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.
Excerpt | Relevance | Reference |
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"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." | 9.17 | Effects 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." | 7.75 | Peroxisome 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." | 7.73 | Marked 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." | 7.68 | Effects 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." | 6.76 | PIOfix-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." | 5.36 | Metformin 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." | 5.34 | PPAR 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." | 5.33 | Effects 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." | 5.19 | The 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." | 5.17 | Effects 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)." | 5.14 | 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. ( 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)." | 5.12 | Effects 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." | 5.10 | Antiatherogenic 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." | 5.10 | Improved 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." | 4.89 | What 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." | 3.83 | The 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." | 3.80 | A 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." | 3.80 | Anti-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." | 3.77 | Dynamic 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." | 3.75 | Peroxisome 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." | 3.73 | Marked 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." | 3.73 | PPARgamma 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." | 3.70 | The 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." | 3.70 | Pioglitazone 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." | 3.68 | Effects 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." | 2.84 | 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. ( 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." | 2.80 | 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. ( 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." | 2.80 | Randomized 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." | 2.78 | Efficacy 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." | 2.76 | PIOfix-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." | 2.72 | Diabetes, stroke, and neuroresilience: looking beyond hyperglycemia. ( Krinock, MJ; Singhal, NS, 2021) |
"Patients with type 2 diabetes mellitus are at high risk of cardiovascular disease." | 2.71 | Pioglitazone 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." | 2.47 | Macrovascular 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." | 2.44 | Initiating insulin in patients with type 2 diabetes. ( Aoki, TJ; White, RD, 2007) |
"Type 2 diabetes is strongly associated with increased risk of cardiovascular disease." | 2.42 | Peroxisome 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)." | 1.46 | Cardiovascular 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." | 1.42 | Hyperglycemia 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." | 1.42 | PPARγ 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)." | 1.39 | Comparative 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." | 1.38 | Oxidative/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." | 1.37 | Metabolic 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." | 1.36 | Metformin 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." | 1.34 | PPAR 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." | 1.33 | Effects 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." | 1.29 | Synthesis and biological activity of metabolites of the antidiabetic, antihyperglycemic agent pioglitazone. ( Colca, JR; Fisher, RM; Kletzein, RF; Parker, TT; Tanis, SP, 1996) |
