tissues of alloxan-treated diabetic animals. ( Gumieniczek, A, 2005)
"A total of 441 individuals with impaired glucose tolerance (IGT) from ACT NOW received an oral glucose tolerance test and were randomized to pioglitazone or placebo for 2."5.19The disposition index does not reflect β-cell function in IGT subjects treated with pioglitazone. ( Abdul-Ghani, M; DeFronzo, RA; Gastaldelli, A; Musi, N; Tripathy, D, 2014)
"Maximal-dose pioglitazone had no effects on BMD or bone turnover, while improving glycemic control as expected, in postmenopausal women with impaired fasting glucose or impaired glucose tolerance."5.17Effects of pioglitazone on bone in postmenopausal women with impaired fasting glucose or impaired glucose tolerance: a randomized, double-blind, placebo-controlled study. ( Bone, HG; Lindsay, R; McClung, MR; Perez, AT; Raanan, MG; Spanheimer, RG, 2013)
"05) between the 2 groups was found in the treatment-induced changes in fasting insulin, the insulin resistance index HOMA, HDL cholesterol, triglycerides, diastolic blood pressure (all in favor of pioglitazone) and in body weight (increase with pioglitazone)."5.14Lack of effects of pioglitazone on cardiac function in patients with type 2 diabetes and evidence of left ventricular diastolic dysfunction: a tissue doppler imaging study. ( Kanioglou, C; Katsouras, CS; Kazakos, N; Liveris, K; Makriyiannis, D; Michalis, LK; Naka, KK; Papamichael, ND; Papathanassiou, K; Pappas, K; Tsatsoulis, A, 2010)
"To investigate the relationship between insulin resistance, postprandial hyperglycemia, postprandial hyperlipidemia, and oxidative stress in type 2 diabetes, changes in postprandial glucose, triglyceride, and nitrotyrosine levels vs baseline after diet loading were examined in type 2 diabetic patients given pioglitazone (PG) or glibenclamide (GB)."5.12Effects of pioglitazone vs glibenclamide on postprandial increases in glucose and triglyceride levels and on oxidative stress in Japanese patients with type 2 diabetes. ( Itoh, Y; Mori, Y; Obata, T; Tajima, N, 2006)
"The pioglitazone treatment significantly reduced hyperglycemia, hyperinsulinemia, and HbA(1c) levels and increased plasma adiponectin concentrations relative to the control group (P < 0."5.10Antiatherogenic effect of pioglitazone in type 2 diabetic patients irrespective of the responsiveness to its antidiabetic effect. ( Kono, S; Kuzuya, H; Nakao, K; Ogawa, Y; Satoh, N; Shimatsu, A; Sugawara, A; Sugiyama, H; Tagami, T; Uesugi, H; Usui, T; Yamada, K, 2003)
"Six months of pioglitazone treatment decreased insulin resistance and improved glycemic control to a significantly greater extent than acarbose treatment."5.10Improved glycemic control and lipid profile in a randomized study of pioglitazone compared with acarbose in patients with type 2 diabetes mellitus. ( Göke, B, 2002)
" The traditional approach involves: i) metformin, acting mainly on fasting blood glucose; ii) sulphonylureas, that have shown a number of drawbacks, including the high risk of hypoglycemia; iii) pioglitazone, with a substantial effect on fasting and postprandial glucose and a low risk of hypoglycaemia; iv) insulin, that can be utilized with the basal or prandial approach."4.89What are the preferred strategies for control of glycaemic variability in patients with type 2 diabetes mellitus? ( Marangoni, A; Zenari, L, 2013)
" Pioglitazone, a thiazolidinedione (TZD) commonly used in the treatment of diabetes due to its ability to improve insulin sensitivity and reverse hyperglycemia, was ineffective in reversing the diabetes-induced changes on lysosomal enzymes."3.83The Role of Oxidized Cholesterol in Diabetes-Induced Lysosomal Dysfunction in the Brain. ( Bakeman, A; Feldman, EL; Glasser, R; Rosko, A; Sims-Robinson, C, 2016)
" In this study, we aim to develop a drug-eluting scaffold with a payload of pioglitazone to simultaneously rein in hyperglycemia and recoup lost renal functions in diabetic mice that underwent islet transplantation."3.80A synergistic therapeutic scheme for hyperglycemia and nephrotic disorders in diabetes. ( Fu, Z; Han, B; He, Q; Tang, K; Xu, J; Yin, H; Zhang, X, 2014)
"Administration of rutin (50 and 100 mg/kg) and pioglitazone (10 mg/kg) orally for 3 weeks treatment significantly improved body weight, reduced plasma glucose and glycosylated hemoglobin, pro-inflammatory cytokines (IL-6 and TNF-alpha), restored the depleted liver antioxidant status and serum lipid profile in high fat diet + streptozotocin induced type 2 diabetic rats."3.80Anti-hyperglycemic activity of rutin in streptozotocin-induced diabetic rats: an effect mediated through cytokines, antioxidants and lipid biomarkers. ( Ansari, AA; Naik, SR; Niture, NT, 2014)
" Here, we tested the effect of a potent and selective peroxisome proliferator-activated receptor-γ agonist, rivoglitazone (Rivo), a newly synthesized thiazolidinedione derivative, on adiponectin, insulin resistance, and atherosclerosis."3.77Dynamic changes of adiponectin and S100A8 levels by the selective peroxisome proliferator-activated receptor-gamma agonist rivoglitazone. ( Funahashi, T; Hirata, A; Hiuge-Shimizu, A; Kihara, S; Maeda, N; Nakamura, K; Nakatsuji, H; Okuno, A; Shimomura, I, 2011)
" Hyperglycemia is an on-target side effect of many inhibitors of PI3K/Akt signaling including the specific PI3K inhibitor PX-866."3.75Peroxisome proliferator-activated receptor gamma agonist pioglitazone prevents the hyperglycemia caused by phosphatidylinositol 3-kinase pathway inhibition by PX-866 without affecting antitumor activity. ( Halter, RJ; Ihle, NT; Kirkpatrick, L; Lemos, R; Oh, J; Powis, G; Schwartz, D; Wipf, P, 2009)
"Here we demonstrate 2 patients who showed marked hyperglycemia after androgen-deprivation therapy for prostate cancer and the efficacy of the thiazolidinedione pioglitazone on their glycemic control."3.73Marked hyperglycemia after androgen-deprivation therapy for prostate cancer and usefulness of pioglitazone for its treatment. ( Azuma, J; Inaba, M; Kasayama, S; Kawase, I; Koga, M; Nishimura, K; Okuyama, A; Otani, Y; Takaha, N, 2005)
" We evaluated the effect of 24- to 48-h 8 microM l-805645 or 10 microM pioglitazone on 25 mM D-glucose-induced markers of fibrosis in HK-2 cells."3.73PPARgamma agonists exert antifibrotic effects in renal tubular cells exposed to high glucose. ( Chen, X; Panchapakesan, U; Pollock, CA; Sumual, S, 2005)
"To determine the relationship between hypoglycemic activity and body weight gain induced by insulin sensitizers, we compared the effects of thiazolidinedione analogs (troglitazone and pioglitazone) and the oxadiazolidinedione analog (Z)-1,4-bis4[(3,5-dioxo-1,2,4-oxadiazolidin-2-yl)methyl]phen oxy¿but-2-ene (YM440) in diabetic db/db mice."3.70The novel hypoglycemic agent YM440 normalizes hyperglycemia without changing body fat weight in diabetic db/db mice. ( Hirayama, R; Kurosaki, E; Nakano, R; Shibasaki, M; Shikama, H; Shimaya, A, 2000)
" Pioglitazone, a thiazolidinedione derivative, sensitizes target tissues to insulin and decreases hyperglycemia and hyperinsulinemia in various insulin-resistant animals."3.70Pioglitazone attenuates basal and postprandial insulin concentrations and blood pressure in the spontaneously hypertensive rat. ( Gonzalez, R; Grinsell, JW; Lardinois, CK; Michaels, JR; Sare, JS; Starich, GH; Swislocki, A, 2000)
"Effects of pioglitazone (5-[4-[2-(5-etyl-2-pyridyl)ethoxy] benzyl]-2,4-thiazolidinedione, AD-4833, also known as U-72, 107E) on peripheral and hepatic insulin resistance were examined using genetically obese-hyperglycemic rats, Wistar fatty."3.68Effects of pioglitazone on hepatic and peripheral insulin resistance in Wistar fatty rats. ( Ikeda, H; Shimura, Y; Sugiyama, Y, 1990)
"These 3-year efficacy data support long-term use of albiglutide in the management of people with T2DM."2.84Three-year data from 5 HARMONY phase 3 clinical trials of albiglutide in type 2 diabetes mellitus: Long-term efficacy with or without rescue therapy. ( Ahrén, B; Ambery, P; Carr, MC; Cirkel, DT; Home, PD; Miller, D; Nauck, MA; Rendell, M; Reusch, JEB; Weissman, PN, 2017)
" The overall incidence rates of treatment-emergent adverse events were similar among the treatment groups."2.80Efficacy and safety of pioglitazone added to alogliptin in Japanese patients with type 2 diabetes mellitus: a multicentre, randomized, double-blind, parallel-group, comparative study. ( Igeta, M; Kaku, K; Katou, M; Ohira, T; Sano, H, 2015)
" We observed a statistically significant trend in the RE dose-response relationship for change from baseline in HbA1c at week 12 (p < 0."2.80Randomized efficacy and safety trial of once-daily remogliflozin etabonate for the treatment of type 2 diabetes. ( Almond, SR; Dobbins, R; Kemp, GL; Kler, L; O'Connor-Semmes, R; Sykes, AP; Walker, S; Wilkison, WO, 2015)
" Overall, lixisenatide once daily was well tolerated, with a similar proportion of treatment-emergent adverse events (TEAEs) and serious TEAEs between groups (lixisenatide: 72."2.78Efficacy and safety of lixisenatide once daily versus placebo in type 2 diabetes insufficiently controlled on pioglitazone (GetGoal-P). ( Aronson, R; Goldenberg, R; Guo, H; Muehlen-Bartmer, I; Niemoeller, E; Pinget, M, 2013)
"A total of 288 type 2 diabetes patients completed this double-blind parallel study (187 men, 101 women; age [mean ± SD], 59 ± 10 years; body mass index, 32."2.76PIOfix-study: effects of pioglitazone/metformin fixed combination in comparison with a combination of metformin with glimepiride on diabetic dyslipidemia. ( Forst, T; Fuchs, W; Lehmann, U; Lobmann, R; Merke, J; Müller, J; Pfützner, A; Schöndorf, T; Tschöpe, D, 2011)
"Ischemic stroke is a leading cause of morbidity and mortality among type 2 diabetic patients."2.72Diabetes, stroke, and neuroresilience: looking beyond hyperglycemia. ( Krinock, MJ; Singhal, NS, 2021)
"Patients with type 2 diabetes mellitus are at high risk of cardiovascular disease."2.71Pioglitazone decreases carotid intima-media thickness independently of glycemic control in patients with type 2 diabetes mellitus: results from a controlled randomized study. ( Forst, T; Füllert, SD; Hohberg, C; Kann, P; Konrad, T; Langenfeld, MR; Lübben, G; Pfützner, A; Sachara, C, 2005)
"Glycemic control in the context of type 2 diabetes, as well as prediabetes, is also intertwined with CV risk factors such as obesity, hypertriglyceridemia, and blood pressure control."2.47Macrovascular effects and safety issues of therapies for type 2 diabetes. ( Plutzky, J, 2011)
"Overall, 7% of the US population has type 2 diabetes mellitus (T2DM), and among people aged 60 years or older, approximately 20% have T2DM, representing a significant health burden in this age group."2.44Initiating insulin in patients with type 2 diabetes. ( Aoki, TJ; White, RD, 2007)
"Type 2 diabetes is strongly associated with increased risk of cardiovascular disease."2.42Peroxisome proliferator-activated receptor-gamma agonists in atherosclerosis: current evidence and future directions. ( Evans, M; Rees, A; Roberts, AW; Thomas, A, 2003)
"Hyperglycemia is the major risk factor for microvascular complications in patients with type 2 diabetes (T2D)."1.46Cardiovascular Disease and Type 2 Diabetes: Has the Dawn of a New Era Arrived? ( Abdul-Ghani, M; Chilton, R; DeFronzo, RA; Del Prato, S; Ryder, REJ; Singh, R, 2017)
"Hyperglycemia was induced by streptozotocin treatment."1.42Hyperglycemia and PPARγ Antagonistically Influence Macrophage Polarization and Infarct Healing After Ischemic Stroke. ( Gliem, M; Hartung, HP; Jander, S; Klotz, L; van Rooijen, N, 2015)
"Diabetic hyperglycemia has been suggested to play a role in osteoarthritis."1.42PPARγ is involved in the hyperglycemia-induced inflammatory responses and collagen degradation in human chondrocytes and diabetic mouse cartilages. ( Chan, DC; Chao, SC; Chen, CM; Chen, YJ; Lan, KC; Liu, SH; Tsai, KS; Wang, CC; Yang, RS, 2015)
"Obesity is often associated with chronic inflammatory state which contributes to the development of insulin resistance (IR) and type 2 diabetes mellitus (T2DM)."1.39Comparative study between atorvastatin and losartan on high fat diet-induced type 2 diabetes mellitus in rats. ( El-Moselhy, MA; Heeba, GH; Mourad, AA; Taye, A, 2013)
"In pioglitazone-treated animals, AA and TAS increased above control values while GSH and PCG were normalized."1.38Oxidative/nitrosative stress and protein damages in aqueous humor of hyperglycemic rabbits: effects of two oral antidiabetics, pioglitazone and repaglinide. ( Gumieniczek, A; Owczarek, B; Pawlikowska, B, 2012)
"Pioglitazone was administered in the diet at two concentrations (10 ppm and 100 ppm), the chemoprevention was initiated 12 days before carcinogenesis induction and lasted until the termination of the experiment."1.37Metabolic effects of pioglitazone in chemically-induced mammary carcinogenesis in rats. ( Ahlers, I; Ahlersová, E; Bojková, B; Garajová, M; Kajo, K; Kassayová, M; Kisková, T; Kubatka, P; Mokáň, M; Orendáš, P; Péč, M, 2011)
"Metformin treatment also improved hyperleptinemia, whereas pioglitazone was ineffective."1.36Metformin reduces body weight gain and improves glucose intolerance in high-fat diet-fed C57BL/6J mice. ( Hirasawa, Y; Ito, M; Kyuki, K; Matsui, Y; Sugiura, T; Toyoshi, T, 2010)
"Treatment with pioglitazone and rosiglitazone significantly decreased the AT(1)R specific binding in HFD fed rats."1.34PPAR gamma agonists partially restores hyperglycemia induced aggravation of vascular dysfunction to angiotensin II in thoracic aorta isolated from rats with insulin resistance. ( Gaikwad, AB; Ramarao, P; Viswanad, B, 2007)
"Pioglitazone treatment for 8 weeks affected GSH-Px activity in diabetic liver (261."1.33Effects of pioglitazone on hyperglycemia-induced alterations in antioxidative system in tissues of alloxan-treated diabetic animals. ( Gumieniczek, A, 2005)
" Metabolites 6-9 have been identified after dosing of rats and dogs."1.29Synthesis and biological activity of metabolites of the antidiabetic, antihyperglycemic agent pioglitazone. ( Colca, JR; Fisher, RM; Kletzein, RF; Parker, TT; Tanis, SP, 1996)

Research

Studies (87)

TimeframeStudies, this research(%)All Research%
pre-19900 (0.00)18.7374
1990's4 (4.60)18.2507
2000's31 (35.63)29.6817
2010's49 (56.32)24.3611
2020's3 (3.45)2.80

Authors

AuthorsStudies
Tanis, SP1
Parker, TT1
Colca, JR1
Fisher, RM1
Kletzein, RF1
Furukawa, A1
Arita, T1
Satoh, S1
Wakabayashi, K1
Hayashi, S1
Matsui, Y3
Araki, K1
Kuroha, M1
Ohsumi, J1
Ushiroda, K1
Maruta, K1
Kitoh, M1
Iwai, K1
Nagamine, J1
Tsuchida, A1
Taiji, M1
Nagata, R1
Ding, LB1
Li, Y1
Liu, GY1
Li, TH1
Li, F1
Guan, J1
Wang, HJ1
Krinock, MJ1
Singhal, NS1
Pires Mendes, C1
Postal, BG1
Silva Frederico, MJ1
Gonçalves Marques Elias, R1
Aiceles de Medeiros Pinto, V1
da Fonte Ramos, C1
Devantier Neuenfeldt, P1
Nunes, RJ1
Mena Barreto Silva, FR1
Katsiki, N1
Mikhailidis, DP1
Inzucchi, SE1
Viscoli, CM1
Young, LH1
Furie, KL1
Gorman, M1
Lovejoy, AM1
Dagogo-Jack, S1
Ismail-Beigi, F1
Korytkowski, MT1
Pratley, RE1
Schwartz, GG1
Kernan, WN1
Li, X1
Wang, E1
Yin, B1
Fang, D1
Chen, P1
Wang, G1
Zhao, J1
Zhang, H1
Chen, W1
Abdul-Ghani, M2
DeFronzo, RA3
Del Prato, S1
Chilton, R1
Singh, R1
Ryder, REJ1
Home, PD1
Ahrén, B1
Reusch, JEB1
Rendell, M1
Weissman, PN1
Cirkel, DT1
Miller, D1
Ambery, P1
Carr, MC1
Nauck, MA1
Campbell, JM1
Adanichkin, N1
Kurmis, R1
Munn, Z1
Motohashi, Y1
Kemmochi, Y1
Maekawa, T1
Tadaki, H1
Sasase, T1
Tanaka, Y1
Kakehashi, A1
Yamada, T1
Ohta, T2
Mudassir, HA1
Qureshi, SA1
Azmi, MB1
Ahsan, M1
Khaloo, P1
Asadi Komeleh, S1
Alemi, H1
Mansournia, MA1
Mohammadi, A1
Yadegar, A1
Afarideh, M2
Esteghamati, S1
Nakhjavani, M2
Esteghamati, A2
Zhuang, Y1
Yin, Q1
Pinget, M1
Goldenberg, R1
Niemoeller, E1
Muehlen-Bartmer, I1
Guo, H1
Aronson, R1
Lee, JO1
Auger, C1
Park, DH1
Kang, M1
Oak, MH1
Kim, KR1
Schini-Kerth, VB1
Zenari, L1
Marangoni, A1
Bone, HG1
Lindsay, R1
McClung, MR1
Perez, AT1
Raanan, MG1
Spanheimer, RG1
He, Q1
Zhang, X1
Han, B1
Xu, J1
Tang, K1
Fu, Z1
Yin, H1
Raccah, D1
Gourdy, P1
Sagnard, L1
Ceriello, A2
Sakata, S1
Mera, Y1
Kuroki, Y1
Nashida, R1
Kakutani, M1
Tripathy, D1
Musi, N1
Gastaldelli, A3
Niture, NT1
Ansari, AA1
Naik, SR1
Sykes, AP2
O'Connor-Semmes, R2
Dobbins, R2
Dorey, DJ1
Lorimer, JD1
Walker, S2
Wilkison, WO2
Kler, L2
Kemp, GL1
Almond, SR1
Chen, YJ1
Chan, DC1
Lan, KC1
Wang, CC1
Chen, CM1
Chao, SC1
Tsai, KS1
Yang, RS1
Liu, SH1
Lecube, A1
Bueno, M1
Suárez, X1
Thakran, S1
Zhang, Q1
Morales-Tirado, V1
Steinle, JJ1
Azizi, R1
Ebadi, M1
Noshad, S1
Mousavizadeh, M1
Hayashi, A1
Takemoto, M1
Shoji, M1
Hattori, A1
Sugita, K1
Yokote, K1
Sims-Robinson, C1
Bakeman, A1
Rosko, A1
Glasser, R1
Feldman, EL1
Matsumoto, Y1
Ishii, M1
Hayashi, Y1
Miyazaki, S1
Sugita, T1
Sumiya, E1
Sekimizu, K1
Kaku, K2
Katou, M1
Igeta, M1
Ohira, T1
Sano, H1
Gliem, M1
Klotz, L1
van Rooijen, N1
Hartung, HP1
Jander, S1
Tai, CJ2
Choong, CY1
Shi, YC1
Lin, YC1
Wang, CW1
Lee, BH1
Joubert, M1
Jagu, B1
Montaigne, D1
Marechal, X1
Tesse, A1
Ayer, A1
Dollet, L1
Le May, C1
Toumaniantz, G1
Manrique, A1
Charpentier, F1
Staels, B1
Magré, J1
Cariou, B1
Prieur, X1
Okoduwa, SI1
Umar, IA1
James, DB1
Inuwa, HM1
Aoki, TJ1
White, RD1
Mizukami, H1
Wada, R1
Yonezawa, A1
Sugawara, A2
Yagihashi, S1
Hirasawa, Y2
Ohtsu, S1
Yamane, K1
Toyoshi, T2
Kyuki, K2
Sakai, T1
Feng, Y1
Nagamatsu, T1
Fujisawa, K1
Nishikawa, T1
Kukidome, D1
Imoto, K1
Yamashiro, T1
Motoshima, H1
Matsumura, T1
Araki, E1
Ihle, NT2
Lemos, R1
Schwartz, D1
Oh, J1
Halter, RJ1
Wipf, P2
Kirkpatrick, L1
Powis, G2
Miyata, T1
van Ypersele de Strihou, C1
Tanaka, S1
Origasa, H1
Kikuchi, M1
Akanuma, Y1
Makino, H1
Shimizu, I1
Murao, S1
Kondo, S1
Tabara, Y1
Fujiyama, M1
Fujii, Y1
Takada, Y1
Nakai, K1
Izumi, K1
Ohashi, J1
Kawamura, R1
Yamauchi, J1
Takata, Y1
Nishida, W1
Hashiramoto, M1
Onuma, H1
Osawa, H1
Gumieniczek, A4
Krzywdzińska, M1
Nowak, M1
Glass, LC1
Cusi, K1
Berria, R1
Petz, R1
Cersosimo, E1
Sugiura, T1
Ito, M1
Vikram, A1
Jena, G1
Naka, KK1
Pappas, K1
Papathanassiou, K1
Papamichael, ND1
Kazakos, N1
Kanioglou, C1
Makriyiannis, D1
Katsouras, CS1
Liveris, K1
Tsatsoulis, A1
Michalis, LK1
Hiuge-Shimizu, A1
Maeda, N1
Hirata, A1
Nakatsuji, H1
Nakamura, K1
Okuno, A1
Kihara, S1
Funahashi, T1
Shimomura, I1
Komsta, L1
Chehab, MR1
Oki, N1
Nonaka, S1
Ozaki, S1
Pfützner, A2
Schöndorf, T1
Tschöpe, D1
Lobmann, R1
Merke, J1
Müller, J1
Lehmann, U1
Fuchs, W1
Forst, T2
Bojková, B1
Garajová, M1
Péč, M1
Kubatka, P1
Kajo, K1
Mokáň, M1
Kassayová, M1
Orendáš, P1
Kisková, T1
Ahlersová, E1
Ahlers, I1
Plutzky, J1
Hempe, J1
Elvert, R1
Schmidts, HL1
Kramer, W1
Herling, AW1
Owczarek, B1
Pawlikowska, B1
Mourad, AA1
Heeba, GH1
Taye, A1
El-Moselhy, MA1
Shen, X1
Li, H1
Li, W1
Wu, X1
Ding, X1
Kotake, H1
Tan, MH2
Satoh, N1
Ogawa, Y1
Usui, T1
Tagami, T1
Kono, S1
Uesugi, H1
Sugiyama, H1
Yamada, K1
Shimatsu, A1
Kuzuya, H1
Nakao, K1
Roberts, AW1
Thomas, A1
Rees, A1
Evans, M1
Inaba, M1
Otani, Y1
Nishimura, K1
Takaha, N1
Okuyama, A1
Koga, M1
Azuma, J1
Kawase, I1
Kasayama, S1
Johns, D1
Widel, M1
Eckland, DJ1
Gilmore, KJ1
Tomono, S1
Uchiyama, T1
Ohyama, Y1
Göke, B1
Langenfeld, MR1
Hohberg, C1
Kann, P1
Lübben, G1
Konrad, T1
Füllert, SD1
Sachara, C1
Panchapakesan, U1
Sumual, S1
Pollock, CA1
Chen, X1
Paine-Murrieta, G1
Berggren, MI1
Baker, A1
Tate, WR1
Abraham, RT1
Kirkpatrick, DL1
Smyth, SS1
Jennings, JL1
Mori, Y1
Itoh, Y1
Obata, T1
Tajima, N1
Casolaro, A1
Pettiti, M1
Nannipieri, M1
Ciociaro, D1
Frascerra, S1
Buzzigoli, E1
Baldi, S1
Mari, A1
Ferrannini, E1
Gaikwad, AB1
Viswanad, B1
Ramarao, P1
Edlinger, M1
Ebenbichler, C1
Rettenbacher, M1
Fleischhacker, WW1
Bourassa, MG1
Berry, C1
Weinstein, SP1
Holand, A1
O'Boyle, E1
Haber, RS1
Pugazhenthi, S1
Khandelwal, RL1
Shimaya, A1
Kurosaki, E1
Nakano, R1
Hirayama, R1
Shibasaki, M1
Shikama, H1
Grinsell, JW1
Lardinois, CK1
Swislocki, A1
Gonzalez, R1
Sare, JS1
Michaels, JR1
Starich, GH1
Kadowaki, T1
Stiefelhagen, P1
Sugiyama, Y1
Shimura, Y1
Ikeda, H1

Clinical Trials (14)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
A Randomized, Double-Blind, Placebo-Controlled, Parallel-Group, Multicenter Study to Determine the Efficacy and Safety of Albiglutide When Used in Combination With Pioglitazone With or Without Metformin in Subjects With Type 2 Diabetes Mellitus[NCT00849056]Phase 3310 participants (Actual)Interventional2009-01-31Completed
A Randomized, Open-label, Parallel-group, Multicenter Study to Determine the Efficacy and Long-term Safety of Albiglutide Compared With Insulin in Subjects With Type 2 Diabetes Mellitus.[NCT00838916]Phase 3779 participants (Actual)Interventional2009-02-28Completed
A Randomized, Double-Blind, Placebo-Controlled, Parallel-Group, Multicenter Study to Determine the Efficacy and Safety of Two Dose Levels of Albiglutide Compared With Placebo in Subjects With Type 2 Diabetes Mellitus[NCT00849017]Phase 3309 participants (Actual)Interventional2009-01-31Completed
A Randomized, Double-blind, Placebo and Active-Controlled, Parallel-group, Multicenter Study to Determine the Efficacy and Safety of Albiglutide Administered in Combination With Metformin and Glimepiride Compared With Metformin Plus Glimepiride and Placeb[NCT00839527]Phase 3685 participants (Actual)Interventional2009-02-28Completed
A Randomized, Double-Blind, Placebo and Active-Controlled, Parallel-Group, Multicenter Study to Determine the Efficacy and Safety of Albiglutide When Used in Combination With Metformin Compared With Metformin Plus Sitagliptin, Metformin Plus Glimepiride, [NCT00838903]Phase 31,049 participants (Actual)Interventional2009-02-28Completed
A Randomized, Double-blind, Placebo-controlled, 2-arm Parallel-group, Multicenter Study With a 24-week Main Treatment Period and an Extension Assessing the Efficacy and Safety of AVE0010 on Top of Pioglitazone in Patients With Type 2 Diabetes Not Adequate[NCT00763815]Phase 3484 participants (Actual)Interventional2008-09-30Completed
Effects of Lixisenatide on Gastric Emptying, Glycaemia and 'Postprandial' Blood Pressure in Type 2 Diabetes and Healthy Subjects.[NCT02308254]Phase 1/Phase 230 participants (Anticipated)Interventional2013-11-30Recruiting
Multicenter, Randomized, Double Blind, Placebo-controlled, Phase II Clinical Trial to Evaluate the Safety and Efficacy of YJP-14 Capsules for the Treatment of Endothelial Dysfunction in Patients With Diabetes Mellitus[NCT01836172]Phase 2136 participants (Anticipated)Interventional2013-04-30Active, not recruiting
A Phase 4, Randomized, Double-Blind, Placebo-Controlled Study to Evaluate the Effect of Pioglitazone Compared to Placebo on Bone Metabolism in Impaired Fasting Glucose, Postmenopausal Women for One Year of Treatment[NCT00708175]Phase 4156 participants (Actual)Interventional2008-05-31Completed
A Double-blind, Randomized 12-week Study to Evaluate the Safety and Efficacy of GSK189075 Tablets vs Pioglitazone in Treatment Naive Subjects With Type 2 Diabetes Mellitus[NCT00500331]Phase 2334 participants (Actual)Interventional2007-01-23Completed
A Once-Daily Dose-Ranging Study of GSK189075 Versus Placebo In The Treatment of Type 2 Diabetes Mellitus in Treatment-Naïve Subjects[NCT00495469]Phase 2250 participants (Actual)Interventional2007-08-17Completed
Comparison of Metformin and Pioglitazone Effects on Serum YKL-40 Concentrations in Patients With Newly Diagnosed Type 2 Diabetes[NCT01963663]84 participants (Actual)Interventional2012-11-30Completed
Effects of a Pioglitazone/Metformin Fixed Combination in Comparison to Metformin in Combination With Glimepiride on Diabetic Dyslipidemia[NCT00770653]Phase 3305 participants (Actual)Interventional2007-04-30Completed
Modulation of Insulin Secretion and Insulin Sensitivity in Bangladeshi Type 2 Diabetic Subjects by an Insulin Sensitizer Pioglitazone and T2DM Association With PPARG Gene Polymorphism.[NCT01589445]Phase 477 participants (Actual)Interventional2008-11-30Completed
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

Change From Baseline (BL) in Glycosylated Hemoglobin (HbA1c) at Week 52

HbA1c is a form of hemoglobin that is measured primarily to identify the average plasma glucose concentration over a 2- to 3-month period. The BL HbA1c value is defined as the last non-missing value before the start of treatment. Change from BL was calculated as the value at Week 52 minus the value at BL. Based on analysis of covariance (ANCOVA): change = treatment + BL HbA1c + prior myocardial infarction history + age category + region + current antidiabetic therapy. The last observation carried forward (LOCF) method was used to impute missing post-BL HbA1c values; the last non-missing post-BL on-treatment measurement was used to impute the missing measurement. HbA1c values obtained after hyperglycemic rescue were treated as missing and were replaced with pre-rescue values. One Intent-to-Treat (ITT) participant (par.) had all post-BL HbA1c measurements occur after hyperglycemic rescue. This par. is included in the ITT Population counts but did not contribute to this analysis. (NCT00849056)
Timeframe: Baseline and Week 52

InterventionPercentage of HbA1c in the blood (Least Squares Mean)
Placebo + Pioglitazone With or Without Metformin-0.05
Albiglutide 30 mg + Pioglitazone With or Without Metformin-0.81

Change From Baseline in Body Weight at Week 156

The Baseline value is the last non-missing value before the start of treatment. Change from Baseline was calculated as the post-Baseline weight minus the Baseline weight. (NCT00849056)
Timeframe: Baseline and Week 156

InterventionKilograms (Mean)
Placebo + Pioglitazone With or Without Metformin1.50
Albiglutide 30 mg + Pioglitazone With or Without Metformin-0.16

Change From Baseline in Body Weight at Week 52

The Baseline value is the last non-missing value before the start of treatment. Change from Baseline was calculated as the post-Baseline weight minus the Baseline weight. The LOCF method was used to impute missing post-Baseline weight values. Weight values obtained after hyperglycemia rescue were treated as missing and replaced with prerescue values. Based on ANCOVA: change = treatment + Baseline weight + prior myocardial infarction history + age category + region + current antidiabetic therapy. (NCT00849056)
Timeframe: Baseline and Week 52

InterventionKilograms (Least Squares Mean)
Placebo + Pioglitazone With or Without Metformin0.45
Albiglutide 30 mg + Pioglitazone With or Without Metformin0.28

Change From Baseline in Fasting Plasma Glucose (FPG) at Week 156

The Baseline FPG value is the last non-missing value before the start of treatment. Change from Baseline was calculated as the post-Baseline FPG minus the Baseline FPG. (NCT00849056)
Timeframe: Baseline and Week 156

InterventionMillimoles per liter (mmol/L) (Mean)
Placebo + Pioglitazone With or Without Metformin0.03
Albiglutide 30 mg + Pioglitazone With or Without Metformin-1.26

Change From Baseline in Fasting Plasma Glucose (FPG) at Week 52

The FPG test measures blood sugar levels after the participant has not eaten (fasted) for 12 to 14 hours. The Baseline FPG value is the last non-missing value before the start of treatment. The LOCF method was used to impute missing post-Baseline FPG values. FPG values obtained after hyperglycemia rescue were treated as missing and replaced with pre-rescue values. Change from Baseline was calculated as the post-Baseline value minus the Baseline value. Based on ANCOVA: change = treatment + Baseline weight + prior myocardial infarction history + age category + region + current antidiabetic therapy. (NCT00849056)
Timeframe: Baseline and Week 52

InterventionMillimoles per liter (mmol/L) (Least Squares Mean)
Placebo + Pioglitazone With or Without Metformin0.35
Albiglutide 30 mg + Pioglitazone With or Without Metformin-1.28

Time to Hyperglycemia Rescue

Participants who experienced persistent hyperglycemia (high blood glucose) could have qualified for hyperglycemia rescue. The conditions for hyperglycemia rescue were as follows: FPG >=280 milligrams/deciliter (mg/dL) between >=Week 2 and =250 mg/dL between >=Week 4 and =8.5% and a <=0.5% reduction from Baseline between >=Week 12 and =8.5% between >=Week 24 and =8.0% between >= Week 48 and NCT00849056)
Timeframe: From the start of study medication until the end of the treatment (up to Week 156)

InterventionWeeks (Median)
Placebo + Pioglitazone With or Without Metformin52.86
Albiglutide 30 mg + Pioglitazone With or Without MetforminNA

Change From Baseline in HbA1c at Weeks 104 and 156

HbA1c is a form of hemoglobin that is measured primarily to identify the average plasma glucose concentration over a 2- to 3-month period. Baseline HbA1c value is defined as the last non-missing value before the start of treatment. Change from Baseline was calculated as the post-Baseline value minus the Baseline value. This analysis used observed HbA1c values, excluding those obtained after hyperglycemia rescue; no missing data imputation was performed. (NCT00849056)
Timeframe: Baseline and Weeks 104 and 156

,
InterventionPercentage of HbA1c in the blood (Mean)
Week 104, n= 29, 72Week 156, n=26, 54
Albiglutide 30 mg + Pioglitazone With or Without Metformin-0.92-0.87
Placebo + Pioglitazone With or Without Metformin-0.72-0.50

Number of Participants Who Achieved Clinically Meaningful HbA1c Response Levels of <6.5%, <7%, and <7.5% at Week 156

The number of participants who achieved the HbA1c treatment goal (i.e., HbA1c response levels of <6.5%, <6.5%, and <7.0% at Week 156) were assessed. (NCT00849056)
Timeframe: Week 156

,
InterventionParticipants (Number)
HbA1c <6.5%HbA1c <7%HbA1c <7.5%
Albiglutide 30 mg + Pioglitazone With or Without Metformin203244
Placebo + Pioglitazone With or Without Metformin71217

Number of Participants Who Achieved Clinically Meaningful HbA1c Response Levels of <6.5%, <7%, and <7.5% at Week 52

The number of participants who achieved the HbA1c treatment goal (i.e., HbA1c response levels of <6.5%, <6.5%, and <7.0% at Week 52) were assessed. (NCT00849056)
Timeframe: Week 52

,
InterventionParticipants (Number)
HbA1c <6.5%HbA1c <7%HbA1c <7.5%
Albiglutide 30 mg + Pioglitazone With or Without Metformin376696
Placebo + Pioglitazone With or Without Metformin82244

Change From Baseline (BL) in Glycosylated Hemoglobin (HbA1c) at Week 52

HbA1c is a form of hemoglobin that is measured primarily to identify the average plasma glucose concentration over a 2- to 3-month period. The BL HbA1c value is defined as the last non-missing value before the start of treatment. Change from BL was calculated as the value at Week 52 minus the value at BL. Based on analysis of covariance (ANCOVA): change = treatment + BL HbA1c + prior myocardial infarction history + age category + region + current antidiabetic therapy. Difference of least squares means (albiglutide - insulin glargine) is from the ANCOVA model. The last observation carried forward (LOCF) method was used to impute missing post-Baseline HbA1c values; the last non-missing post-BL on-treatment measurement was used to impute the missing measurement. HbA1c values obtained after hyperglycemic rescue were treated as missing and were replaced with pre-rescue values. (NCT00838916)
Timeframe: Baseline and Week 52

InterventionPercentage of HbA1c in the blood (Least Squares Mean)
Albiglutide 30 mg + Metformin +/- Sulfonylurea-0.67
Insulin Glargine 10 Units + Metformin +/- Sulfonylurea-0.79

Change From Baseline in Body Weight at Week 156

The Baseline value is the last non-missing value before the start of treatment. Change from Baseline was calculated as the post-Baseline weight minus the Baseline weight. (NCT00838916)
Timeframe: Baseline and Week 156

InterventionKilograms (Mean)
Albiglutide 30 mg + Metformin +/- Sulfonylurea-3.47
Insulin Glargine 10 Units + Metformin +/- Sulfonylurea0.90

Change From Baseline in Body Weight at Week 52

The Baseline value is the last non-missing value before the start of treatment. Change from Baseline was calculated as the post-Baseline weight minus the Baseline weight. The LOCF method was used to impute missing post-Baseline weight values. Weight values obtained after hyperglycemia rescue were treated as missing and replaced with prerescue values. Based on ANCOVA: change = treatment + Baseline weight + Baseline HbA1c category + prior myocardial infarction history + age category + region + current antidiabetic therapy. (NCT00838916)
Timeframe: Baseline and Week 52

InterventionKilograms (Least Squares Mean)
Albiglutide 30 mg + Metformin +/- Sulfonylurea-1.05
Insulin Glargine 10 Units + Metformin +/- Sulfonylurea1.56

Change From Baseline in Fasting Plasma Glucose (FPG) at Week 156

The FPG test measures blood sugar levels after the participant has not eaten (fasted) for 12 to 14 hours. The Baseline FPG value is the last non-missing value before the start of treatment. Change from Baseline was calculated as the post-Baseline value minus the Baseline value. (NCT00838916)
Timeframe: Baseline and Week 156

InterventionMillimoles per liter (mmol/L) (Mean)
Albiglutide 30 mg + Metformin +/- Sulfonylurea-0.83
Insulin Glargine 10 Units + Metformin +/- Sulfonylurea-2.19

Change From Baseline in Fasting Plasma Glucose (FPG) at Week 52

The FPG test measures blood sugar levels after the participant has not eaten (fasted) for 12 to 14 hours. The Baseline FPG value is the last non-missing value before the start of treatment. The LOCF method was used to impute missing post-Baseline FPG values. FPG values obtained after hyperglycemia rescue were treated as missing and replaced with pre-rescue values. Change from Baseline was calculated as the post-Baseline value minus the Baseline value. Based on ANCOVA: change = treatment + Baseline FPG + Baseline HbA1c category + prior myocardial infarction history + age category + region + current antidiabetic therapy. (NCT00838916)
Timeframe: Baseline and Week 52

InterventionMillimoles per liter (mmol/L) (Least Squares Mean)
Albiglutide 30 mg + Metformin +/- Sulfonylurea-0.87
Insulin Glargine 10 Units + Metformin +/- Sulfonylurea-2.06

Change From Baseline in Glucose Profile Measured by 24-hour Area Under Curve (AUC) at Week 52

A 24-hour glucose profile was collected at Baseline and Week 52 at a subset of sites in a subset of participants per treatment group using the continuous glucose monitoring device. Glucose measurements were obtained at 5 minute increments in the 24-hour period. The area under the curve (AUC) was determined using the trapezoidal method on the measurements obtained during the first 24 hours of continuous monitoring. This analysis used observed values excluding those obtained after hyperglycemia rescue; no missing data imputation was performed. The Baseline value is the last non-missing value before the start of treatment. (NCT00838916)
Timeframe: Baseline and Week 52

InterventionMillimoles per hour per liter (mmol.h/L) (Mean)
Albiglutide 30 mg + Metformin +/- Sulfonylurea0.457
Insulin Glargine 10 Units + Metformin +/- Sulfonylurea-1.657

Change From Baseline in HbA1c at Week 156

HbA1c is a form of hemoglobin that is measured primarily to identify the average plasma glucose concentration over a 2- to 3-month period. Baseline HbA1c value is defined as the last non-missing value before the start of treatment. Change from Baseline was calculated as the post-Baseline value minus the Baseline value. This analysis used observed HbA1c values, excluding those obtained after hyperglycemia rescue; no missing data imputation was performed. (NCT00838916)
Timeframe: Baseline and Week 156

InterventionPercentage of HbA1c in the blood (Mean)
Albiglutide 30 mg + Metformin +/- Sulfonylurea-0.83
Insulin Glargine 10 Units + Metformin +/- Sulfonylurea-1.00

Time to Hyperglycemia Rescue

Participants who experienced persistent hyperglycemia (high blood glucose) could have qualified for hyperglycemia rescue. The conditions for hyperglycemia rescue were as follows: FPG >=280 milligrams/deciliter (mg/dL) between >=Week 2 and =250 mg/dL between >=Week 4 and =8.5% and a <=0.5% reduction from Baseline between >=Week 12 and =8.5% between >=Week 24 and =8.0% between >= Week 48 and NCT00838916)
Timeframe: From the start of study medication until the end of the treatment (up to Week 156)

InterventionWeeks (Median)
Albiglutide 30 mg + Metformin +/- Sulfonylurea107.57
Insulin Glargine 10 Units + Metformin +/- SulfonylureaNA

Albiglutide Plasma Concentrations at Week 8 and Week 24

Albiglutide plasma concentration data was analyzed at Week 8 pre-dose, Week 8 post-dose, Week 24 pre-dose and Week 24 post-dose. All participants receiving albiglutide were initiated on a 30 mg weekly dosing regimen; however, beginning at Week 4, uptitration of albiglutide was allowed based on glycemic response. As such, albiglutide plasma concentrations achieved at each sampling time represent a mixed population of participants receiving either 30 mg or 50 mg weekly for various durations. (NCT00838916)
Timeframe: Weeks 8 and 24

Interventionnanograms/milliliter (ng/mL) (Mean)
Week 8, Pre-dose, n=408Week 8, Post-dose, n=398Week 24, Pre-dose, n=416Week 24, Post-dose, n=401
Albiglutide 30 mg + Metformin +/- Sulfonylurea1642.831911.352159.302748.15