Timeframe | Studies, this research(%) | All Research% |
---|---|---|
pre-1990 | 0 (0.00) | 18.7374 |
1990's | 4 (4.60) | 18.2507 |
2000's | 31 (35.63) | 29.6817 |
2010's | 49 (56.32) | 24.3611 |
2020's | 3 (3.45) | 2.80 |
Authors | Studies |
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Tanis, SP | 1 |
Parker, TT | 1 |
Colca, JR | 1 |
Fisher, RM | 1 |
Kletzein, RF | 1 |
Furukawa, A | 1 |
Arita, T | 1 |
Satoh, S | 1 |
Wakabayashi, K | 1 |
Hayashi, S | 1 |
Matsui, Y | 3 |
Araki, K | 1 |
Kuroha, M | 1 |
Ohsumi, J | 1 |
Ushiroda, K | 1 |
Maruta, K | 1 |
Kitoh, M | 1 |
Iwai, K | 1 |
Nagamine, J | 1 |
Tsuchida, A | 1 |
Taiji, M | 1 |
Nagata, R | 1 |
Ding, LB | 1 |
Li, Y | 1 |
Liu, GY | 1 |
Li, TH | 1 |
Li, F | 1 |
Guan, J | 1 |
Wang, HJ | 1 |
Krinock, MJ | 1 |
Singhal, NS | 1 |
Pires Mendes, C | 1 |
Postal, BG | 1 |
Silva Frederico, MJ | 1 |
Gonçalves Marques Elias, R | 1 |
Aiceles de Medeiros Pinto, V | 1 |
da Fonte Ramos, C | 1 |
Devantier Neuenfeldt, P | 1 |
Nunes, RJ | 1 |
Mena Barreto Silva, FR | 1 |
Katsiki, N | 1 |
Mikhailidis, DP | 1 |
Inzucchi, SE | 1 |
Viscoli, CM | 1 |
Young, LH | 1 |
Furie, KL | 1 |
Gorman, M | 1 |
Lovejoy, AM | 1 |
Dagogo-Jack, S | 1 |
Ismail-Beigi, F | 1 |
Korytkowski, MT | 1 |
Pratley, RE | 1 |
Schwartz, GG | 1 |
Kernan, WN | 1 |
Li, X | 1 |
Wang, E | 1 |
Yin, B | 1 |
Fang, D | 1 |
Chen, P | 1 |
Wang, G | 1 |
Zhao, J | 1 |
Zhang, H | 1 |
Chen, W | 1 |
Abdul-Ghani, M | 2 |
DeFronzo, RA | 3 |
Del Prato, S | 1 |
Chilton, R | 1 |
Singh, R | 1 |
Ryder, REJ | 1 |
Home, PD | 1 |
Ahrén, B | 1 |
Reusch, JEB | 1 |
Rendell, M | 1 |
Weissman, PN | 1 |
Cirkel, DT | 1 |
Miller, D | 1 |
Ambery, P | 1 |
Carr, MC | 1 |
Nauck, MA | 1 |
Campbell, JM | 1 |
Adanichkin, N | 1 |
Kurmis, R | 1 |
Munn, Z | 1 |
Motohashi, Y | 1 |
Kemmochi, Y | 1 |
Maekawa, T | 1 |
Tadaki, H | 1 |
Sasase, T | 1 |
Tanaka, Y | 1 |
Kakehashi, A | 1 |
Yamada, T | 1 |
Ohta, T | 2 |
Mudassir, HA | 1 |
Qureshi, SA | 1 |
Azmi, MB | 1 |
Ahsan, M | 1 |
Khaloo, P | 1 |
Asadi Komeleh, S | 1 |
Alemi, H | 1 |
Mansournia, MA | 1 |
Mohammadi, A | 1 |
Yadegar, A | 1 |
Afarideh, M | 2 |
Esteghamati, S | 1 |
Nakhjavani, M | 2 |
Esteghamati, A | 2 |
Zhuang, Y | 1 |
Yin, Q | 1 |
Pinget, M | 1 |
Goldenberg, R | 1 |
Niemoeller, E | 1 |
Muehlen-Bartmer, I | 1 |
Guo, H | 1 |
Aronson, R | 1 |
Lee, JO | 1 |
Auger, C | 1 |
Park, DH | 1 |
Kang, M | 1 |
Oak, MH | 1 |
Kim, KR | 1 |
Schini-Kerth, VB | 1 |
Zenari, L | 1 |
Marangoni, A | 1 |
Bone, HG | 1 |
Lindsay, R | 1 |
McClung, MR | 1 |
Perez, AT | 1 |
Raanan, MG | 1 |
Spanheimer, RG | 1 |
He, Q | 1 |
Zhang, X | 1 |
Han, B | 1 |
Xu, J | 1 |
Tang, K | 1 |
Fu, Z | 1 |
Yin, H | 1 |
Raccah, D | 1 |
Gourdy, P | 1 |
Sagnard, L | 1 |
Ceriello, A | 2 |
Sakata, S | 1 |
Mera, Y | 1 |
Kuroki, Y | 1 |
Nashida, R | 1 |
Kakutani, M | 1 |
Tripathy, D | 1 |
Musi, N | 1 |
Gastaldelli, A | 3 |
Niture, NT | 1 |
Ansari, AA | 1 |
Naik, SR | 1 |
Sykes, AP | 2 |
O'Connor-Semmes, R | 2 |
Dobbins, R | 2 |
Dorey, DJ | 1 |
Lorimer, JD | 1 |
Walker, S | 2 |
Wilkison, WO | 2 |
Kler, L | 2 |
Kemp, GL | 1 |
Almond, SR | 1 |
Chen, YJ | 1 |
Chan, DC | 1 |
Lan, KC | 1 |
Wang, CC | 1 |
Chen, CM | 1 |
Chao, SC | 1 |
Tsai, KS | 1 |
Yang, RS | 1 |
Liu, SH | 1 |
Lecube, A | 1 |
Bueno, M | 1 |
Suárez, X | 1 |
Thakran, S | 1 |
Zhang, Q | 1 |
Morales-Tirado, V | 1 |
Steinle, JJ | 1 |
Azizi, R | 1 |
Ebadi, M | 1 |
Noshad, S | 1 |
Mousavizadeh, M | 1 |
Hayashi, A | 1 |
Takemoto, M | 1 |