Number of Participants Who Achieved Clinically Meaningful HbA1c Response Levels of <6.5%, <7%, and <7.5% at Week 156

The number of participants who achieved the HbA1c treatment goal (i.e., HbA1c response levels of <6.5%, <7%, and <7.5% at Week 156) were assessed. (NCT00838916)
Timeframe: Week 156

,
InterventionParticipants (Number)
HbA1c <6.5%HbA1c <7%HbA1c <7.5%
Albiglutide 30 mg + Metformin +/- Sulfonylurea335985
Insulin Glargine 10 Units + Metformin +/- Sulfonylurea184671

Number of Participants Who Achieved Clinically Meaningful HbA1c Response Levels of <6.5%, <7%, and <7.5% at Week 52

The number of participants who achieved the HbA1c treatment goal (i.e., HbA1c response levels of <6.5%, <7%, and <7.5% at Week 52) were assessed. (NCT00838916)
Timeframe: Week 52

,
InterventionParticipants (Number)
HbA1c <6.5%HbA1c <7%HbA1c <7.5%
Albiglutide 30 mg + Metformin +/- Sulfonylurea54156268
Insulin Glargine 10 Units + Metformin +/- Sulfonylurea2578135

Change From Baseline (BL) in Glycosylated Hemoglobin (HbA1c) at Week 52

Glycated hemoglobin (HbA1c) is a form of hemoglobin that is measured primarily to identify the average plasma glucose concentration over a 2- to 3-month period. The BL HbA1c is defined as the last non-missing value before the start of treatment. Change from BL was calculated as the value at Week 52 minus the value at BL. The analysis was performed using an Analysis of Covariance (ANCOVA) model with treatment group, region, history of prior myocardial infarction (yes versus no), and age category (<65 years versus ≥65 years) as factors and Baseline HbA1c as a continuous covariate. The last observation carried forward (LOCF) method was used to impute missing post-BL HbA1c values; the last non-missing post-BL on-treatment measurement was used to impute the missing measurement. HbA1c values obtained after hyperglycemic rescue were treated as missing and were replaced with pre-rescue values. (NCT00849017)
Timeframe: Baseline and Week 52

InterventionPercentage of HbA1c in the blood (Least Squares Mean)
Placebo0.15
Albiglutide 30 mg-0.70
Albiglutide 50 mg-0.89

Change From Baseline in Body Weight at Week 156

The Baseline value is the last non-missing value before the start of treatment. Change from Baseline was calculated as the post-Baseline weight minus the Baseline weight. (NCT00849017)
Timeframe: Baseline and Week 156

InterventionKilograms (Mean)
Placebo-2.91
Albiglutide 30 mg-1.32
Albiglutide 50 mg-2.24

Change From Baseline in Body Weight at Week 52

The Baseline value is the last non-missing value before the start of treatment. Change from Baseline was calculated as the post-Baseline weight minus the Baseline weight. The LOCF method was used to impute missing post-Baseline weight values. Weight values obtained after hyperglycemia rescue were treated as missing and replaced with prerescue values. Based on ANCOVA: change = treatment + Baseline weight + prior myocardial infarction history + age category + region + current antidiabetic therapy. (NCT00849017)
Timeframe: Baseline and Week 52

InterventionKilograms (Least Squares Mean)
Placebo-0.66
Albiglutide 30 mg-0.39
Albiglutide 50 mg-0.86

Change From Baseline in Fasting Plasma Glucose (FPG) at Week 156

The Baseline FPG value is the last non-missing value before the start of treatment. Change from Baseline was calculated as the post-Baseline FPG minus the Baseline FPG. (NCT00849017)
Timeframe: Baseline and Week 156

InterventionMillimoles per liter (mmol/L) (Mean)
Placebo-0.23
Albiglutide 30 mg-1.31
Albiglutide 50 mg-1.83

Change From Baseline in Fasting Plasma Glucose (FPG) at Week 52

The FPG test measures blood sugar levels after the participant has not eaten (fasted) for 12 to 14 hours. The Baseline FPG value is the last non-missing value before the start of treatment. The LOCF method was used to impute missing post-Baseline FPG values. FPG values obtained after hyperglycemia rescue were treated as missing and replaced with pre-rescue values. Change from Baseline was calculated as the post-Baseline value minus the Baseline value. Based on ANCOVA: change = treatment + Baseline weight + prior myocardial infarction history + age category + region + current antidiabetic therapy. (NCT00849017)
Timeframe: Baseline and Week 52

InterventionMillimoles per liter (mmol/L) (Least Squares Mean)
Placebo1.00
Albiglutide 30 mg-0.88
Albiglutide 50 mg-1.38

Change From Baseline in Postprandial Blood Glucose Profile Parameter- 4 Hour Blood Glucose AUC

Changes from Baseline at Week 52 in postprandial parameters after a mixed-meal (MM) tolerance test were analyzed. Post prandial blood glucose parameter analyzed was: 4 hour blood glucose area under urve AUC The AUC was determined using the trapezoidal method using measurements until 4 hours following the meal. The standardized AUC is the total AUC divided by elapsed time. Those parameters were analyzed analogous to the primary endpoint using an ANCOVA model with treatment group as a factor, and corresponding Baseline postprandial profile as a continuous covariate. This analysis used observed values excluding those obtained after hyperglycemia rescue; no missing data imputation was performed. (NCT00849017)
Timeframe: Baseline and Week 52

InterventionNanomoles/Liter (nmol/L) (Least Squares Mean)
Placebo-0.51
Albiglutide 30 mg-1.74
Albiglutide 50 mg-2.05

Change From Baseline in Postprandial Blood Glucose Profile Parameter-4 Hour C-peptide AUC

Changes from Baseline at Week 52 in postprandial parameters after a mixed-meal (MM) tolerance test were analyzed. Post prandial blood glucose parameter analyzed was 4 hour c-peptide AUC. The AUC was determined using the trapezoidal method using measurements until 4 hours following the meal. The standardized AUC is the total AUC divided by elapsed time. Those parameters were analyzed analogous to the primary endpoint using an ANCOVA model with treatment group as a factor, and corresponding Baseline postprandial profile as a continuous covariate. This analysis used observed values excluding those obtained after hyperglycemia rescue; no missing data imputation was performed. (NCT00849017)
Timeframe: Baseline and Week 52

InterventionNanomoles/Liter (nmol/L) (Least Squares Mean)
Placebo0.05
Albiglutide 30 mg Weekly0.03
Albiglutide 50 mg Weekly0.08

Time to Hyperglycemia Rescue

Participants who experienced persistent hyperglycemia (high blood glucose) could have qualified for hyperglycemia rescue. The conditions for hyperglycemia rescue were as follows: FPG >=280 milligrams/deciliter (mg/dL) between >=Week 2 and =250 mg/dL between >=Week 4 and =8.5% and a <=0.5% reduction from Baseline between >=Week 12 and =8.5% between >=Week 24 and =8.0% between >= Week 48 and NCT00849017)
Timeframe: From the start of study medication until the end of the treatment (up to Week 156)

InterventionWeeks (Median)
Placebo49.71
Albiglutide 30 mg118.43
Albiglutide 50 mgNA

Albiglutide Plasma Concentration at Weeks 8 and 24

Albiglutide plasma concentration data was analyzed at Week 8 pre-dose, Week 8 post dose, Week 24 pre-dose and Week 24 post-dose. All participants who received albiglutide were initiated on a 30mg weekly dosing regimen; however, beginning at Week 12, participants in the albiglutide 50 mg treatment group were uptitrated to receive albiglutide 50 mg for the remainder of the study. (NCT00849017)
Timeframe: Weeks 8 and 24

,
Interventionnanograms/milliliter (ng/mL) (Mean)
Week 8 Pre-dose, n=85, 85Week 8 Post-dose, n=87, 80Week 24 Pre-dose, n=79, 74Week 24 Post-dose, n=81, 72
Albiglutide 30 mg1582190019122289
Albiglutide 50 mg1433175930603484

Change From Baseline in HbA1c at Weeks 104 and 156

HbA1c is a form of hemoglobin that is measured primarily to identify the average plasma glucose concentration over a 2- to 3-month period. Baseline HbA1c value is defined as the last non-missing value before the start of treatment. Change from Baseline was calculated as the post-Baseline value minus the Baseline value. This analysis used observed HbA1c values, excluding those obtained after hyperglycemia rescue; no missing data imputation was performed. (NCT00849017)
Timeframe: Baseline and Weeks 104 and 156

,,
InterventionPercentage of HbA1c in the blood (Mean)
Week 104, n=21, 39, 42Week 156, n=14, 30, 32
Albiglutide 30 mg-0.93-0.96
Albiglutide 50 mg-1.18-1.07
Placebo-0.40-0.61

Change From Baseline in Postprandial Blood Glucose Profile Parameters-4 Hour Insulin AUC and 4 Hour Proinsulin AUC

Changes from Baseline at Week 52 in postprandial parameters after a mixed-meal (MM) tolerance test were analyzed. Post prandial blood glucose parameters analyzed were: 4-hour insulin AUC (4 hr Ins AUC), and 4-hour proinsulin AUC (4 hr pro-Ins AUC). The AUC was determined using the trapezoidal method using measurements until 4 hours following the meal. The standardized AUC is the total AUC divided by elapsed time. Those parameters were analyzed analogous to the primary endpoint using an ANCOVA model with treatment group as a factor, and corresponding Baseline postprandial profile as a continuous covariate. This analysis used observed values excluding those obtained after hyperglycemia rescue; no missing data imputation was performed. (NCT00849017)
Timeframe: Baseline and Week 52

,,
Interventionpicomoles/Liter (pmol/L) (Least Squares Mean)
4hr Ins AUC4hr Pro-Ins AUC
Albiglutide 30 mg2.91.9
Albiglutide 50 mg39.9-10.7
Placebo49.21.0

Number of Participants Who Achieved Clinically Meaningful HbA1c Response Levels of <6.5%, <7%, and <7.5% at Week 156

The number of participants who acheieved the HbA1c treatment goal (i.e., HbA1c response levels of <6.5%, <7%, and <7.5% at Week 156) were assessed. (NCT00849017)
Timeframe: Week 156

,,
InterventionParticipants (Number)
Week 156, HbA1c <6.5%Week 156, HbA1c <7.0%Week 156, HbA1c <7.5%
Albiglutide 30 mg101824
Albiglutide 50 mg111929
Placebo6813

Number of Participants Who Achieved Clinically Meaningful HbA1c Response Levels of <6.5%, <7%, and <7.5% at Week 52

The number of participants who acheieved the HbA1c treatment goal (i.e., HbA1c response levels of <6.5%, <7%, and <7.5% at Week 52) were assessed. (NCT00849017)
Timeframe: Week 52

,,
InterventionParticipants (Number)
Week 52, HbA1c <6.5%Week 52, HbA1c <7.0%Week 52, HbA1c <7.5%
Albiglutide 30 mg254959
Albiglutide 50 mg243962
Placebo102134

Change From Baseline (BL) in Glycosylated Hemoglobin (HbA1c) at Week 52

HbA1c is a form of hemoglobin that is measured primarily to identify the average plasma glucose concentration over a 2- to 3-month period. The BL HbA1c value is defined as the last non-missing value before the start of treatment. Change from BL was calculated as the value at Week 52 minus the value at BL. Based on analysis of covariance (ANCOVA): change = treatment + BL HbA1c + prior myocardial infarction history + age category + region. The last observation carried forward (LOCF) method was used to impute missing post-BL HbA1c values; the last non-missing post-BL on-treatment measurement was used to impute the missing measurement. HbA1c values obtained after hyperglycemic rescue were treated as missing and were replaced with pre-rescue values. Nine par. with post-BL values obtained >14 days after the last dose or after hyperglycemic rescue were included in the analysis population but were not analyzed for this endpoint. (NCT00839527)
Timeframe: Baseline and Week 52

InterventionPercentage of HbA1c in the blood (Least Squares Mean)
Placebo + Metformin + Glimepiride0.33
Pioglitazone + Metformin + Glimepiride-0.80
Albiglutide + Metformin + Glimepiride-0.55

Change From Baseline in Body Weight at Week 52

The Baseline value is the last non-missing value before the start of treatment. Change from Baseline was calculated as the post-Baseline weight minus the Baseline weight. The LOCF method was used to impute missing post-Baseline weight values. Weight values obtained after hyperglycemia rescue were treated as missing and replaced with pre-rescue values. Based on ANCOVA: change = treatment + Baseline weight + Baseline HbA1c category + prior myocardial infarction history + age category + region. (NCT00839527)
Timeframe: Baseline and Week 52

InterventionKilograms (Least Squares Mean)
Placebo + Metformin + Glimepiride-0.40
Pioglitazone + Metformin + Glimepiride4.43
Albiglutide + Metformin + Glimepiride-0.42

Change From Baseline in Fasting Plasma Glucose (FPG) at Week 52

The FPG test measures blood sugar levels after the participant has not eaten (fasted) for 12 to 14 hours. The Baseline FPG value is the last non-missing value before the start of treatment. The LOCF method was used to impute missing post-Baseline FPG values. FPG values obtained after hyperglycemia rescue were treated as missing and replaced with pre-rescue values. Change from Baseline was calculated as the post-Baseline value minus the Baseline value. Based on ANCOVA: change = treatment + Baseline FPG + Baseline HbA1c category + prior myocardial infarction history + age category + region. (NCT00839527)
Timeframe: Baseline and Week 52

InterventionMillimoles per liter (mmol/L) (Least Squares Mean)
Placebo + Metformin + Glimepiride0.64
Pioglitazone + Metformin + Glimepiride-1.74
Albiglutide + Metformin + Glimepiride-0.69

Time to Hyperglycemia Rescue

Participants who experienced persistent hyperglycemia (high blood glucose) could have qualified for hyperglycemia rescue. The conditions for hyperglycemia rescue were as follows: FPG >=280 milligrams/deciliter (mg/dL) between >=Week 2 and =250 mg/dL between >=Week 4 and =8.5% and a <=0.5% reduction from Baseline between >=Week 12 and =8.5% between >=Week 24 and =8.0% between >= Week 48 and NCT00839527)
Timeframe: From the start of study medication until the end of the treatment (up to Week 156)

InterventionWeeks (Median)
Placebo + Metformin + Glimepiride49.57
Pioglitazone + Metformin + GlimepirideNA
Albiglutide + Metformin + Glimepiride137.71

Change From Baseline in Body Weight at Week 104 and Week 156

The Baseline value is the last non-missing value before the start of treatment. Change from Baseline was calculated as the post-Baseline weight minus the Baseline weight. This analysis used observed body weight values excluding those obtained after hyperglycemia rescue; no missing data imputation was performed. (NCT00839527)
Timeframe: Baseline, Week 104, and Week 156

,,
InterventionKilograms (Mean)
Week 104, n=12, 130, 104Week 156, n=9, 90, 71
Albiglutide + Metformin + Glimepiride-0.90-1.53
Pioglitazone + Metformin + Glimepiride6.286.52
Placebo + Metformin + Glimepiride-2.16-4.47

Change From Baseline in FPG at Week 104 and Week 156

The FPG test measures blood sugar levels after the participant has not eaten (fasted) for 12 to 14 hours. The Baseline FPG value is the last non-missing value before the start of treatment. Change from Baseline was calculated as the post-Baseline value minus the Baseline value. This analysis used observed FPG values excluding those obtained after hyperglycemia rescue; no missing data imputation was performed. (NCT00839527)
Timeframe: Baseline, Week 104, and Week 156

,,
InterventionMillimoles per liter (mmol/L) (Mean)
Week 104, n=12, 128, 103Week 156, n=9, 88, 71
Albiglutide + Metformin + Glimepiride-0.99-0.88
Pioglitazone + Metformin + Glimepiride-1.98-1.94
Placebo + Metformin + Glimepiride0.43-0.50

Change From Baseline in HbA1c at Week 104 and Week 156

HbA1c is a form of hemoglobin that is measured primarily to identify the average plasma glucose concentration over a 2- to 3-month period. The Baseline HbA1c value is defined as the last non-missing value before the start of treatment. Change from Baseline was calculated as the post-Baseline value minus the Baseline value. This analysis used observed HbA1c values, excluding those obtained after hyperglycemia rescue; no missing data imputation was performed. (NCT00839527)
Timeframe: Baseline, Week 104, and Week 156

,,
InterventionPercentage of HbA1c in the blood (Mean)
Week 104, n=12, 130, 104Week 156, n=9, 89, 71
Albiglutide + Metformin + Glimepiride-0.76-0.46
Pioglitazone + Metformin + Glimepiride-1.09-0.97
Placebo + Metformin + Glimepiride-0.32-0.10

Number of Participants Who Achieved Clinically Meaningful HbA1c Response Levels of <6.5%, <7%, and <7.5% at Week 156

The number of participants who acheieved the HbA1c treatment goal (i.e., HbA1c response levels of <6.5%, <7%, and <7.5% at Week 156) was assessed. (NCT00839527)
Timeframe: Week 156

,,
InterventionParticipants (Number)
HbA1c <6.5%HbA1c <7.0%HbA1c <7.5%
Albiglutide + Metformin + Glimepiride162645
Pioglitazone + Metformin + Glimepiride234468
Placebo + Metformin + Glimepiride135

Number of Participants Who Achieved Clinically Meaningful HbA1c Response Levels of <6.5%, <7%, and <7.5% at Week 52

The number of participants who acheieved the HbA1c treatment goal (i.e., HbA1c response levels of <6.5%, <7%, and <7.5% at Week 52) was assessed. Values were carried forward for participants who were rescued or discontinued from active treatment before Week 52. (NCT00839527)
Timeframe: Week 52

,,
InterventionParticipants (Number)
HbA1c <6.5%HbA1c <7.0%HbA1c <7.5%
Albiglutide + Metformin + Glimepiride2779126
Pioglitazone + Metformin + Glimepiride3794150
Placebo + Metformin + Glimepiride41019

Change From Baseline (BL) in Glycosylated Hemoglobin (HbA1c) at Week 104

HbA1c is a form of hemoglobin that is measured primarily to identify the average plasma glucose concentration over a 2- to 3-month period. The BL HbA1c value is defined as the last non-missing value before the start of treatment. Change from BL was calculated as the value at Week 104 minus the value at BL. Based on analysis of covariance (ANCOVA): change = treatment + BL HbA1c + prior myocardial infarction history + age category + region. Difference of least squares means (albiglutide - placebo, albiglutide - sitagliptin, albiglutide - glimepiride) is from the ANCOVA model. The last observation carried forward (LOCF) method was used to impute missing post-Baseline HbA1c values; the last non-missing post-BL on-treatment measurement was used to impute the missing measurement. HbA1c values obtained after hyperglycemic rescue were treated as missing and were replaced with pre-rescue values. (NCT00838903)
Timeframe: Baseline and Week 104

InterventionPercentage of HbA1c in the blood (Least Squares Mean)
Placebo Plus Metformin0.27
Sitagliptin 100 mg Plus Metformin-0.28
Glimepiride 2 mg Plus Metformin-0.36
Albiglutide 30 mg Plus Metformin-0.63

Change From Baseline in Body Weight at Week 104

The Baseline value is the last non-missing value before the start of treatment. Change from Baseline was calculated as the post-Baseline weight minus the Baseline weight. The LOCF method was used to impute missing post-Baseline weight values. Weight values obtained after hyperglycemia rescue were treated as missing and replaced with prerescue values. Based on ANCOVA: change = treatment + Baseline weight + Baseline HbA1c category + prior myocardial infarction history + age category + region. (NCT00838903)
Timeframe: Baseline and Week 104

InterventionKilograms (Least Squares Mean)
Placebo Plus Metformin-1.00
Sitagliptin 100 mg Plus Metformin-0.86
Glimepiride 2 mg Plus Metformin1.17
Albiglutide 30 mg Plus Metformin-1.21

Change From Baseline in Body Weight at Week 156

The Baseline value is the last non-missing value before the start of treatment. Change from Baseline was calculated as the post-Baseline weight minus the Baseline weight. This analysis used observed body weight values excluding those obtained after hyperglycemia rescue; no missing data imputation was performed. (NCT00838903)
Timeframe: Baseline and Week 156

InterventionKilograms (Mean)
Placebo Plus Metformin-3.61
Sitagliptin 100 mg Plus Metformin-2.05
Glimepiride 2 mg Plus Metformin0.98
Albiglutide 30 mg Plus Metformin-2.31

Change From Baseline in Fasting Plasma Glucose (FPG) at Week 104

The FPG test measures blood sugar levels after the participant has not eaten (fasted) for 12 to 14 hours. The Baseline FPG value is the last non-missing value before the start of treatment. The LOCF method was used to impute missing post-Baseline FPG values. FPG values obtained after hyperglycemia rescue were treated as missing and replaced with pre-rescue values. Change from Baseline was calculated as the post-Baseline value minus the Baseline value. Based on ANCOVA: change = treatment + Baseline FPG + Baseline HbA1c category + prior myocardial infarction history + age category + region. (NCT00838903)
Timeframe: Baseline and Week 104

InterventionMillimoles per liter (mmol/L) (Least Squares Mean)
Placebo Plus Metformin0.55
Sitagliptin 100 mg Plus Metformin-0.12
Glimepiride 2 mg Plus Metformin-0.41
Albiglutide 30 mg Plus Metformin-0.98

Change From Baseline in FPG at Week 156

The FPG test measures blood sugar levels after the participant has not eaten (fasted) for 12 to 14 hours. The Baseline FPG value is the last non-missing value before the start of treatment. Change from Baseline was calculated as the post-Baseline value minus the Baseline value. This analysis used observed FPG values excluding those obtained after hyperglycemia rescue; no missing data imputation was performed. (NCT00838903)
Timeframe: Baseline and Week 156

InterventionMillimoles per liter (mmol/L) (Mean)
Placebo Plus Metformin-0.11
Sitagliptin 100 mg Plus Metformin-0.50
Glimepiride 2 mg Plus Metformin-0.71
Albiglutide 30 mg Plus Metformin-1.30

Change From Baseline in HbA1c at Week 156

HbA1c is a form of hemoglobin that is measured primarily to identify the average plasma glucose concentration over a 2- to 3-month period. Baseline HbA1c value is defined as the last non-missing value before the start of treatment. Change from Baseline was calculated as the post-Baseline value minus the Baseline value. This analysis used observed HbA1c values, excluding those obtained after hyperglycemia rescue; no missing data imputation was performed . (NCT00838903)
Timeframe: Baseline and Week 156

InterventionPercentage of HbA1c in the blood (Mean)
Placebo Plus Metformin-0.46
Sitagliptin 100 mg Plus Metformin-0.56
Glimepiride 2 mg Plus Metformin-0.59
Albiglutide 30 mg Plus Metformin-0.88

Time to Hyperglycemia Rescue

Participants who experienced persistent hyperglycemia (high blood glucose) could have qualified for hyperglycemia rescue.The conditions for hyperglycemic rescue were as follows: FPG >=280 milligrams/deciliter (mg/dL) between >=Week 2 and =250 mg/dL between >=Week 4 and =8.5% and a <=0.5% reduction from Baseline between >=Week 12 and =8.5% between >=Week 24 and =8.0% between >= Week 48 and NCT00838903)
Timeframe: From the start of study medication until the end of the treatment (up to Week 156)

InterventionWeeks (Median)
Placebo Plus Metformin67.71
Sitagliptin 100 mg Plus MetforminNA
Glimepiride 2 mg Plus MetforminNA
Albiglutide 30 mg Plus MetforminNA

Number of Participants Who Achieved Clinically Meaningful HbA1c Response Levels of <6.5%, <7%, and <7.5% at Week 104

The number of participants who achieved the HbA1c treatment goal (i.e., HbA1c response levels of <6.5%, <7%, and <7.5% at Week 52) were assessed. (NCT00838903)
Timeframe: Week 104

,,,
InterventionParticipants (Number)
HbA1c <6.5%HbA1c <7.0%HbA1c <7.5%
Albiglutide 30 mg Plus Metformin50113172
Glimepiride 2 mg Plus Metformin4094147
Placebo Plus Metformin71527
Sitagliptin 100 mg Plus Metformin4594132

Number of Participants Who Achieved Clinically Meaningful HbA1c Response Levels of <6.5%, <7%, and <7.5% at Week 156

The number of participants who achieved the HbA1c treatment goal (i.e., HbA1c response levels of <6.5%, <7%, and <7.5% at Week 156) were assessed. (NCT00838903)
Timeframe: Week 156

,,,
InterventionParticipants (Number)
HbA1c <6.5%HbA1c <7.0%HbA1c <7.5%
Albiglutide 30 mg Plus Metformin316990
Glimepiride 2 mg Plus Metformin154469
Placebo Plus Metformin4713
Sitagliptin 100 mg Plus Metformin234469

Absolute Change From Baseline in Glycosylated Hemoglobin (HbA1c) at Week 24

Absolute change = HbA1c value at Week 24 minus HbA1c value at baseline. The on-treatment period for this efficacy variable is time from the first dose of study drug and up to 3 days after the last dose of study drug, on or before Visit 12 (Week 24) or Day 169 if Visit 12 is not available, and before the introduction of rescue therapy. For a patient to be included in mITT population, both baseline and at least 1 post baseline assessment for at least 1 efficacy variable, were required. (NCT00763815)
Timeframe: Baseline, Week 24

Interventionpercentage of hemoglobin (Least Squares Mean)
Placebo-0.34
Lixisenatide-0.90

Change From Baseline in Beta-cell Function Assessed by Homeostasis Model Assessment for Beta-cell Function (HOMA-beta) at Week 24

Beta cell function was assessed by HOMA-beta. HOMA-beta (% of normal beta cells function) = (20 multiplied by fasting plasma insulin [micro unit per milliliter]) divided by (fasting plasma glucose [mmol/L] minus 3.5). Change was calculated by subtracting baseline value from Week 24 value. The on-treatment period for this efficacy variable is time from the first dose of study drug and up to 1 day after the last dose of study drug, on or before Visit 12 (Week 24) or Day 169 if Visit 12 is not available, and before the introduction of rescue therapy. For a patient to be included in mITT population, both baseline and at least 1 post baseline assessment for at least 1 efficacy variable, were required. (NCT00763815)
Timeframe: Baseline, Week 24

Intervention% of normal beta cells function (Least Squares Mean)
Placebo6.98
Lixisenatide6.72

Change From Baseline in Body Weight at Week 24

Change was calculated by subtracting baseline value from Week 24 value. The on-treatment period for this efficacy variable is time from the first dose of study drug and up to 3 days after the last dose of study drug, on or before Visit 12 (Week 24) or Day 169 if Visit 12 is not available, and before the introduction of rescue therapy. For a patient to be included in mITT population, both baseline and at least 1 post baseline assessment for at least 1 efficacy variable, were required. (NCT00763815)
Timeframe: Baseline, Week 24

Interventionkilogram (Least Squares Mean)
Placebo0.21
Lixisenatide-0.21

Change From Baseline in Fasting Plasma Glucose (FPG) at Week 24

Change was calculated by subtracting baseline value from Week 24 value. The on-treatment period for this efficacy variable is time from the first dose of study drug and up to 1 day after the last dose of study drug, on or before Visit 12 (Week 24) or Day 169 if Visit 12 is not available, and before the introduction of rescue therapy. For a patient to be included in mITT population, both baseline and at least 1 post baseline assessment for at least 1 efficacy variable, were required. (NCT00763815)
Timeframe: Baseline, Week 24

Interventionmmol/L (Least Squares Mean)
Placebo-0.32
Lixisenatide-1.16

Change From Baseline in Fasting Plasma Insulin (FPI) at Week 24

Change was calculated by subtracting baseline value from Week 24 value. The on-treatment period for this efficacy variable is time from the first dose of study drug and up to 1 day after the last dose of study drug, on or before Visit 12 (Week 24) or Day 169 if Visit 12 is not available, and before the introduction of rescue therapy. For a patient to be included in mITT population, both baseline and at least 1 post baseline assessment for at least 1 efficacy variable, were required. (NCT00763815)
Timeframe: Baseline, Week 24

Interventionpmol/L (Least Squares Mean)
Placebo-1.01
Lixisenatide-10.36

Percentage of Patients Requiring Rescue Therapy During Main 24-Week Period

Routine fasting self-monitored plasma glucose (SMPG) and central laboratory FPG (and HbA1c after week 12) values were used to determine the requirement of rescue medication. If fasting SMPG value exceeded the specified limit for 3 consecutive days, the central laboratory FPG (and HbA1c after week 12) were performed. Threshold values - from baseline to Week 8: fasting SMPG/FPG >270 milligram/deciliter (mg/dL) (15.0 mmol/L), from Week 8 to Week 12: fasting SMPG/FPG >240 mg/dL (13.3 mmol/L), and from Week 12 to Week 24: fasting SMPG/FPG >200 mg/dL (11.1 mmol/L) or HbA1c >8.5%. For a patient to be included in mITT population, both baseline and at least 1 post baseline assessment for at least 1 efficacy variable, were required. (NCT00763815)
Timeframe: Baseline up to Week 24

Interventionpercentage of participants (Number)
Placebo11.3
Lixisenatide3.8

Percentage of Patients With at Least 5% Weight Loss From Baseline at Week 24

The on-treatment period for this efficacy variable is time from the first dose of study drug and up to 3 days after the last dose of study drug, on or before Visit 12 (Week 24) or Day 169 if Visit 12 is not available, and before the introduction of rescue therapy. For a patient to be included in mITT population, both baseline and at least 1 post baseline assessment for at least 1 efficacy variable, were required. (NCT00763815)
Timeframe: Baseline, Week 24

Interventionpercentage of participants (Number)
Placebo5.1
Lixisenatide9.2

Percentage of Patients With Glycosylated Hemoglobin (HbA1c) Level Less Than 7% at Week 24

The on-treatment period for this efficacy variable is the time from the first dose of study drug up to 3 days after the last dose of study drug or up to the introduction of rescue therapy, whichever is the earliest. For a patient to be included in mITT population, both baseline and at least 1 post baseline assessment for at least 1 efficacy variable, were required. (NCT00763815)
Timeframe: Week 24

Interventionpercentage of participants (Number)
Placebo26.4
Lixisenatide52.3

Percentage of Patients With HbA1c Level Less Than or Equal to 6.5% at Week 24

The on-treatment period for this efficacy variable is the time from the first dose of study drug up to 3 days after the last dose of study drug or up to the introduction of rescue therapy, whichever is the earliest. For a patient to be included in mITT population, both baseline and at least 1 post baseline assessment for at least 1 efficacy variable, were required. (NCT00763815)
Timeframe: Week 24

Interventionpercentage of participants (Number)
Placebo10.1
Lixisenatide28.9

Number of Patients With Symptomatic Hypoglycemia and Severe Symptomatic Hypoglycemia

Symptomatic hypoglycemia was an event with clinical symptoms that were considered to result from a hypoglycemic episode with an accompanying plasma glucose less than 60 mg/dL (3.3 mmol/L) or associated with prompt recovery after oral carbohydrate, intravenous glucose, or glucagon administration if no plasma glucose measurement was available. Severe symptomatic hypoglycemia was symptomatic hypoglycemia event in which the patient required the assistance of another person and was associated with either a plasma glucose level below 36 mg/dL (2.0 mmol/L) or prompt recovery after oral carbohydrate, intravenous glucose, or glucagon administration, if no plasma glucose measurement was available. (NCT00763815)
Timeframe: First dose of study drug up to 3 days after the last dose administration, for up to 132 weeks

,
Interventionparticipants (Number)
Symptomatic HypoglycemiaSevere Symptomatic Hypoglycemia
Lixisenatide230
Placebo70

Number of Participants With Fracture

Number of participants with confirmed (through an adjudication process) fractures during the study. Circumstances surrounding the fracture, available X-ray and other diagnostic results and healing status were collected for the adjudication process. (NCT00708175)
Timeframe: Up to 18 months.

Interventionparticipants (Number)
Pioglitazone1
Placebo3

Percent Change From Baseline to Month 12 in Bone Mineral Density in the Total Proximal Femur by Dual-Energy-Ray Absorptiometry (DXA)

The change in bone mineral density in the total proximal femur at month 12 relative to baseline. DXA is a means of measuring BMD through x-ray. (NCT00708175)
Timeframe: Baseline and Month 12.

Interventionpercent (Least Squares Mean)
Pioglitazone-0.69
Placebo-0.14

Percent Change From Month 12 to Month 18 in Bone Mineral Density in the Total Proximal Femur by DXA

The change in bone mineral density in the total proximal femur at month 18 relative to month 12. DXA is a means of measuring BMD through x-ray. (NCT00708175)
Timeframe: Month 12 and Month 18.

Interventionpercent (Least Squares Mean)
Pioglitazone-0.14
Placebo0.04

Change in Fasting Plasma Glucose (FPG)

The change between the fasting plasma glucose value collected at each time frame indicated. (NCT00708175)
Timeframe: Baseline and Month 12; Month 12 and Month 18.

,
Interventionmg/dL (Least Squares Mean)
Baseline to Month 12 (n=57; n=61)Month 12 to Month 18 (n=54; n=57)
Pioglitazone-2.80.4
Placebo6.0-1.0

Number of Participants Who Converted to Type 2 Diabetes Mellitus (T2DM)

Participants were considered to have converted to T2DM if there were ≥2 consecutive post-Baseline FPG measurements ≥126 mg/dL. Participants meeting criteria were tabulated and summarized by Study Period (Treatment and Follow-up). Conversion to T2DM during Treatment Period occurred if either both of the consecutive post-Baseline high FPG values, or the first of the 2 consecutive high values occurred on or before the first day off study drug. Conversion to T2DM occurred during the Follow-up Period if both consecutive high values occurred after at least 1 day after the Treatment Period. (NCT00708175)
Timeframe: Up to 18 months.

,
Interventionparticipants (Number)
Double-Blind Period (n=76; n=75)Follow-up Period (n=63; n=59)
Pioglitazone10
Placebo71

Change From Baseline (Week 0) in Glycosylated Hemoglobin (HbA1c) (%) at Week 12

Fasted blood samples for HbA1c were collected at Baseline and Week 12. Participants were required to fast for at least 8 hours prior to laboratory samples and were told not to take the morning dose of study medication on these visit days and to refrain from eating until instructed to do so by study personnel in the clinic. When the participant had not fasted, the participant was rescheduled to return to the clinic to have a fasted sample taken. Baseline was Week 0. Change from Baseline was calculated by subtracting Baseline values from post-Baseline values. Only those participants with a value at Baseline and at Week 12 (after Last Observation Carried Forward [LOCF]) were used for this analysis. Adjusted mean is presented as least square mean. (NCT00500331)
Timeframe: Baseline (Week 0) and Week 12

InterventionPercentage of hemoglobin (Least Squares Mean)
Placebo-0.31
GSK189075 50 mg-1.04
GSK189075 100 mg-0.96
GSK189075 250 mg-1.05
GSK189075 500 mg-1.21
GSK189075 1000 mg-1.38
Pioglitazone 30 mg-1.07

Change From Baseline in 24-hour Percent of Filtered Glucose Excreted in Urine

A 24-hour urine collection was obtained from all participants at Baseline (Week 0) and Week 12 to measure glucose. Participants were provided with urine collection bottles and cooler prior to these visits and instructed that the urine collections must be kept cold and dropped off at the clinic prior to or at the scheduled visits. Site staff queried participants to determine whether the sample represented a full 24-hour collection. The total volume and the sample date and time were recorded. The entire 24-hour urine collection was well mixed in one container and a urine aliquot obtained. Samples were assayed for glucose. The 24-hour collections were used to derive 24-hour urine glucose excretion corrected for filtered load. Baseline was Week 0. Change from Baseline was calculated by subtracting Baseline values from post-Baseline values. (NCT00500331)
Timeframe: Baseline (Week 0) and Week 12 (24-hour urine collection)

InterventionPercentage of filtered glucose molecules (Mean)
Placebo-1.09
GSK189075 50 mg27.96
GSK189075 100 mg40.43
GSK189075 250 mg38.98
GSK189075 500 mg42.41
GSK189075 1000 mg52.39
Pioglitazone 30 mg-0.99

Change From Baseline in C-peptide AUC During a 2-hr OGTT

"Post-prandial assessments of C-peptide were performed at Baseline (Week 0) and at Week 12 using a 2-hour OGTT in a subgroup of participants at selected sites who agreed to participate. Participants were required to fast for at least 8 hours prior to the test. Seventy-five (75) g of standard oral glucose solution was administered 15 minutes after the morning administration of study medication (Week 12) and in the place of breakfast at Week 0 (i.e., at Week 0 the OGTT was completed prior to administration of study medication). Time 0 started when the participants drank the glucose solution. Blood samples were collected at the following times relative to the administration of oral glucose: -30 min (pre-glucose), -20 min (pre-glucose), 20 min, 30 min, 1 hour, 1.5 hour and 2 hour post glucose administration. Baseline was Week 0. Change from Baseline was calculated by subtracting Baseline values from post-Baseline values." (NCT00500331)
Timeframe: Baseline (Week 0) and Week 12 (0 to 2 hour OGTT)

InterventionNanomol*hour per Liter (nmol*hr/L) (Mean)
Placebo-0.140
GSK189075 50 mg0.654
GSK189075 100 mg-0.156
GSK189075 250 mg-0.026
GSK189075 500 mg-0.476
GSK189075 1000 mg-0.175
Pioglitazone 30 mg-0.239

Change From Baseline in Insulin AUC During a 2-hour OGTT

"Post-prandial assessments of insulin were performed at Baseline (Week 0) and at Week 12 using a 2-hour OGTT in a subgroup of participants at selected sites who agreed to participate. Participants were required to fast for at least 8 hours prior to the test. Seventy-five (75) g of standard oral glucose solution was administered 15 minutes after the morning administration of study medication (Week 12) and in the place of breakfast at Week 0 (i.e., at Week 0 the OGTT was completed prior to administration of study medication). Time 0 started when the participants drank the glucose solution. Blood samples were collected at the following times relative to the administration of oral glucose: -30 min (pre-glucose), -20 min (pre-glucose), 20 min, 30 min, 1 hour, 1.5 hour and 2 hour post glucose administration. Baseline was Week 0. Change from Baseline was calculated by subtracting Baseline values from post-Baseline values." (NCT00500331)
Timeframe: Baseline (Week 0) and Week 12 (0 to 2-hour OGTT)

InterventionPicomol*hour per Liter (pmol*hr/L) (Mean)
Placebo-5.3
GSK189075 50 mg162.4
GSK189075 100 mg-70.9
GSK189075 250 mg66.6
GSK189075 500 mg-173.9
GSK189075 1000 mg-97.8
Pioglitazone 30 mg10.0

Change From Baseline in Plasma Glucose Area Under the Curve (AUC) During a 2-hour Oral Glucose Tolerance Test (OGTT)

"Post-prandial assessments of glucose were performed at Baseline (Week 0) and at Week 12 using a 2-hour OGTT in a subgroup of participants at selected sites who agreed to participate. Participants were required to fast for at least 8 hours prior to the test. Seventy-five (75) g of standard oral glucose solution was administered 15 minutes after the morning administration of study medication (Week 12) and in the place of breakfast at Week 0 (i.e., at Week 0 the OGTT was completed prior to administration of study medication). Time 0 started when the participants drank the glucose solution. Blood samples were collected at the following times relative to the administration of oral glucose: -30 min (pre-glucose), -20 min (pre-glucose), 20 min, 30 min, 1 hour, 1.5 hour and 2 hour post glucose administration. Baseline was Week 0. Change from Baseline was calculated by subtracting Baseline values from post-Baseline values." (NCT00500331)
Timeframe: Baseline (Week 0) and Week 12 (0 to 2 hour OGTT)

InterventionMillimol*hour per Liter (mmol*hr/L) (Mean)
Placebo-0.90
GSK189075 50 mg-6.31
GSK189075 100 mg-6.71
GSK189075 250 mg-7.69
GSK189075 500 mg-6.06
GSK189075 1000 mg-7.59
Pioglitazone 30 mg-6.55

Change From Baseline to Week 12 in Body Weight

Weight of participants was measured from Baseline (Week 0) to Week 12 and recorded in the case report form (CRF). Baseline was Week 0. Change from Baseline was calculated by subtracting Baseline values from post-Baseline values. (NCT00500331)
Timeframe: Baseline (Week 0) to Week 12

InterventionKilograms (Mean)
Placebo-0.49
GSK189075 50 mg-1.78
GSK189075 100 mg-2.41
GSK189075 250 mg-2.38
GSK189075 500 mg-3.52
GSK189075 1000 mg-4.00
Pioglitazone 30 mg0.96

Change From Baseline to Week 12 in Fasting Insulin

Fasted blood samples for insulin were collected up to Week 12. Participants were required to fast for at least 8 hours prior to laboratory samples and were told not to take the morning dose of study medication on these visit days and to refrain from eating until instructed to do so by study personnel in the clinic. When the participant had not fasted, the participant was rescheduled to return to the clinic to have a fasted sample taken. Baseline was Week 0. Change from Baseline was calculated by subtracting Baseline values from post-Baseline values. (NCT00500331)
Timeframe: Baseline (Week 0) to Week 12

InterventionPicomol per Liter (pmol/L) (Mean)
Placebo-30.6
GSK189075 50 mg0.3
GSK189075 100 mg-20.7
GSK189075 250 mg-9.7
GSK189075 500 mg-25.8
GSK189075 1000 mg-15.1
Pioglitazone 30 mg-2.1

Change From Baseline to Week 12 in Fructosamine

Fasted blood samples for fructosamine were collected up to Week 12. Participants were required to fast for at least 8 hours prior to laboratory samples and were told not to take the morning dose of study medication on these visit days and to refrain from eating until instructed to do so by study personnel in the clinic. When the participant had not fasted, the participant was rescheduled to return to the clinic to have a fasted sample taken. Baseline was Week 0. Change from Baseline was calculated by subtracting Baseline values from post-Baseline values. (NCT00500331)
Timeframe: Baseline (Week 0) to Week 12

InterventionMicromol per Liter (mcmol/L) (Mean)
Placebo5.7
GSK189075 50 mg-33.8
GSK189075 100 mg-35.7
GSK189075 250 mg-38.9
GSK189075 500 mg-41.9
GSK189075 1000 mg-55.2
Pioglitazone 30 mg-34.7

Change From Baseline to Week 12 in Waist Circumference

Waist circumference of participants was measured from Baseline (Week 0) to Week 12 and recorded in the CRF. Baseline was Week 0. Change from Baseline was calculated by subtracting Baseline values from post-Baseline values. (NCT00500331)
Timeframe: Baseline (Week 0) to Week 12

InterventionCentimeters (Mean)
Placebo-0.7
GSK189075 50 mg-1.2
GSK189075 100 mg-2.0
GSK189075 250 mg-2.2
GSK189075 500 mg-2.6
GSK189075 1000 mg-2.4
Pioglitazone 30 mg1.3

Number of Participants With On-therapy Hypoglycemia

Hypoglycemia is low blood glucose or low blood sugar. Hypoglycemic events were collected separately and reported separately from AE, including supplemental data which were not collected for AE. However, any hypoglycemic event which met the criteria for a SAE was included in the SAE summaries. The number of participants in each group that experienced a hypoglycemic event was summarized by frequency of the events. (NCT00500331)
Timeframe: Up to 14 weeks

InterventionParticipants (Count of Participants)
Placebo1
GSK189075 50 mg1
GSK189075 100 mg0
GSK189075 250 mg0
GSK189075 500 mg1
GSK189075 1000 mg0
Pioglitazone 30 mg0

Change From Baseline in HbA1c (%) at Weeks 4 and 8

Fasted blood samples for HbA1c were collected at Baseline and Weeks 4 and 8. Participants were required to fast for at least 8 hours prior to laboratory samples and were told not to take the morning dose of study medication on these visit days and to refrain from eating until instructed to do so by study personnel in the clinic. When the participant had not fasted, the participant was rescheduled to return to the clinic to have a fasted sample taken. Baseline was Week 0. Change from Baseline was calculated by subtracting Baseline values from post-Baseline values. (NCT00500331)
Timeframe: Baseline (Week 0) and Week 4 and Week 8

,,,,,,
InterventionPercentage of hemoglobin (Mean)
Week 4Week 8
GSK189075 100 mg-0.69-0.96
GSK189075 1000 mg-0.84-1.28
GSK189075 250 mg-0.64-0.99
GSK189075 50 mg-0.77-0.98
GSK189075 500 mg-0.83-1.07
Pioglitazone 30 mg-0.39-0.88
Placebo-0.30-0.41

Change From Baseline to Week 12 in Fasting Plasma Glucose (FPG) at Weeks 4, 8 and 12

Fasted blood samples for FPG were collected up to Week 12. Participants were required to fast for at least 8 hours prior to laboratory samples and were told not to take the morning dose of study medication on these visit days and to refrain from eating until instructed to do so by study personnel in the clinic. When the participant had not fasted, the participant was rescheduled to return to the clinic to have a fasted sample taken. Baseline was Week 0. Change from Baseline was calculated by subtracting Baseline values from post-Baseline values. (NCT00500331)
Timeframe: Baseline (Week 0) and Week 4, Week 8 and Week 12

,,,,,,
InterventionMillimoles per Liter (mmol/L) (Mean)
Week 4Week 8Week 12
GSK189075 100 mg-1.43-1.30-1.63
GSK189075 1000 mg-2.48-2.78-2.76
GSK189075 250 mg-1.49-1.76-1.80
GSK189075 50 mg-0.56-0.91-0.89
GSK189075 500 mg-1.90-2.14-2.07
Pioglitazone 30 mg-1.26-1.73-1.71
Placebo-0.49-0.62-0.51

Number of Participants at Week 12 With: HbA1c <= 6.5%, HbA1c <7.0%; FPG <7 Mmo/L, FPG <7.8 mmol/L; FPG <5.5 mmol/L; a Decrease From Baseline of HbA1c >= 0.7%; a Decrease From Baseline of FPG ≥1.7 mmol/L

Fasted blood samples for HbA1c were collected at Week 12. Participants were required to fast for at least 8 hours prior to laboratory samples and were told not to take the morning dose of study medication on these visit days and to refrain from eating until instructed to do so by study personnel in the clinic. When the participant had not fasted, the participant was rescheduled to return to the clinic to have a fasted sample taken. Number of participants at Week 12 with: HbA1c <= 6.5%, HbA1c <7.0%; FPG <7 mmo/L (126 milligram/deciliter [mg/dL]), FPG <7.8 mmol/L (140 mg/dL); FPG <5.5 mmol/L (100 mg/dL); a decrease from Baseline of HbA1c >= 0.7%; a decrease from Baseline of FPG ≥1.7 mmol/L (30 mg/dL) are presented. (NCT00500331)
Timeframe: Week 12

,,,,,,
InterventionParticipants (Count of Participants)
HbA1c <= 6.5%HbA1c <7.0%FPG <7 mmo/LFPG <7.8 mmol/LFPG <5.5 mmol/LDecrease from Baseline of HbA1c >= 0.7%Decrease from Baseline of FPG ≥1.7 mmol/L
GSK189075 100 mg818202622719
GSK189075 1000 mg1729223433930
GSK189075 250 mg1122182753321
GSK189075 50 mg1020162443315
GSK189075 500 mg1728223343624
Pioglitazone 30 mg821213122823
Placebo394130168

Number of Participants With Change From Baseline in Standard Laboratory Parameters of Potential Clinical Concern

Participants were instructed to fast for at least 8 hours prior to all study visits for the collection of laboratory samples. An additional fasting blood sample (serum and plasma) was drawn at Week 0, Week 4, Week 6 and Week 12 or at early withdrawal (up to 14 weeks) and kept in long-term storage for future testing of biomarkers for diabetes and complications of the disease. Baseline was Week 0. Change from Baseline was calculated by subtracting Baseline values from post-Baseline values. (NCT00500331)
Timeframe: Up to 14 weeks

,,,,,,
InterventionParticipants (Count of Participants)
Low HemoglobinLow Hematocrit
GSK189075 100 mg00
GSK189075 1000 mg00
GSK189075 250 mg00
GSK189075 50 mg00
GSK189075 500 mg00
Pioglitazone 30 mg00
Placebo11

Number of Participants With Change From Baseline Vital Signs of Potential Clinical Concern

Vital signs included heart rate and blood pressure. Heart rate and blood pressure were taken before blood draws were performed. Participants were asked to refrain from smoking for at least 30 minutes prior to vital sign measurements. Heart rate and blood pressure was measured pre-dose in duplicate at the specified visits, after the participant had been lying quietly for 5 minutes, and then in duplicate 3 minutes after standing up. Heart rate was measured at the same time as blood pressure using the standardized blood pressure equipment that was provided. Baseline was Week 0. Change from Baseline was calculated by subtracting Baseline values from post-Baseline values. (NCT00500331)
Timeframe: Up to 14 weeks

,,,,,,
InterventionParticipants (Count of Participants)
High SBPLow SBPHigh DBPLow DBPHigh heart rateLow heart rate
GSK189075 100 mg210200
GSK189075 1000 mg122101
GSK189075 250 mg020000
GSK189075 50 mg000110
GSK189075 500 mg020001
Pioglitazone 30 mg000300
Placebo301000

Number of Participants With Electrocardiogram (ECG) Values of Potential Clinical Concern

Full 12-lead ECGs were recorded at screening, Baseline (Week 0), Week 4, Week 12 or early withdrawal, and Week 14 (Follow-up) using an ECG machine that automatically calculated the heart rate and measured the PR, QRS, QT and corrected QT (QTc) intervals. All 12-lead ECGs were read locally by the Investigator or his/her designate and were forwarded electronically to the central reader for interpretation. If the QTc was >500 milliseconds (msec) on the locally read ECG recording, an additional 2 ECG recordings at 10 minute intervals were made at that visit. If the average QTc for the 3 recordings was >500 msec, the participant was withdrawn from the study. (NCT00500331)
Timeframe: Up to Early withdrawal (Between Week 12 and Week 14)

,,,,,,
InterventionParticipants (Count of Participants)
PR interval > 300 msecQRS Duration > 200 msecQTc(Bazett) > 500 msecQTc(Fridericia) > 500 msec
GSK189075 100 mg0000
GSK189075 1000 mg0000
GSK189075 250 mg0000
GSK189075 50 mg0000
GSK189075 500 mg0000
Pioglitazone 30 mg0000
Placebo0000

Number of Participants With On-therapy Adverse Events (AE) and Serious Adverse Events (SAE)

AE is any untoward medical occurrence in a participant or clinical investigation participant, temporally associated with the use of a medicinal product, whether or not considered related to the medicinal product. An AE can therefore be any unfavorable and unintended sign (including an abnormal laboratory finding), symptom, or disease (new or exacerbated) temporally associated with the use of a medicinal product. For marketed medicinal products, this also includes failure to produce expected benefits (i.e., lack of efficacy), abuse or misuse. SAE is any untoward medical occurrence that, at any dose results in death, is life-threatening, requires hospitalization or prolongation of existing hospitalization, results in disability/incapacity, or is a congenital anomaly/birth defect or is medically significant. (NCT00500331)
Timeframe: Up to 12 weeks

,,,,,,
InterventionParticipants (Count of Participants)
AESAE
GSK189075 100 mg170
GSK189075 1000 mg220
GSK189075 250 mg190
GSK189075 50 mg180
GSK189075 500 mg180
Pioglitazone 30 mg220
Placebo180

Percent Change From Baseline in Lipid Parameters at Weeks 4, 8 and 12(Triglycerides [TG], Total Cholesterol [TC], Low-density Lipoprotein Cholesterol [LDL-C] and High-density Lipoprotein Cholesterol [HDL-C])

Fasted samples for TC, LDL-C, HDL-C and TG were collected at Week 12. When the participant had not fasted, the participant was rescheduled to return to the clinic to have a fasted sample taken. Baseline was Week 0. Change from Baseline was calculated by subtracting Baseline values from post-Baseline values. Percent Change based on log-transformed data: 100*(exponentiated(mean change on log scale)-1) (NCT00500331)
Timeframe: Baseline (Week 0) and Week 4, Week 8 and Week 12

,,,,,,
InterventionPercent change (Median)
TG: Week 4TG: Week 8TG: Week 12TC: Week 4TC: Week 8TC: Week 12LDL-C: Week 4LDL-C: Week 8LDL-C: Week 12HDL-C: Week 4HDL-C: Week 8HDL-C: Week 12
GSK189075 100 mg6.320.5910.921.623.645.450.373.623.573.695.004.96
GSK189075 1000 mg-4.62-7.30-9.972.390.002.777.024.4414.890.000.004.27
GSK189075 250 mg-13.42-10.01-4.714.134.493.976.918.963.935.133.096.70
GSK189075 50 mg-3.45-9.09-10.911.853.493.390.838.676.695.436.205.56
GSK189075 500 mg-13.04-13.35-15.284.435.319.8210.037.5711.435.697.1411.93
Pioglitazone 30mg-7.22-0.79-7.192.291.06-2.050.00-2.241.189.188.2010.00
Placebo-8.35-1.663.320.470.824.750.823.173.17-1.970.000.00

Mean Change From Baseline in Hemoglobin A1c (Glycosylated Hemoglobin) (HbA1c) at Week 12

The blood samples were collected at Baseline, Week 4, Week 8 and at Week 12 (or early withdrawal). Baseline was defined as the period immediately preceding treatment with study medication (Week 0). For participants with missing Baseline assessment, the last pre-therapy value prior to the Baseline visit was used as the Baseline value. Change from Baseline was the value at Week 12 minus Baseline value. The primary analysis was performed on the Intent-to-Treat (ITT) Population with Last observation carried forward (LOCF). Adjusted mean is presented as least square (LS) mean. (NCT00495469)
Timeframe: Baseline (Week 0) and at Week 12

InterventionPercentage (Least Squares Mean)
Placebo-0.19
GSK189075 100 mg QD-0.53
GSK189075 250 mg QD-0.75
GSK189075 500 mg QD-0.53
GSK189075 1000 mg QD-0.85
GSK189075 250 mg BID-0.78
Pioglitazone 30 mg QD-0.38

Mean Change From Baseline to Week 12 in Body Weight

Body weight measurement was taken at Baseline, Week 2, Week 4, Week 8, Week 12 and at Week 14 (follow up). Baseline was defined as the period immediately preceding treatment with study medication (Week 0). For participants with missing Baseline assessment, the last pre-therapy value prior to the Baseline visit was used as the Baseline value. Change from Baseline was the value at Week 12 minus Baseline value. Adjusted mean is presented as LS mean. (NCT00495469)
Timeframe: Baseline (Week 0) and Week 12

Interventionkilograms (Least Squares Mean)
Placebo-1.03
GSK189075 100 mg QD-1.52
GSK189075 250 mg QD-2.54
GSK189075 500 mg QD-2.46
GSK189075 1000 mg QD-2.47
GSK189075 250 mg BID-2.11
Pioglitazone 30 mg QD0.00

Mean Change From Baseline to Week 12 in Fasting Plasma Glucose (FPG)

The samples were collected at Baseline, Week 2, Week 4, Week 8, Week 12 and Week 14 (follow up). Participants were asked to be on fast for at least 8 hours prior to each study visits and collection of lab samples. Baseline was defined as the period immediately preceding treatment with study medication (Week 0). For participants with missing Baseline assessment, the last pre-therapy value prior to the Baseline visit was used as the Baseline value. Change from Baseline was the value at Week 12 minus Baseline value. The primary analysis was performed on the ITT Population with LOCF. Adjusted mean is presented as LS mean. (NCT00495469)
Timeframe: Baseline (Week 0) and at Week 12

Interventionmillimoles per liter (mmol/L) (Least Squares Mean)
Placebo-0.50
GSK189075 100 mg QD-1.35
GSK189075 250 mg QD-1.56
GSK189075 500 mg QD-1.13
GSK189075 1000 mg QD-1.45
GSK189075 250 mg BID-1.63
Pioglitazone 30 mg QD-1.01

Mean Change From Baseline to Week 12 in Fructosamine (Corrected)

The blood samples were collected at Baseline, Week 2, Week 4, Week 8, Week 12 and Week 14 (follow up). Participants were asked to be on fast for at least 8 hours prior to each study visits and collection of lab samples. Baseline was defined as the period immediately preceding treatment with study medication (Week 0). For participants with missing Baseline assessment, the last pre-therapy value prior to the Baseline visit was used as the Baseline value. Change from Baseline was the value at Week 12 minus Baseline value. The primary analysis was performed on the ITT Population with LOCF. Adjusted mean is presented as LS mean. (NCT00495469)
Timeframe: Baseline (Week 0) and at Week 12

Interventionmicromoles per liter (µmol/L) (Least Squares Mean)
Placebo-1.4
GSK189075 100 mg QD-25.5
GSK189075 250 mg QD-36.3
GSK189075 500 mg QD-31.2
GSK189075 1000 mg QD-37.9
GSK189075 250 mg BID-30.9
Pioglitazone 30 mg QD-15.2

Mean Change From Baseline to Week 12 in High Density Lipoprotein Cholesterol (HDL-c)

Blood samples were collected at Baseline and at Week 12 (or early withdrawal). Baseline was defined as the period immediately preceding treatment with study medication (Week 0). For participants with missing Baseline assessment, the last pre-therapy value prior to the Baseline visit was used as the Baseline value. Change from Baseline was the value at Week 12 minus Baseline value. Adjusted mean is presented as LS mean. (NCT00495469)
Timeframe: Baseline (Week 0) and Week 12

Interventionmmol/L (Least Squares Mean)
Placebo-0.02
GSK189075 100 mg QD0.00
GSK189075 250 mg QD0.02
GSK189075 500 mg QD0.06
GSK189075 1000 mg QD0.05
GSK189075 250 mg BID0.04
Pioglitazone 30 mg QD0.09

Mean Change From Baseline to Week 12 in LDL-c/HDL-c Ratio

Blood samples were collected at Baseline and at Week 12 (or early withdrawal). Baseline was defined as the period immediately preceding treatment with study medication (Week 0). For participants with missing Baseline assessment, the last pre-therapy value prior to the Baseline visit was used as the Baseline value. Change from Baseline was the value at Week 12 minus Baseline value. Adjusted mean is presented as LS mean. (NCT00495469)
Timeframe: Baseline (Week 0) and Week 12

InterventionRatio (Least Squares Mean)
Placebo0.06
GSK189075 100 mg QD-0.19
GSK189075 250 mg QD-0.06
GSK189075 500 mg QD-0.13
GSK189075 1000 mg QD-0.07
GSK189075 250 mg BID0.10
Pioglitazone 30 mg QD-0.07

Mean Change From Baseline to Week 12 in Low Density Lipoprotein Cholesterol (LDL-c)

Blood samples were collected at Baseline and at Week 12 (or early withdrawal). Baseline was defined as the period immediately preceding treatment with study medication (Week 0). For participants with missing Baseline assessment, the last pre-therapy value prior to the Baseline visit was used as the Baseline value. Change from Baseline was the value at Week 12 minus Baseline value. Adjusted mean is presented as LS mean. (NCT00495469)
Timeframe: Baseline (Week 0) and Week 12

Interventionmmol/L (Least Squares Mean)
Placebo-0.02
GSK189075 100 mg QD-0.17
GSK189075 250 mg QD-0.03
GSK189075 500 mg QD0.08
GSK189075 1000 mg QD-0.04
GSK189075 250 mg BID0.23
Pioglitazone 30 mg QD0.07

Mean Change From Baseline to Week 12 in Total Cholesterol

Samples were collected at Baseline and at Week 12 (or early withdrawal). Baseline was defined as the period immediately preceding treatment with study medication (Week 0). For participants with missing Baseline assessment, the last pre-therapy value prior to the Baseline visit was used as the Baseline value. Change from Baseline was the value at Week 12 minus Baseline value. Adjusted mean is presented as LS mean. (NCT00495469)
Timeframe: Baseline (Week 0) and at Week 12

Interventionmmol/L (Least Squares Mean)
Placebo-0.03
GSK189075 100 mg QD-0.08
GSK189075 250 mg QD-0.12
GSK189075 500 mg QD0.10
GSK189075 1000 mg QD-0.02
GSK189075 250 mg BID0.22
Pioglitazone 30 mg QD0.00

Mean Change From Baseline to Week 12 in Total Cholesterol/HDL-c Ratio

Blood samples were collected at Baseline and at Week 12 (or early withdrawal). Baseline was defined as the period immediately preceding treatment with study medication (Week 0). For participants with missing Baseline assessment, the last pre-therapy value prior to the Baseline visit was used as the Baseline value. Change from Baseline was the value at Week 12 minus Baseline value. Adjusted mean is presented as LS mean. (NCT00495469)
Timeframe: Baseline (Week 0) and Week 12

InterventionRatio (Least Squares Mean)
Placebo0.14
GSK189075 100 mg QD-0.05
GSK189075 250 mg QD-0.20
GSK189075 500 mg QD-0.22
GSK189075 1000 mg QD-0.09
GSK189075 250 mg BID0.01
Pioglitazone 30 mg QD-0.26

Mean Change From Baseline to Week 12 in Triglycerides

Samples were collected at Baseline and at Week 12 (or early withdrawal). Baseline was defined as the period immediately preceding treatment with study medication (Week 0). For participants with missing Baseline assessment, the last pre-therapy value prior to the Baseline visit was used as the Baseline value. Change from Baseline was the value at Week 12 minus Baseline value. Adjusted mean is presented as LS mean. (NCT00495469)
Timeframe: Baseline (Week 0) and at Week 12

Interventionmmol/L (Least Squares Mean)
Placebo-0.01
GSK189075 100 mg QD0.19
GSK189075 250 mg QD-0.32
GSK189075 500 mg QD-0.16
GSK189075 1000 mg QD-0.05
GSK189075 250 mg BID-0.18
Pioglitazone 30 mg QD-0.37

Number of Participants With Abnormal Electrocardiogram (ECG) Findings at Any Time Post-Baseline

Full 12-lead ECGs were recorded at Randomization (Week 0), Week 4, and Week 12 or early withdrawal. If the QTc was >500 milliseconds on the locally read ECG recording, an additional 2 ECG recordings at 10 minute intervals were made at that visit. If the average QTc for the 3 recordings was >500 milliseconds, the participant was withdrawn from the study. (NCT00495469)
Timeframe: Up to Week 12

InterventionParticipants (Count of Participants)
Placebo9
GSK189075 100 mg QD12
GSK189075 250 mg QD11
GSK189075 500 mg QD7
GSK189075 1000 mg QD14
GSK189075 250 mg BID7
Pioglitazone 30 mg QD8

Number of Participants With On-therapy Hypoglycemia

Participants were provided with a Daily Glucose Monitoring Log to record glucose meter readings and to record symptoms of hypoglycemia. A separate electronic case report form (eCRF) page was provided to capture events of hypoglycemia. (NCT00495469)
Timeframe: Up to Week 12

InterventionParticipants (Count of Participants)
Placebo0
GSK189075 100 mg QD1
GSK189075 250 mg QD0
GSK189075 500 mg QD2
GSK189075 1000 mg QD1
GSK189075 250 mg BID1
Pioglitazone 30 mg QD0

Mean Change From Baseline in HbA1c at Weeks 4 and 8

The blood samples were collected at Baseline, Week 4, Week 8 and at Week 12 (or early withdrawal). Baseline was defined as the period immediately preceding treatment with study medication (Week 0). For participants with missing Baseline assessment, the last pre-therapy value prior to the Baseline visit was used as the Baseline value. Change from Baseline was the value at Week 4 and 8 minus Baseline value. The primary analysis was performed on the ITT Population with LOCF. (NCT00495469)
Timeframe: Baseline (Week 0) and at Week 4 nad 8

,,,,,,
InterventionPercentage (Mean)
Week 4Week 8
GSK189075 100 mg QD-0.37-0.42
GSK189075 1000 mg QD-0.45-0.77
GSK189075 250 mg BID-0.31-0.67
GSK189075 250 mg QD-0.57-0.76
GSK189075 500 mg QD-0.40-0.60
Pioglitazone 30 mg QD-0.07-0.25
Placebo-0.18-0.08

Number of Participants Who Were Fasting Plasma Glucose (FPG) Responders at Week 12

Differences between treatment groups in the proportion of participants who achieved FPG targets of <7.0 millimoles per liter (mmol/L) (126 milligrams per deciliter [mg/dL]) and <7.8 mmol/L (140 mg/dL) at Week 12 in the ITT population with LOCF were assessed based on a logistic regression model with terms included for treatment and Baseline FPG. The proportion of participants who achieved the target of <5.5 mmol/L (100 mg/dL) at Week 12 within each treatment group were summarized only. Differences between treatment groups in the proportion of participants who achieved a clinically meaningful decreases from Baseline in FPG (1.7 mmol/L [>=30 mg/dL]) at Week 12 were assessed in the same manner. (NCT00495469)
Timeframe: Week 12

,,,,,,
InterventionParticipants (Count of Participants)
Responders (<7 mmol/L)Responders (<7.8 mmol/L)Responders (reduction >=1.7 mmol/L)
GSK189075 100 mg QD10209
GSK189075 1000 mg QD122114
GSK189075 250 mg BID142219
GSK189075 250 mg QD141913
GSK189075 500 mg QD111711
Pioglitazone 30 mg QD131517
Placebo6135

Number of Participants Who Were HbA1c Responders at Week 12

Differences between treatment groups in the proportion of participants who achieved HbA1c targets of <=6.5% and <7% at Week 12 in the ITT population with LOCF were assessed based on a logistic regression model with terms included for treatment and Baseline HbA1c. Differences between treatment groups in the proportion of participants who achieved a clinically meaningful decreases from Baseline in HbA1c (>=0.7%) at Week 12 were assessed in the same manner. (NCT00495469)
Timeframe: Week 12

,,,,,,
InterventionParticipants (Count of Participants)
Responders (<=6.5%)Responders (<7%)Responders (reduction>=0.7%)
GSK189075 100 mg QD51113
GSK189075 1000 mg QD71318
GSK189075 250 mg BID61521
GSK189075 250 mg QD41218
GSK189075 500 mg QD41013
Pioglitazone 30 mg QD41113
Placebo379

Number of Participants With Abnormal Chemistry Value of PCI at Any Time on Therapy

Chemistry parameters: Albumin, Alkaline phosphatase, Alanine animotransferase, Aspartate aminotransferase, Total billirubin, Calcium, Carbon dioxide/Bicarbonate, Glucose, Potassium, Sodium, Phosphorus and Total protein were assessed for abnormal PCI values. Participants were instructed to fast for at least 8 hours prior to all study visits for the collection of laboratory samples. Samples were collected at Baseline, Week 2, Week 4, Week 8, Week 12 and at Week 14 (follow up). (NCT00495469)
Timeframe: Up to Week 12

,,,,,,
InterventionParticipants (Count of Participants)
Albumin, lowAlkaline phosphatase, highAlanine aminotransferase, highAspartate aminotransferase, highTotal bilirubin, highCalcium, lowcarbon dioxide content/Bicarbonate, lowGlucose, highPotassium, highPotassium, lowSodium, highPhosphorus, highTotal protein, highTotal protein, low
GSK189075 100 mg QD11111120011011
GSK189075 1000 mg QD00001010200000
GSK189075 250 mg BID00001210100000
GSK189075 250 mg QD00000300100000
GSK189075 500 mg QD00000010000100
Pioglitazone 30 mg QD00002000000000
Placebo00001001000000

Number of Participants With Abnormal Hematology Value of PCI at Any Time on Therapy

Hematology parameters: Hemoglobin, Hematocrit, Platelet count and White blood cells were assessed for abnormal PCI values. Participants were instructed to fast for at least 8 hours prior to all study visits for the collection of laboratory samples. Samples were collected at Baseline, Week 2, Week 4, Week 8, Week 12 and at Week 14 (follow up). (NCT00495469)
Timeframe: Up to Week 12

,,,,,,
InterventionParticipants (Count of Participants)
Hemoglobin, highHemoglobin, lowHematocrit, highHematocrit, lowPlatelet count, highPlatelet count, lowWhite blood cell count, low
GSK189075 100 mg QD0002000
GSK189075 1000 mg QD2020011
GSK189075 250 mg BID0000200
GSK189075 250 mg QD0000000
GSK189075 500 mg QD1010000
Pioglitazone 30 mg QD0100001
Placebo1211010

Number of Participants With Any On-therapy Adverse Events (AEs) and Serious Adverse Events (SAEs)

AE was defined as any untoward medical occurrence in a clinical investigation participant, temporally associated with the use of a medicinal product, whether or not considered related to the medicinal product. SAE was defined as any untoward event resulting in death, life threatening, requires hospitalization or prolongation of existing hospitalization, results in disability/incapacity, congenital anomaly/birth defect or any other situation according to medical or scientific judgment. (NCT00495469)
Timeframe: Up to Week 12

,,,,,,
InterventionParticipants (Count of Participants)
Any AEsAny SAEs
GSK189075 100 mg QD151
GSK189075 1000 mg QD210
GSK189075 250 mg BID201
GSK189075 250 mg QD200
GSK189075 500 mg QD110
Pioglitazone 30 mg QD120
Placebo80

Number of Participants With Vital Signs of Potential Clinical Importance (PCI) at Any Time on Therapy

Systolic blood pressure (SBP), diastolic blood pressure (DBP), heart rate (HR) were measured pre-dose in duplicate, after the participant has been lying quietly for 5 minutes, and then in duplicate 3 minutes after standing up. Participants were asked to refrain from smoking for at least 30 minutes prior to vital sign measurements. (NCT00495469)
Timeframe: Up to Week 12

,,,,,,
InterventionParticipants (Count of Participants)
SBP, supine, lowDBP, supine, highHR, supine, lowOrthostatic SBP, standing, lowOrthostatic DBP, standing, lowOrthostatic HR, standing, high
GSK189075 100 mg QD200015
GSK189075 1000 mg QD201005
GSK189075 250 mg BID210117
GSK189075 250 mg QD000336
GSK189075 500 mg QD300425
Pioglitazone 30 mg QD301015
Placebo101114

Change From Baseline in Adiponectin.

The change between Adiponectin collected at week 24 or final visit and Adiponectin collected at baseline. (NCT00770653)
Timeframe: Baseline and Week 24.

Interventionμg/mL (Least Squares Mean)
Pioglitazone 15 mg and Metformin 850 mg BID6.79
Glimepiride 2 mg and Metformin 850 mg BID0.72

Change From Baseline in Diastolic Blood Pressure.

The change between Diastolic Blood Pressure measured at week 24 or final visit and Diastolic Blood Pressure measured at baseline. (NCT00770653)
Timeframe: Baseline and Week 24.

InterventionmmHg (Least Squares Mean)
Pioglitazone 15 mg and Metformin 850 mg BID-1.3
Glimepiride 2 mg and Metformin 850 mg BID-0.1

Change From Baseline in E-Selectin.

The change between the value of E-Selectin collected at week 24 or final visit and E-Selectin collected at baseline. (NCT00770653)
Timeframe: Baseline and Week 24.

Interventionng/mL (Least Squares Mean)
Pioglitazone 15 mg and Metformin 850 mg BID-3.7
Glimepiride 2 mg and Metformin 850 mg BID-0.5

Change From Baseline in Erythrocyte Deformability (0.30%).

The change between the 0.30 percent value of Erythrocyte (Red Blood Cell) Deformability collected at week 24 or final visit and Erythrocyte Deformability collected at baseline. (NCT00770653)
Timeframe: Baseline and Week 24.

Interventionpercent (Mean)
Pioglitazone 15 mg and Metformin 850 mg BID1.3
Glimepiride 2 mg and Metformin 850 mg BID-0.4

Change From Baseline in Erythrocyte Deformability (0.60%)

The change between the 0.60 percent value of Erythrocyte (Red Blood Cell) Deformability collected at week 24 or final visit and Erythrocyte Deformability collected at baseline. (NCT00770653)
Timeframe: Baseline and Week 24.

Interventionpercent (Mean)
Pioglitazone 15 mg and Metformin 850 mg BID2.4
Glimepiride 2 mg and Metformin 850 mg BID-0.5

Change From Baseline in Erythrocyte Deformability (1.20).

The change between the 1.20 percent value of Erythrocyte (Red Blood Cell) Deformability collected at week 24 or final visit and Erythrocyte Deformability collected at baseline. (NCT00770653)
Timeframe: Baseline and Week 24.

Interventionpercent (Mean)
Pioglitazone 15 mg and Metformin 850 mg BID3.2
Glimepiride 2 mg and Metformin 850 mg BID-1.1

Change From Baseline in Erythrocyte Deformability (12.00).

The change between the 12.00 percent value of Erythrocyte (Red Blood Cell) Deformability collected at week 24 or final visit and Erythrocyte Deformability collected at baseline. (NCT00770653)
Timeframe: Baseline and Week 24.

Interventionpercent (Mean)
Pioglitazone 15 mg and Metformin 850 mg BID2.7
Glimepiride 2 mg and Metformin 850 mg BID-1.3

Change From Baseline in Erythrocyte Deformability (3.00).

The change between the 3.00 percent value of Erythrocyte (Red Blood Cell) Deformability collected at week 24 or final visit and Erythrocyte Deformability collected at baseline. (NCT00770653)
Timeframe: Baseline and Week 24.

Interventionpercent (Mean)
Pioglitazone 15 mg and Metformin 850 mg BID3.3
Glimepiride 2 mg and Metformin 850 mg BID-.15

Change From Baseline in Erythrocyte Deformability (30.00).

The change between the 30.00 percent value of Erythrocyte (Red Blood Cell) Deformability collected at week 24 or final visit and Erythrocyte Deformability collected at baseline. (NCT00770653)
Timeframe: Baseline and Week 24.

Interventionpercent (Mean)
Pioglitazone 15 mg and Metformin 850 mg BID2.5
Glimepiride 2 mg and Metformin 850 mg BID-1.3

Change From Baseline in Erythrocyte Deformability (6.00).

The change between the 6.00 percent value of Erythrocyte (Red Blood Cell) Deformability collected at week 24 or final visit and Erythrocyte Deformability collected at baseline. (NCT00770653)
Timeframe: Baseline and Week 24.

Interventionpercent (Mean)
Pioglitazone 15 mg and Metformin 850 mg BID3.1
Glimepiride 2 mg and Metformin 850 mg BID-1.4

Change From Baseline in Erythrocyte Deformability (60.00).

The change between the 60.00 percent value of Erythrocyte (Red Blood Cell) Deformability collected at week 24 or final visit and Erythrocyte Deformability collected at baseline. (NCT00770653)
Timeframe: Baseline and Week 24.

Interventionpercent (Mean)
Pioglitazone 15 mg and Metformin 850 mg BID2.7
Glimepiride 2 mg and Metformin 850 mg BID-1.3

Change From Baseline in Fasting Glucose.

The change between Fasting Glucose collected at week 24 or final visit and Fasting Glucose collected at baseline. (NCT00770653)
Timeframe: Baseline and Week 24.

Interventionmg/dL (Least Squares Mean)
Pioglitazone 15 mg and Metformin 850 mg BID-21.6
Glimepiride 2 mg and Metformin 850 mg BID-21.1

Change From Baseline in Fasting Intact Proinsulin.

The change between Fasting Intact Proinsulin collected at week 24 or final visit and Fasting Intact Proinsulin collected at baseline. (NCT00770653)
Timeframe: Baseline and Week 24.

Interventionpmol/L (Least Squares Mean)
Pioglitazone 15 mg and Metformin 850 mg BID-5.18
Glimepiride 2 mg and Metformin 850 mg BID-0.11

Change From Baseline in Glycosylated Hemoglobin.

The change between the value of Glycosylated Hemoglobin (the concentration of glucose bound to hemoglobin as a percent of the absolute maximum that can be bound) collected at week 24 or final visit and Glycosylated Hemoglobin collected at baseline. (NCT00770653)
Timeframe: Baseline and Week 24.

Interventionmg/dL (Least Squares Mean)
Pioglitazone 15 mg and Metformin 850 mg BID-0.83
Glimepiride 2 mg and Metformin 850 mg BID-0.95

Change From Baseline in High Sensitivity C-reactive Protein (≤ 10 mg/L).

The change between the value of High Sensitivity C-reactive Protein less than or equal to 10 mg/L collected at week 24 or final visit and High Sensitivity C-reactive Protein less than or equal to 10 mg/L collected at baseline. (NCT00770653)
Timeframe: Baseline and Week 24.

Interventionmg/L (Mean)
Pioglitazone 15 mg and Metformin 850 mg BID-0.87
Glimepiride 2 mg and Metformin 850 mg BID0.00

Change From Baseline in High Sensitivity C-reactive Protein (Original).

The change between the value of High Sensitivity C-reactive Protein collected at week 24 or final visit and High Sensitivity C-reactive Protein collected at baseline. (NCT00770653)
Timeframe: Baseline and Week 24.

Interventionmg/L (Least Squares Mean)
Pioglitazone 15 mg and Metformin 850 mg BID-0.21
Glimepiride 2 mg and Metformin 850 mg BID-0.04

Change From Baseline in High-Density Lipoprotein Cholesterol.

The change between HDL-Cholesterol collected at week 24 or final visit and HDL-Cholesterol collected at baseline. (NCT00770653)
Timeframe: Baseline and Week 24.

Interventionmg/dL (Least Squares Mean)
Pioglitazone 15 mg and Metformin 850 mg BID3.3
Glimepiride 2 mg and Metformin 850 mg BID-0.4

Change From Baseline in High-Density Lipoprotein/Low-Density Lipoprotein Ratio.

The change between High-Density Lipoprotein/Low-Density Lipoprotein Ratio collected at week 24 or final visit and High-Density Lipoprotein/Low-Density Lipoprotein Ratio collected at baseline. (NCT00770653)
Timeframe: Baseline and Week 24.

Interventionmg/dL (Least Squares Mean)
Pioglitazone 15 mg and Metformin 850 mg BID0.1
Glimepiride 2 mg and Metformin 850 mg BID0.3

Change From Baseline in Low-Density Lipoprotein Cholesterol.

The change between Low-Density Lipoprotein Cholesterol collected at week 24 or final visit and Low-Density Lipoprotein Cholesterol collected at baseline. (NCT00770653)
Timeframe: Baseline and Week 24.

Interventionmg/dL (Least Squares Mean)
Pioglitazone 15 mg and Metformin 850 mg BID9.7
Glimepiride 2 mg and Metformin 850 mg BID11.2

Change From Baseline in Low-Density Lipoprotein Subfractions.

The change between the value of Low-Density Lipoprotein Subfractions collected at week 24 or final visit and Low-Density Lipoprotein Subfractions collected at baseline. (NCT00770653)
Timeframe: Baseline and Week 24.

Interventionmg/dL (Least Squares Mean)
Pioglitazone 15 mg and Metformin 850 mg BID6.2
Glimepiride 2 mg and Metformin 850 mg BID6.1

Change From Baseline in Matrix Metallo Proteinase-9.

The change between the value of Baseline in Matrix Metallo Proteinase-9 collected at week 24 or final visit and Baseline in Matrix Metallo Proteinase-9 collected at baseline. (NCT00770653)
Timeframe: Baseline and Week 24.

Interventionng/mL (Least Squares Mean)
Pioglitazone 15 mg and Metformin 850 mg BID31.4
Glimepiride 2 mg and Metformin 850 mg BID51.6

Change From Baseline in Nitrotyrosine.

The change between the value of Nitrotyrosine collected at week 24 or final visit and Nitrotyrosine collected at baseline. (NCT00770653)
Timeframe: Baseline and Week 24.

Interventionnmol/L (Least Squares Mean)
Pioglitazone 15 mg and Metformin 850 mg BID-2.7
Glimepiride 2 mg and Metformin 850 mg BID32.5

Change From Baseline in Platelet Function.

The change between the value of Platelet Function by PFA 100 collected at week 24 or final visit and Platelet Function by PFA 100 collected at baseline. (NCT00770653)
Timeframe: Baseline and Week 24.

Interventionsec (Least Squares Mean)
Pioglitazone 15 mg and Metformin 850 mg BID-30.3
Glimepiride 2 mg and Metformin 850 mg BID-1.0

Change From Baseline in Soluble CD40 Ligand.

The change between the value of Soluble CD40 Ligand collected at week 24 or final visit and Soluble CD40 Ligand collected at baseline. (NCT00770653)
Timeframe: Baseline and Week 24.

Interventionpg/mL (Least Squares Mean)
Pioglitazone 15 mg and Metformin 850 mg BID-40.7
Glimepiride 2 mg and Metformin 850 mg BID102.4

Change From Baseline in Soluble Intracellular Adhesion Molecule.

The change between the value of Baseline in Soluble Intracellular Adhesion molecule at week 24 or final visit and Baseline in Soluble Intracellular Adhesion molecule collected at baseline. (NCT00770653)
Timeframe: Baseline and Week 24.

Interventionng/mL (Least Squares Mean)
Pioglitazone 15 mg and Metformin 850 mg BID-13.0
Glimepiride 2 mg and Metformin 850 mg BID-3.2

Change From Baseline in Soluble Vascular Cell Adhesion Molecule.

The change between the value of Soluble Vascular Cell Adhesion Molecule collected at week 24 or final visit and Soluble Vascular Cell Adhesion Molecule collected at baseline. (NCT00770653)
Timeframe: Baseline and Week 24.

Interventionng/mL (Least Squares Mean)
Pioglitazone 15 mg and Metformin 850 mg BID11.6
Glimepiride 2 mg and Metformin 850 mg BID3.3

Change From Baseline in Systolic Blood Pressure.

The change between Systolic Blood Pressure measured at week 24 or final visit and Systolic Blood Pressure measured at baseline. (NCT00770653)
Timeframe: Baseline and Week 24.

InterventionmmHg (Least Squares Mean)
Pioglitazone 15 mg and Metformin 850 mg BID-2.5
Glimepiride 2 mg and Metformin 850 mg BID0.5

Change From Baseline in Thromboxane B2.

The change between the value of Thromboxane B2 collected at week 24 or final visit and Thromboxane B2 collected at baseline. (NCT00770653)
Timeframe: Baseline and Week 24.

Interventionpg/mL (Least Squares Mean)
Pioglitazone 15 mg and Metformin 850 mg BID-216.4
Glimepiride 2 mg and Metformin 850 mg BID527.8

Change From Baseline in Triglycerides.

The change between the value of Triglycerides collected at week 24 or final visit and Triglycerides collected at baseline. (NCT00770653)
Timeframe: Baseline and Week 24.

Interventionmg/dL (Least Squares Mean)
Pioglitazone 15 mg and Metformin 850 mg BID-40.9
Glimepiride 2 mg and Metformin 850 mg BID-16.7

Change From Baseline in Von-Willebrand Factor.

The change between the value of Von-Willebrand Factor collected at week 24 or final visit and Von-Willebrand Factor collected at baseline. (NCT00770653)
Timeframe: Baseline and Week 24.

Interventionpercent (Least Squares Mean)
Pioglitazone 15 mg and Metformin 850 mg BID-19.5
Glimepiride 2 mg and Metformin 850 mg BID1.4

Intake of Study Medication Greater Than 80% and Less Than 120%.

The change between the Intake of study medication greater than 80% at week 24 or final visit and Baseline and the Intake of study medication greater than 80% at baseline. (NCT00770653)
Timeframe: Baseline and Week 24.

Interventionparticipants (Number)
Pioglitazone 15 mg and Metformin 850 mg BID136
Glimepiride 2 mg and Metformin 850 mg BID137

The Mean Increase From Baseline in High-Density Lipoprotein Cholesterol.

The increase in High-Density Lipoprotein (HDL) Cholesterol collected at week 24 or final visit and HDL-Cholesterol collected at baseline. (NCT00770653)
Timeframe: Baseline and Week 24.

Interventionmg/dL (Least Squares Mean)
Pioglitazone 15 mg and Metformin 850 mg BID3.2
Glimepiride 2 mg and Metformin 850 mg BID-0.3

Comparison of Changes in Fasting Serum Glucose (FSG)With Pioglitazone and Metformin

Response rate was defined by ≥10% decrease of FSG or/and ≥1% decrease of HbA1c from the baseline values after 3 months treatment.48 responded to pioglitazone and 32 responded to metformin. (NCT01589445)
Timeframe: 3 months for each drug

,
Interventionmmol/l (Mean)
Baseline FSG3rd Month FSG
Metformin ( 002 Group)6.26.5
Pioglitazone (001 Group)6.95.4

Comparison of Changes in Fasting Serum Insulin (FSI)With Pioglitazone and Metformin

Response rate was defined by ≥10% decrease of FSG or/and ≥1% decrease of HbA1c from the baseline values after 3 months treatment.48 responded to pioglitazone and 32 responded to metformin. (NCT01589445)
Timeframe: 3 months for each drug

,
InterventionμU/ml (Mean)
Baseline FSI3rd month FSI
Metformin ( 002 Group)13.013.9
Pioglitazone (001 Group)16.212.3

Comparison of Changes in Glycosylated Hemoglobin (HbA1c)With Pioglitazone and Metformin

Response rate was defined by ≥10% decrease of FSG or/and ≥1% decrease of HbA1c from the baseline values after 3 months treatment.48 responded to pioglitazone and 32 responded to metformin. (NCT01589445)
Timeframe: 3 months for each drug

,
Interventionpercentage (Mean)
Baseline HbA1c3rd month HbA1c
Metformin ( 002 Group)7.87.0
Pioglitazone (001 Group)7.36.7

Comparison of Changes in HOMA Percent B and HOMA Percent S With Pioglitazone and Metformin

"Response rate was defined by ≥10% decrease of FSG or/and ≥1% decrease of HbA1c from the baseline values after 3 months treatment.48 responded to pioglitazone and 32 responded to metformin.~Analysis 1: Homeostatic Model Assessment of Beta cell function(HOMA percent B) Analysis 2: Homeostatic Model Assessment of Insulin Sensitivity (Homa percent S)" (NCT01589445)
Timeframe: 3 months for each drug

,
Interventionpercentage (Mean)
Baseline HOMA percent beta cells function3rd month HOMA percent beta cells functionBaseline HOMA percent sensitivity3rd month HOMA percent sensitivity
Metformin ( 002 Group)109.3116.076.267.2
Pioglitazone (001 Group)118.9132.351.169.3

Comparison of Changes in Insulin Levels (HOMA IR,QUICKI) With Pioglitazone and Metformin

"Response rate was defined by ≥10% decrease of FSG or/and ≥1% decrease of HbA1c from the baseline values after 3 months treatment.48 responded to pioglitazone and 32 responded to metformin.~Analysis 1: Homeostasis Model Assessment Insulin Resistance(HOMA IR) Analysis 2: Quantitative Insulin sensitivity Check Index(QUICKI)" (NCT01589445)
Timeframe: 3 months for each drug

,
InterventionScore on a scale ( SI unit) (Mean)
Baseline QUICKI3rd month QUICKIBaseline HOMA IR3rd month HOMA IR
Metformin ( 002 Group)0.570.543.74.3
Pioglitazone (001 Group)0.520.595.12.9

Comparison of Changes in Lipid Profiles With Pioglitazone and Metformin

"Response rate was defined by ≥10% decrease of FSG or/and ≥1% decrease of HbA1c from the baseline values after 3 months treatment.48 responded to pioglitazone and 32 responded to metformin.~Analysis 1:Total Cholesterol(TC) Analysis 2:Triglyceride(TG) Analysis 3:High Density Lipoprotein(HDL) Analysis 4:Low Density Lipoprotein(LDL)" (NCT01589445)
Timeframe: 3 months for each drug

,
Interventionmg/dl (Mean)
Baseline TC3rd month TCBaseline TG3rd month TGBaseline HDL3rd month HDLBaseline LDL3rd month LDL
Metformin (002 Group)193.0177.0166.0175.034.434.7125.6112.0
Pioglitazone (001 Group)182.01781831953333.2112.8105.5

Reviews

12 reviews available for pioglitazone and Hyperglycemia, Postprandial

ArticleYear
Diabetes, stroke, and neuroresilience: looking beyond hyperglycemia.
    Annals of the New York Academy of Sciences, 2021, Volume: 1495, Issue:1

    Topics: Diabetes Mellitus, Type 2; Humans; Hyperglycemia; Hypoglycemic Agents; Inflammation; Insulin; Insuli

2021
Intensive insulin therapy, insulin sensitisers and insulin secretagogues for burns: A systematic review of effectiveness and safety.
    Burns : journal of the International Society for Burn Injuries, 2018, Volume: 44, Issue:6

    Topics: Burns; Dipeptidyl-Peptidase IV Inhibitors; Disease Management; Exenatide; Glipizide; Humans; Hypergl

2018
What are the preferred strategies for control of glycaemic variability in patients with type 2 diabetes mellitus?
    Diabetes, obesity & metabolism, 2013, Volume: 15 Suppl 2

    Topics: Blood Glucose; Body Weight; Diabetes Mellitus, Type 2; Diet, Reducing; Dipeptidyl-Peptidase IV Inhib

2013
Lixisenatide as add-on to oral anti-diabetic therapy: an effective treatment for glycaemic control with body weight benefits in type 2 diabetes.
    Diabetes/metabolism research and reviews, 2014, Volume: 30, Issue:8

    Topics: Administration, Oral; Clinical Trials, Phase III as Topic; Combined Modality Therapy; Diabetes Melli

2014
[Twice-daily and weekly exenatide: clinical profile of two pioneer formulations in incretin therapy].
    Medicina clinica, 2014, Volume: 143 Suppl 2

    Topics: Delayed-Action Preparations; Diabetes Mellitus, Type 2; Dipeptidyl-Peptidase IV Inhibitors; Drug Adm

2014
Initiating insulin in patients with type 2 diabetes.
    The Journal of family practice, 2007, Volume: 56, Issue:8 Suppl Ho

    Topics: Blood Glucose; Cholesterol; Comorbidity; Diabetes Mellitus, Type 2; Drug Monitoring; Drug Therapy, C

2007
Macrovascular effects and safety issues of therapies for type 2 diabetes.
    The American journal of cardiology, 2011, Aug-02, Volume: 108, Issue:3 Suppl

    Topics: Atherosclerosis; Diabetes Mellitus, Type 2; Diabetic Angiopathies; Diabetic Retinopathy; Disease Pro

2011
[Syndrome X].
    Nihon rinsho. Japanese journal of clinical medicine, 2002, Volume: 60 Suppl 10

    Topics: Animals; Bezafibrate; Biguanides; Fatty Acids, Nonesterified; Humans; Hyperglycemia; Hyperinsulinism

2002
[Thiazolidinediones: effect of the pioglitazone on hyperglycemia, dyslipidemia and cardiovascular risk].
    Revista clinica espanola, 2003, Volume: 203, Issue:1

    Topics: Cardiovascular Diseases; Humans; Hyperglycemia; Hyperlipidemias; Hypoglycemic Agents; Pioglitazone;

2003
Peroxisome proliferator-activated receptor-gamma agonists in atherosclerosis: current evidence and future directions.
    Current opinion in lipidology, 2003, Volume: 14, Issue:6

    Topics: Albuminuria; Arteriosclerosis; Blood Pressure; C-Reactive Protein; Carotid Arteries; Coronary Resten

2003
[Pathophysiological conditions progressing from impaired glucose tolerance: coronary artery disease (ischemic heart disease)].
    Nihon rinsho. Japanese journal of clinical medicine, 2005, Volume: 63 Suppl 2

    Topics: Acarbose; Cyclohexanes; Fasting; Glucose Intolerance; Glycation End Products, Advanced; Humans; Hype

2005
[Hypoglycemic agents to improve insulin resistance].
    Nihon rinsho. Japanese journal of clinical medicine, 2000, Volume: 58, Issue:2

    Topics: Adipocytes; Animals; Cell Differentiation; Chromans; Diabetes Mellitus, Type 2; Disease Models, Anim

2000

Trials

19 trials available for pioglitazone and Hyperglycemia, Postprandial

ArticleYear
Three-year data from 5 HARMONY phase 3 clinical trials of albiglutide in type 2 diabetes mellitus: Long-term efficacy with or without rescue therapy.
    Diabetes research and clinical practice, 2017, Volume: 131

    Topics: Blood Glucose; Body Weight; Diabetes Mellitus, Type 2; Drug Therapy, Combination; Female; Glucagon-L

2017
Three-year data from 5 HARMONY phase 3 clinical trials of albiglutide in type 2 diabetes mellitus: Long-term efficacy with or without rescue therapy.
    Diabetes research and clinical practice, 2017, Volume: 131

    Topics: Blood Glucose; Body Weight; Diabetes Mellitus, Type 2; Drug Therapy, Combination; Female; Glucagon-L

2017
Three-year data from 5 HARMONY phase 3 clinical trials of albiglutide in type 2 diabetes mellitus: Long-term efficacy with or without rescue therapy.
    Diabetes research and clinical practice, 2017, Volume: 131

    Topics: Blood Glucose; Body Weight; Diabetes Mellitus, Type 2; Drug Therapy, Combination; Female; Glucagon-L

2017
Three-year data from 5 HARMONY phase 3 clinical trials of albiglutide in type 2 diabetes mellitus: Long-term efficacy with or without rescue therapy.
    Diabetes research and clinical practice, 2017, Volume: 131

    Topics: Blood Glucose; Body Weight; Diabetes Mellitus, Type 2; Drug Therapy, Combination; Female; Glucagon-L

2017
Three-year data from 5 HARMONY phase 3 clinical trials of albiglutide in type 2 diabetes mellitus: Long-term efficacy with or without rescue therapy.
    Diabetes research and clinical practice, 2017, Volume: 131

    Topics: Blood Glucose; Body Weight; Diabetes Mellitus, Type 2; Drug Therapy, Combination; Female; Glucagon-L

2017
Three-year data from 5 HARMONY phase 3 clinical trials of albiglutide in type 2 diabetes mellitus: Long-term efficacy with or without rescue therapy.
    Diabetes research and clinical practice, 2017, Volume: 131

    Topics: Blood Glucose; Body Weight; Diabetes Mellitus, Type 2; Drug Therapy, Combination; Female; Glucagon-L

2017
Three-year data from 5 HARMONY phase 3 clinical trials of albiglutide in type 2 diabetes mellitus: Long-term efficacy with or without rescue therapy.
    Diabetes research and clinical practice, 2017, Volume: 131

    Topics: Blood Glucose; Body Weight; Diabetes Mellitus, Type 2; Drug Therapy, Combination; Female; Glucagon-L

2017
Three-year data from 5 HARMONY phase 3 clinical trials of albiglutide in type 2 diabetes mellitus: Long-term efficacy with or without rescue therapy.
    Diabetes research and clinical practice, 2017, Volume: 131

    Topics: Blood Glucose; Body Weight; Diabetes Mellitus, Type 2; Drug Therapy, Combination; Female; Glucagon-L

2017
Three-year data from 5 HARMONY phase 3 clinical trials of albiglutide in type 2 diabetes mellitus: Long-term efficacy with or without rescue therapy.
    Diabetes research and clinical practice, 2017, Volume: 131

    Topics: Blood Glucose; Body Weight; Diabetes Mellitus, Type 2; Drug Therapy, Combination; Female; Glucagon-L

2017
Three-year data from 5 HARMONY phase 3 clinical trials of albiglutide in type 2 diabetes mellitus: Long-term efficacy with or without rescue therapy.
    Diabetes research and clinical practice, 2017, Volume: 131

    Topics: Blood Glucose; Body Weight; Diabetes Mellitus, Type 2; Drug Therapy, Combination; Female; Glucagon-L

2017
Three-year data from 5 HARMONY phase 3 clinical trials of albiglutide in type 2 diabetes mellitus: Long-term efficacy with or without rescue therapy.
    Diabetes research and clinical practice, 2017, Volume: 131

    Topics: Blood Glucose; Body Weight; Diabetes Mellitus, Type 2; Drug Therapy, Combination; Female; Glucagon-L

2017
Three-year data from 5 HARMONY phase 3 clinical trials of albiglutide in type 2 diabetes mellitus: Long-term efficacy with or without rescue therapy.
    Diabetes research and clinical practice, 2017, Volume: 131

    Topics: Blood Glucose; Body Weight; Diabetes Mellitus, Type 2; Drug Therapy, Combination; Female; Glucagon-L

2017
Three-year data from 5 HARMONY phase 3 clinical trials of albiglutide in type 2 diabetes mellitus: Long-term efficacy with or without rescue therapy.
    Diabetes research and clinical practice, 2017, Volume: 131

    Topics: Blood Glucose; Body Weight; Diabetes Mellitus, Type 2; Drug Therapy, Combination; Female; Glucagon-L

2017
Three-year data from 5 HARMONY phase 3 clinical trials of albiglutide in type 2 diabetes mellitus: Long-term efficacy with or without rescue therapy.
    Diabetes research and clinical practice, 2017, Volume: 131

    Topics: Blood Glucose; Body Weight; Diabetes Mellitus, Type 2; Drug Therapy, Combination; Female; Glucagon-L

2017
Three-year data from 5 HARMONY phase 3 clinical trials of albiglutide in type 2 diabetes mellitus: Long-term efficacy with or without rescue therapy.
    Diabetes research and clinical practice, 2017, Volume: 131

    Topics: Blood Glucose; Body Weight; Diabetes Mellitus, Type 2; Drug Therapy, Combination; Female; Glucagon-L

2017
Three-year data from 5 HARMONY phase 3 clinical trials of albiglutide in type 2 diabetes mellitus: Long-term efficacy with or without rescue therapy.
    Diabetes research and clinical practice, 2017, Volume: 131

    Topics: Blood Glucose; Body Weight; Diabetes Mellitus, Type 2; Drug Therapy, Combination; Female; Glucagon-L

2017
Three-year data from 5 HARMONY phase 3 clinical trials of albiglutide in type 2 diabetes mellitus: Long-term efficacy with or without rescue therapy.
    Diabetes research and clinical practice, 2017, Volume: 131

    Topics: Blood Glucose; Body Weight; Diabetes Mellitus, Type 2; Drug Therapy, Combination; Female; Glucagon-L

2017
Three-year data from 5 HARMONY phase 3 clinical trials of albiglutide in type 2 diabetes mellitus: Long-term efficacy with or without rescue therapy.
    Diabetes research and clinical practice, 2017, Volume: 131

    Topics: Blood Glucose; Body Weight; Diabetes Mellitus, Type 2; Drug Therapy, Combination; Female; Glucagon-L

2017
Three-year data from 5 HARMONY phase 3 clinical trials of albiglutide in type 2 diabetes mellitus: Long-term efficacy with or without rescue therapy.
    Diabetes research and clinical practice, 2017, Volume: 131

    Topics: Blood Glucose; Body Weight; Diabetes Mellitus, Type 2; Drug Therapy, Combination; Female; Glucagon-L

2017
Three-year data from 5 HARMONY phase 3 clinical trials of albiglutide in type 2 diabetes mellitus: Long-term efficacy with or without rescue therapy.
    Diabetes research and clinical practice, 2017, Volume: 131

    Topics: Blood Glucose; Body Weight; Diabetes Mellitus, Type 2; Drug Therapy, Combination; Female; Glucagon-L

2017
Three-year data from 5 HARMONY phase 3 clinical trials of albiglutide in type 2 diabetes mellitus: Long-term efficacy with or without rescue therapy.
    Diabetes research and clinical practice, 2017, Volume: 131

    Topics: Blood Glucose; Body Weight; Diabetes Mellitus, Type 2; Drug Therapy, Combination; Female; Glucagon-L

2017
Three-year data from 5 HARMONY phase 3 clinical trials of albiglutide in type 2 diabetes mellitus: Long-term efficacy with or without rescue therapy.
    Diabetes research and clinical practice, 2017, Volume: 131

    Topics: Blood Glucose; Body Weight; Diabetes Mellitus, Type 2; Drug Therapy, Combination; Female; Glucagon-L

2017
Three-year data from 5 HARMONY phase 3 clinical trials of albiglutide in type 2 diabetes mellitus: Long-term efficacy with or without rescue therapy.
    Diabetes research and clinical practice, 2017, Volume: 131

    Topics: Blood Glucose; Body Weight; Diabetes Mellitus, Type 2; Drug Therapy, Combination; Female; Glucagon-L

2017
Three-year data from 5 HARMONY phase 3 clinical trials of albiglutide in type 2 diabetes mellitus: Long-term efficacy with or without rescue therapy.
    Diabetes research and clinical practice, 2017, Volume: 131

    Topics: Blood Glucose; Body Weight; Diabetes Mellitus, Type 2; Drug Therapy, Combination; Female; Glucagon-L

2017
Three-year data from 5 HARMONY phase 3 clinical trials of albiglutide in type 2 diabetes mellitus: Long-term efficacy with or without rescue therapy.
    Diabetes research and clinical practice, 2017, Volume: 131

    Topics: Blood Glucose; Body Weight; Diabetes Mellitus, Type 2; Drug Therapy, Combination; Female; Glucagon-L

2017
Sitagliptin vs. pioglitazone as add-on treatments in patients with uncontrolled type 2 diabetes on the maximal dose of metformin plus sulfonylurea.
    Journal of endocrinological investigation, 2019, Volume: 42, Issue:7

    Topics: Biomarkers; Blood Glucose; Diabetes Mellitus, Type 2; Drug Therapy, Combination; Female; Follow-Up S

2019
Efficacy and safety of lixisenatide once daily versus placebo in type 2 diabetes insufficiently controlled on pioglitazone (GetGoal-P).
    Diabetes, obesity & metabolism, 2013, Volume: 15, Issue:11

    Topics: Aged; Diabetes Mellitus, Type 2; Double-Blind Method; Drug Administration Schedule; Drug Monitoring;

2013
Efficacy and safety of lixisenatide once daily versus placebo in type 2 diabetes insufficiently controlled on pioglitazone (GetGoal-P).
    Diabetes, obesity & metabolism, 2013, Volume: 15, Issue:11

    Topics: Aged; Diabetes Mellitus, Type 2; Double-Blind Method; Drug Administration Schedule; Drug Monitoring;

2013
Efficacy and safety of lixisenatide once daily versus placebo in type 2 diabetes insufficiently controlled on pioglitazone (GetGoal-P).
    Diabetes, obesity & metabolism, 2013, Volume: 15, Issue:11

    Topics: Aged; Diabetes Mellitus, Type 2; Double-Blind Method; Drug Administration Schedule; Drug Monitoring;

2013
Efficacy and safety of lixisenatide once daily versus placebo in type 2 diabetes insufficiently controlled on pioglitazone (GetGoal-P).
    Diabetes, obesity & metabolism, 2013, Volume: 15, Issue:11

    Topics: Aged; Diabetes Mellitus, Type 2; Double-Blind Method; Drug Administration Schedule; Drug Monitoring;

2013
Effects of pioglitazone on bone in postmenopausal women with impaired fasting glucose or impaired glucose tolerance: a randomized, double-blind, placebo-controlled study.
    The Journal of clinical endocrinology and metabolism, 2013, Volume: 98, Issue:12

    Topics: Adiposity; Aged; Biomarkers; Bone and Bones; Bone Density; Bone Remodeling; Bone Resorption; Double-

2013
The disposition index does not reflect β-cell function in IGT subjects treated with pioglitazone.
    The Journal of clinical endocrinology and metabolism, 2014, Volume: 99, Issue:10

    Topics: Blood Glucose; Body Mass Index; Drug Monitoring; Female; Follow-Up Studies; Glucose Intolerance; Glu

2014
Randomized trial showing efficacy and safety of twice-daily remogliflozin etabonate for the treatment of type 2 diabetes.
    Diabetes, obesity & metabolism, 2015, Volume: 17, Issue:1

    Topics: Diabetes Mellitus, Type 2; Dose-Response Relationship, Drug; Double-Blind Method; Drug Administratio

2015
Randomized efficacy and safety trial of once-daily remogliflozin etabonate for the treatment of type 2 diabetes.
    Diabetes, obesity & metabolism, 2015, Volume: 17, Issue:1

    Topics: Cohort Studies; Diabetes Mellitus, Type 2; Dose-Response Relationship, Drug; Double-Blind Method; Dr

2015
The comparative effect of pioglitazone and metformin on serum osteoprotegerin, adiponectin and intercellular adhesion molecule concentrations in patients with newly diagnosed type 2 diabetes: a randomized clinical trial.
    Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association, 2015, Volume: 123, Issue:5

    Topics: Adiponectin; Anti-Inflammatory Agents, Non-Steroidal; Blood Glucose; C-Reactive Protein; Diabetes Me

2015
Efficacy and safety of pioglitazone added to alogliptin in Japanese patients with type 2 diabetes mellitus: a multicentre, randomized, double-blind, parallel-group, comparative study.
    Diabetes, obesity & metabolism, 2015, Volume: 17, Issue:12

    Topics: Combined Modality Therapy; Diabetes Mellitus, Type 2; Diet, Diabetic; Dipeptidyl-Peptidase IV Inhibi

2015
Effect of mitiglinide on glycemic control over 52 weeks in Japanese type 2 diabetic patients insufficiently controlled with pioglitazone monotherapy.
    Endocrine journal, 2009, Volume: 56, Issue:6

    Topics: Aged; Blood Glucose; Diabetes Mellitus, Type 2; Drug Therapy, Combination; Female; Glycated Hemoglob

2009
Pioglitazone improvement of fasting and postprandial hyperglycaemia in Mexican-American patients with Type 2 diabetes: a double tracer OGTT study.
    Clinical endocrinology, 2010, Volume: 73, Issue:3

    Topics: Blood Glucose; Carbon Radioisotopes; Diabetes Mellitus, Type 2; Fasting; Female; Glucose; Glucose To

2010
Lack of effects of pioglitazone on cardiac function in patients with type 2 diabetes and evidence of left ventricular diastolic dysfunction: a tissue doppler imaging study.
    Cardiovascular diabetology, 2010, Sep-23, Volume: 9

    Topics: Aged; Blood Pressure; Diabetes Mellitus, Type 2; Diastole; Echocardiography, Doppler; Heart Function

2010
PIOfix-study: effects of pioglitazone/metformin fixed combination in comparison with a combination of metformin with glimepiride on diabetic dyslipidemia.
    Diabetes technology & therapeutics, 2011, Volume: 13, Issue:6

    Topics: Adiponectin; Aged; Anticholesteremic Agents; C-Reactive Protein; Cholesterol, HDL; Cholesterol, LDL;

2011
Antiatherogenic effect of pioglitazone in type 2 diabetic patients irrespective of the responsiveness to its antidiabetic effect.
    Diabetes care, 2003, Volume: 26, Issue:9

    Topics: Adiponectin; Arteriosclerosis; Blood Pressure; Body Mass Index; C-Reactive Protein; Diabetes Mellitu

2003
Comparison of effect of pioglitazone with metformin or sulfonylurea (monotherapy and combination therapy) on postload glycemia and composite insulin sensitivity index during an oral glucose tolerance test in patients with type 2 diabetes.
    Diabetes care, 2005, Volume: 28, Issue:2

    Topics: Adult; Aged; Blood Glucose; Body Weight; Diabetes Mellitus, Type 2; Drug Therapy, Combination; Femal

2005
Improved glycemic control and lipid profile in a randomized study of pioglitazone compared with acarbose in patients with type 2 diabetes mellitus.
    Treatments in endocrinology, 2002, Volume: 1, Issue:5

    Topics: Acarbose; Adult; Aged; Cholesterol, HDL; Cholesterol, LDL; Cholesterol, VLDL; Diabetes Mellitus, Typ

2002
Pioglitazone decreases carotid intima-media thickness independently of glycemic control in patients with type 2 diabetes mellitus: results from a controlled randomized study.
    Circulation, 2005, May-17, Volume: 111, Issue:19

    Topics: Aged; Cardiovascular Diseases; Carotid Arteries; Diabetes Mellitus, Type 2; Female; Humans; Hypergly

2005
Effects of pioglitazone vs glibenclamide on postprandial increases in glucose and triglyceride levels and on oxidative stress in Japanese patients with type 2 diabetes.
    Endocrine, 2006, Volume: 29, Issue:1

    Topics: Aged; Blood Glucose; Diabetes Mellitus, Type 2; Dose-Response Relationship, Drug; Fatty Acids, Nones

2006
Effect of pioglitazone on the metabolic and hormonal response to a mixed meal in type II diabetes.
    Clinical pharmacology and therapeutics, 2007, Volume: 81, Issue:2

    Topics: Adiponectin; Blood Glucose; Diabetes Mellitus, Type 2; Double-Blind Method; Drug Administration Sche

2007

Other Studies

56 other studies available for pioglitazone and Hyperglycemia, Postprandial

ArticleYear
Synthesis and biological activity of metabolites of the antidiabetic, antihyperglycemic agent pioglitazone.
    Journal of medicinal chemistry, 1996, Dec-20, Volume: 39, Issue:26

    Topics: Animals; Dogs; Half-Life; Humans; Hyperglycemia; Hypoglycemic Agents; Insulin Resistance; Magnetic R

1996
Discovery of a novel selective PPARgamma modulator from (-)-Cercosporamide derivatives.
    Bioorganic & medicinal chemistry letters, 2010, Apr-01, Volume: 20, Issue:7

    Topics: Animals; Benzofurans; Crystallography, X-Ray; Diabetes Mellitus; Glucose; Humans; Hyperglycemia; Hyp

2010
Development of a new class of benzoylpyrrole-based PPARα/γ activators.
    Bioorganic & medicinal chemistry letters, 2011, Jan-01, Volume: 21, Issue:1

    Topics: Acetates; Animals; Carboxylic Acids; Hyperglycemia; Hypoglycemic Agents; Male; Mice; Mice, Obese; Ob

2011
Long non-coding RNA PVT1, a molecular sponge of miR-26b, is involved in the progression of hyperglycemia-induced collagen degradation in human chondrocytes by targeting CTGF/TGF-
    Innate immunity, 2020, Volume: 26, Issue:3

    Topics: Aged; Cartilage; Chondrocytes; Collagen; Connective Tissue Growth Factor; Diabetes Mellitus; Female;

2020
Synthesis of a novel glibenclamide-pioglitazone hybrid compound and its effects on glucose homeostasis in normal and insulin-resistant rats.
    Bioorganic chemistry, 2021, Volume: 114

    Topics: Animals; Blood Glucose; Diabetes Mellitus, Type 2; Dose-Response Relationship, Drug; Glyburide; Home

2021
Comment on Inzucchi et al. Pioglitazone Prevents Diabetes in Patients With Insulin Resistance and Cerebrovascular Disease. Diabetes Care 2016;39:1684-1692.
    Diabetes care, 2017, Volume: 40, Issue:4

    Topics: Cerebrovascular Disorders; Diabetes Mellitus, Type 2; Humans; Hyperglycemia; Hypoglycemic Agents; In

2017
Response to Comment on Inzucchi et al. Pioglitazone Prevents Diabetes in Patients With Insulin Resistance and Cerebrovascular Disease. Diabetes Care 2016;39:1684-1692.
    Diabetes care, 2017, Volume: 40, Issue:4

    Topics: Cerebrovascular Disorders; Diabetes Mellitus, Type 2; Humans; Hyperglycemia; Hypoglycemic Agents; In

2017
Effects of Lactobacillus casei CCFM419 on insulin resistance and gut microbiota in type 2 diabetic mice.
    Beneficial microbes, 2017, May-30, Volume: 8, Issue:3

    Topics: Animals; Bacteroides; Blood Glucose; Cytokines; Diabetes Mellitus, Experimental; Diabetes Mellitus,

2017
Cardiovascular Disease and Type 2 Diabetes: Has the Dawn of a New Era Arrived?
    Diabetes care, 2017, Volume: 40, Issue:7

    Topics: Animals; Benzhydryl Compounds; Cardiovascular Diseases; Diabetes Mellitus, Type 2; Glucagon-Like Pep

2017
Diabetic macular edema-like ocular lesions in male spontaneously diabetic torii fatty rats.
    Physiological research, 2018, 07-17, Volume: 67, Issue:3

    Topics: Animals; Capillary Permeability; Diabetic Retinopathy; Disease Models, Animal; Hyperglycemia; Hypogl

2018
Ethanolic seeds extract of Centratherum anthelminticum reduces oxidative stress in type 2 diabetes.
    Pakistan journal of pharmaceutical sciences, 2018, Volume: 31, Issue:3(Suppleme

    Topics: Alanine Transaminase; Animals; Antioxidants; Asteraceae; Bilirubin; Creatine Kinase; Diabetes Mellit

2018
Peroxisome proliferator-activated receptor γ agonists attenuate hyperglycaemia-induced hyaluronan secretion in vascular smooth muscle cells by inhibiting PKCβ2.
    Cell biochemistry and biophysics, 2013, Volume: 67, Issue:2

    Topics: Gene Expression Regulation; Glucuronosyltransferase; Humans; Hyaluronan Synthases; Hyaluronic Acid;

2013
An ethanolic extract of Lindera obtusiloba stems, YJP-14, improves endothelial dysfunction, metabolic parameters and physical performance in diabetic db/db mice.
    PloS one, 2013, Volume: 8, Issue:6

    Topics: Albuminuria; Angiotensin II; Animals; Aorta; Blood Glucose; Body Weight; Diabetes Mellitus, Type 2;

2013
A synergistic therapeutic scheme for hyperglycemia and nephrotic disorders in diabetes.
    Theranostics, 2014, Volume: 4, Issue:5

    Topics: Animals; Blood Urea Nitrogen; Creatinine; Diabetes Complications; Diabetes Mellitus; Humans; Hypergl

2014
Combination therapy of an intestine-specific inhibitor of microsomal triglyceride transfer protein and peroxisome proliferator-activated receptor γ agonist in diabetic rat.
    Journal of diabetes research, 2014, Volume: 2014

    Topics: Adipose Tissue, White; Animals; Benzamides; Carrier Proteins; Diabetes Mellitus, Type 2; Drug Therap

2014
Anti-hyperglycemic activity of rutin in streptozotocin-induced diabetic rats: an effect mediated through cytokines, antioxidants and lipid biomarkers.
    Indian journal of experimental biology, 2014, Volume: 52, Issue:7

    Topics: Animals; Antioxidants; Biomarkers; Blood Glucose; Body Weight; Diabetes Complications; Diabetes Mell

2014
PPARγ is involved in the hyperglycemia-induced inflammatory responses and collagen degradation in human chondrocytes and diabetic mouse cartilages.
    Journal of orthopaedic research : official publication of the Orthopaedic Research Society, 2015, Volume: 33, Issue:3

    Topics: Adult; Aged; Animals; Cartilage; Chondrocytes; Collagen; Diabetes Mellitus, Experimental; Dinoprosto

2015
Pioglitazone restores IGFBP-3 levels through DNA PK in retinal endothelial cells cultured in hyperglycemic conditions.
    Investigative ophthalmology & visual science, 2014, Dec-18, Volume: 56, Issue:1

    Topics: Apoptosis; Blotting, Western; Cells, Cultured; Culture Media; Diabetic Retinopathy; DNA; DNA-Activat

2014
Pioglitazone improves fat tissue distribution and hyperglycemia in a case of cockayne syndrome with diabetes.
    Diabetes care, 2015, Volume: 38, Issue:5

    Topics: Body Fat Distribution; Cockayne Syndrome; Comorbidity; Diabetes Mellitus; Humans; Hyperglycemia; Hyp

2015
The Role of Oxidized Cholesterol in Diabetes-Induced Lysosomal Dysfunction in the Brain.
    Molecular neurobiology, 2016, Volume: 53, Issue:4

    Topics: Animals; Brain; Cathepsin D; Cerebral Cortex; Cholesterol; Diabetes Mellitus, Type 2; Fluorescence;

2016
Diabetic silkworms for evaluation of therapeutically effective drugs against type II diabetes.
    Scientific reports, 2015, May-29, Volume: 5

    Topics: Animals; Bombyx; Diabetes Mellitus, Experimental; Diabetes Mellitus, Type 2; Diet; Drug Evaluation,

2015
Hyperglycemia and PPARγ Antagonistically Influence Macrophage Polarization and Infarct Healing After Ischemic Stroke.
    Stroke, 2015, Volume: 46, Issue:10

    Topics: Animals; Anticoagulants; Cell Polarity; Cerebral Hemorrhage; Diabetes Mellitus, Experimental; Diseas

2015
Solanum nigrum Protects against Hepatic Fibrosis via Suppression of Hyperglycemia in High-Fat/Ethanol Diet-Induced Rats.
    Molecules (Basel, Switzerland), 2016, Feb-25, Volume: 21, Issue:3

    Topics: Animals; Diet, High-Fat; Ethanol; Gene Expression Regulation; Glycation End Products, Advanced; Hepa

2016
The Sodium-Glucose Cotransporter 2 Inhibitor Dapagliflozin Prevents Cardiomyopathy in a Diabetic Lipodystrophic Mouse Model.
    Diabetes, 2017, Volume: 66, Issue:4

    Topics: Animals; Benzhydryl Compounds; Blood Glucose; Cardiomyopathy, Hypertrophic; Diabetes Mellitus, Type

2017
Appropriate Insulin Level in Selecting Fortified Diet-Fed, Streptozotocin-Treated Rat Model of Type 2 Diabetes for Anti-Diabetic Studies.
    PloS one, 2017, Volume: 12, Issue:1

    Topics: Animals; Blood Glucose; Cholesterol; Diabetes Mellitus, Experimental; Diabetes Mellitus, Type 2; Dis

2017
Suppression of post-prandial hyperglycaemia by pioglitazone improved islet fibrosis and macrophage migration in the Goto-Kakizaki rat.
    Diabetes, obesity & metabolism, 2008, Volume: 10, Issue:9

    Topics: Animals; Cell Death; Diabetes Mellitus, Experimental; Hyperglycemia; Hypoglycemic Agents; Insulin-Se

2008
Involvement of hyperglycemia in deposition of aggregated protein in glomeruli of diabetic mice.
    European journal of pharmacology, 2008, Dec-28, Volume: 601, Issue:1-3

    Topics: Animals; Blood Glucose; Diabetes Mellitus; Glucose; Glycated Hemoglobin; Glycated Serum Albumin; Gly

2008
TZDs reduce mitochondrial ROS production and enhance mitochondrial biogenesis.
    Biochemical and biophysical research communications, 2009, Jan-30, Volume: 379, Issue:1

    Topics: Cells, Cultured; DNA, Mitochondrial; Heat-Shock Proteins; Humans; Hyperglycemia; Hypoglycemic Agents

2009
Peroxisome proliferator-activated receptor gamma agonist pioglitazone prevents the hyperglycemia caused by phosphatidylinositol 3-kinase pathway inhibition by PX-866 without affecting antitumor activity.
    Molecular cancer therapeutics, 2009, Volume: 8, Issue:1

    Topics: Animals; Antineoplastic Agents; Cell Line, Tumor; Disease Progression; Glucose; Glucose Transport Pr

2009
Translation of basic science into clinical medicine: novel targets for diabetic nephropathy.
    Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association, 2009, Volume: 24, Issue:5

    Topics: Angiotensin II Type 1 Receptor Blockers; Animals; Biomedical Research; Clinical Medicine; Diabetic N

2009
A pilot study suggests that the G/G genotype of resistin single nucleotide polymorphism at -420 may be an independent predictor of a reduction in fasting plasma glucose and insulin resistance by pioglitazone in type 2 diabetes.
    Endocrine journal, 2009, Volume: 56, Issue:9

    Topics: Adult; Aged; Blood Glucose; Diabetes Mellitus, Type 2; Female; Glycated Hemoglobin; Homeostasis; Hom

2009
Modulation of nitrosative/oxidative stress in the lung of hyperglycemic rabbits by two antidiabetics, pioglitazone and repaglinide.
    Experimental lung research, 2009, Volume: 35, Issue:5

    Topics: Administration, Oral; Animals; Blood Glucose; Carbamates; Catalase; Diabetes Mellitus, Experimental;

2009
Metformin reduces body weight gain and improves glucose intolerance in high-fat diet-fed C57BL/6J mice.
    Biological & pharmaceutical bulletin, 2010, Volume: 33, Issue:6

    Topics: Animals; Blood Glucose; Body Weight; Dietary Fats; Energy Intake; Glucagon-Like Peptide 1; Glucose I

2010
S961, an insulin receptor antagonist causes hyperinsulinemia, insulin-resistance and depletion of energy stores in rats.
    Biochemical and biophysical research communications, 2010, Jul-23, Volume: 398, Issue:2

    Topics: Animals; Cell Line; Glucose; Glucose Tolerance Test; Hyperglycemia; Hyperinsulinism; Hypoglycemic Ag

2010
Dynamic changes of adiponectin and S100A8 levels by the selective peroxisome proliferator-activated receptor-gamma agonist rivoglitazone.
    Arteriosclerosis, thrombosis, and vascular biology, 2011, Volume: 31, Issue:4

    Topics: 3T3-L1 Cells; Adipocytes; Adiponectin; Adipose Tissue, White; Animals; Apolipoproteins E; Atheroscle

2011
Effects of two oral antidiabetics, pioglitazone and repaglinide, on aconitase inactivation, inflammation and oxidative/nitrosative stress in tissues under alloxan-induced hyperglycemia.
    European journal of pharmacology, 2011, May-20, Volume: 659, Issue:1

    Topics: Aconitate Hydratase; Administration, Oral; Alloxan; Animals; Blood Glucose; Body Weight; Carbamates;

2011
The effects of an arabinogalactan-protein from the white-skinned sweet potato (Ipomoea batatas L.) on blood glucose in spontaneous diabetic mice.
    Bioscience, biotechnology, and biochemistry, 2011, Volume: 75, Issue:3

    Topics: Animals; Blood Glucose; Diabetes Mellitus; Disease Models, Animal; Female; Glucose Tolerance Test; H

2011
Metabolic effects of pioglitazone in chemically-induced mammary carcinogenesis in rats.
    Pathology oncology research : POR, 2011, Volume: 17, Issue:4

    Topics: Animals; Corticosterone; Female; Glycogen; Heart; Hyperglycemia; Hyperinsulinism; Lipid Peroxidation

2011
Appropriateness of the Zucker Diabetic Fatty rat as a model for diabetic microvascular late complications.
    Laboratory animals, 2012, Volume: 46, Issue:1

    Topics: Animals; Blood Chemical Analysis; Caloric Restriction; Diabetes Mellitus, Type 2; Diabetic Nephropat

2012
Oxidative/nitrosative stress and protein damages in aqueous humor of hyperglycemic rabbits: effects of two oral antidiabetics, pioglitazone and repaglinide.
    Experimental diabetes research, 2012, Volume: 2012

    Topics: Animals; Antioxidants; Aqueous Humor; Carbamates; Diabetes Mellitus, Experimental; Glutathione Perox

2012
Comparative study between atorvastatin and losartan on high fat diet-induced type 2 diabetes mellitus in rats.
    Fundamental & clinical pharmacology, 2013, Volume: 27, Issue:5

    Topics: Angiotensin II Type 1 Receptor Blockers; Animals; Atorvastatin; Cholesterol, LDL; Diabetes Mellitus,

2013
Pioglitazone prevents hyperglycemia induced decrease of AdipoR1 and AdipoR2 in coronary arteries and coronary VSMCs.
    Molecular and cellular endocrinology, 2012, Nov-05, Volume: 363, Issue:1-2

    Topics: Adiponectin; Animals; Blood Pressure; Cells, Cultured; Coronary Vessels; Diabetes Mellitus, Experime

2012
Marked hyperglycemia after androgen-deprivation therapy for prostate cancer and usefulness of pioglitazone for its treatment.
    Metabolism: clinical and experimental, 2005, Volume: 54, Issue:1

    Topics: Aged; Aged, 80 and over; Androgen Receptor Antagonists; Glycated Hemoglobin; Humans; Hyperglycemia;

2005
Effects of pioglitazone on hyperglycemia-induced alterations in antioxidative system in tissues of alloxan-treated diabetic animals.
    Experimental and toxicologic pathology : official journal of the Gesellschaft fur Toxikologische Pathologie, 2005, Volume: 56, Issue:4-5

    Topics: Alloxan; Animals; Antioxidants; Diabetes Mellitus, Experimental; Glutathione; Glutathione Peroxidase

2005
PPARgamma agonists exert antifibrotic effects in renal tubular cells exposed to high glucose.
    American journal of physiology. Renal physiology, 2005, Volume: 289, Issue:5

    Topics: Cell Culture Techniques; Cell Proliferation; Fibrosis; Glucose; Humans; Hyperglycemia; Hypoglycemic

2005
The phosphatidylinositol-3-kinase inhibitor PX-866 overcomes resistance to the epidermal growth factor receptor inhibitor gefitinib in A-549 human non-small cell lung cancer xenografts.
    Molecular cancer therapeutics, 2005, Volume: 4, Issue:9

    Topics: Animals; Antineoplastic Agents; Carcinoma, Non-Small-Cell Lung; Drug Resistance, Neoplasm; Enzyme In

2005
PPARgamma agonists: a new strategy for antithrombotic therapy.
    Journal of thrombosis and haemostasis : JTH, 2005, Volume: 3, Issue:10

    Topics: Diabetic Angiopathies; Fibrinolytic Agents; Humans; Hyperglycemia; Hypoglycemic Agents; Pioglitazone

2005
PPAR gamma agonists partially restores hyperglycemia induced aggravation of vascular dysfunction to angiotensin II in thoracic aorta isolated from rats with insulin resistance.
    Pharmacological research, 2007, Volume: 55, Issue:5

    Topics: Angiotensin II; Animals; Aorta, Thoracic; Blood Pressure; Dietary Fats; Disease Models, Animal; Dose

2007
Treatment of antipsychotic-associated hyperglycemia with pioglitazone: a case series.
    Journal of clinical psychopharmacology, 2007, Volume: 27, Issue:4

    Topics: Adult; Aged; Antipsychotic Agents; Blood Glucose; Female; Homeostasis; Humans; Hyperglycemia; Hypogl

2007
Prevention and noninvasive management of coronary atherosclerosis in patients with diabetes.
    Current atherosclerosis reports, 2008, Volume: 10, Issue:2

    Topics: Antihypertensive Agents; Cholesterol, HDL; Cholesterol, LDL; Coronary Artery Disease; Diabetes Melli

2008
Effects of thiazolidinediones on glucocorticoid-induced insulin resistance and GLUT4 glucose transporter expression in rat skeletal muscle.
    Metabolism: clinical and experimental, 1993, Volume: 42, Issue:10

    Topics: Animals; Benzopyrans; Blood Glucose; Deoxyglucose; Dexamethasone; Glucocorticoids; Glucose Transport

1993
Insulin action on protein phosphatase-1 activation is enhanced by the antidiabetic agent pioglitazone in cultured diabetic hepatocytes.
    Molecular and cellular biochemistry, 1998, Volume: 182, Issue:1-2

    Topics: Animals; Cells, Cultured; Enzyme Activation; Glycogen Synthase; Hyperglycemia; Hypoglycemic Agents;

1998
The novel hypoglycemic agent YM440 normalizes hyperglycemia without changing body fat weight in diabetic db/db mice.
    Metabolism: clinical and experimental, 2000, Volume: 49, Issue:3

    Topics: 3T3 Cells; Adipose Tissue; Animals; Blood Glucose; Cell Differentiation; Chromans; Diabetes Mellitus

2000
Pioglitazone attenuates basal and postprandial insulin concentrations and blood pressure in the spontaneously hypertensive rat.
    American journal of hypertension, 2000, Volume: 13, Issue:4 Pt 1

    Topics: Animals; Area Under Curve; Blood Glucose; Blood Pressure; Body Weight; Diabetes Mellitus, Type 2; Gl

2000
[New development in diabetes therapy. 35th Annual Meeting of the German Diabetes Society, Munich, May 5-June 3, 2000].
    Der Internist, 2000, Volume: 41, Issue:9

    Topics: Chromans; Diabetes Mellitus, Type 2; Germany; Humans; Hyperglycemia; Hypoglycemic Agents; Insulin; P

2000
Effects of pioglitazone on hepatic and peripheral insulin resistance in Wistar fatty rats.
    Arzneimittel-Forschung, 1990, Volume: 40, Issue:4

    Topics: Animals; Blood Glucose; Body Weight; Hyperglycemia; Hypoglycemic Agents; Insulin; Insulin Resistance

1990