Shoji, M | 1 |
Hattori, A | 1 |
Sugita, K | 1 |
Yokote, K | 1 |
Sims-Robinson, C | 1 |
Bakeman, A | 1 |
Rosko, A | 1 |
Glasser, R | 1 |
Feldman, EL | 1 |
Matsumoto, Y | 1 |
Ishii, M | 1 |
Hayashi, Y | 1 |
Miyazaki, S | 1 |
Sugita, T | 1 |
Sumiya, E | 1 |
Sekimizu, K | 1 |
Kaku, K | 2 |
Katou, M | 1 |
Igeta, M | 1 |
Ohira, T | 1 |
Sano, H | 1 |
Gliem, M | 1 |
Klotz, L | 1 |
van Rooijen, N | 1 |
Hartung, HP | 1 |
Jander, S | 1 |
Tai, CJ | 2 |
Choong, CY | 1 |
Shi, YC | 1 |
Lin, YC | 1 |
Wang, CW | 1 |
Lee, BH | 1 |
Joubert, M | 1 |
Jagu, B | 1 |
Montaigne, D | 1 |
Marechal, X | 1 |
Tesse, A | 1 |
Ayer, A | 1 |
Dollet, L | 1 |
Le May, C | 1 |
Toumaniantz, G | 1 |
Manrique, A | 1 |
Charpentier, F | 1 |
Staels, B | 1 |
Magré, J | 1 |
Cariou, B | 1 |
Prieur, X | 1 |
Okoduwa, SI | 1 |
Umar, IA | 1 |
James, DB | 1 |
Inuwa, HM | 1 |
Aoki, TJ | 1 |
White, RD | 1 |
Mizukami, H | 1 |
Wada, R | 1 |
Yonezawa, A | 1 |
Sugawara, A | 2 |
Yagihashi, S | 1 |
Hirasawa, Y | 2 |
Ohtsu, S | 1 |
Yamane, K | 1 |
Toyoshi, T | 2 |
Kyuki, K | 2 |
Sakai, T | 1 |
Feng, Y | 1 |
Nagamatsu, T | 1 |
Fujisawa, K | 1 |
Nishikawa, T | 1 |
Kukidome, D | 1 |
Imoto, K | 1 |
Yamashiro, T | 1 |
Motoshima, H | 1 |
Matsumura, T | 1 |
Araki, E | 1 |
Ihle, NT | 2 |
Lemos, R | 1 |
Schwartz, D | 1 |
Oh, J | 1 |
Halter, RJ | 1 |
Wipf, P | 2 |
Kirkpatrick, L | 1 |
Powis, G | 2 |
Miyata, T | 1 |
van Ypersele de Strihou, C | 1 |
Tanaka, S | 1 |
Origasa, H | 1 |
Kikuchi, M | 1 |
Akanuma, Y | 1 |
Makino, H | 1 |
Shimizu, I | 1 |
Murao, S | 1 |
Kondo, S | 1 |
Tabara, Y | 1 |
Fujiyama, M | 1 |
Fujii, Y | 1 |
Takada, Y | 1 |
Nakai, K | 1 |
Izumi, K | 1 |
Ohashi, J | 1 |
Kawamura, R | 1 |
Yamauchi, J | 1 |
Takata, Y | 1 |
Nishida, W | 1 |
Hashiramoto, M | 1 |
Onuma, H | 1 |
Osawa, H | 1 |
Gumieniczek, A | 4 |
Krzywdzińska, M | 1 |
Nowak, M | 1 |
Glass, LC | 1 |
Cusi, K | 1 |
Berria, R | 1 |
Petz, R | 1 |
Cersosimo, E | 1 |
Sugiura, T | 1 |
Ito, M | 1 |
Vikram, A | 1 |
Jena, G | 1 |
Naka, KK | 1 |
Pappas, K | 1 |
Papathanassiou, K | 1 |
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Pfützner, A | 2 |
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Forst, T | 2 |
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Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
---|---|---|---|---|---|---|---|
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 3 | 310 participants (Actual) | Interventional | 2009-01-31 | Completed | ||
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 3 | 779 participants (Actual) | Interventional | 2009-02-28 | Completed | ||
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 3 | 309 participants (Actual) | Interventional | 2009-01-31 | Completed | ||
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 3 | 685 participants (Actual) | Interventional | 2009-02-28 | Completed | ||
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 3 | 1,049 participants (Actual) | Interventional | 2009-02-28 | Completed | ||
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 3 | 484 participants (Actual) | Interventional | 2008-09-30 | Completed | ||
Effects of Lixisenatide on Gastric Emptying, Glycaemia and 'Postprandial' Blood Pressure in Type 2 Diabetes and Healthy Subjects.[NCT02308254] | Phase 1/Phase 2 | 30 participants (Anticipated) | Interventional | 2013-11-30 | Recruiting | ||
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 2 | 136 participants (Anticipated) | Interventional | 2013-04-30 | Active, 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 4 | 156 participants (Actual) | Interventional | 2008-05-31 | Completed | ||
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 2 | 334 participants (Actual) | Interventional | 2007-01-23 | Completed | ||
A Once-Daily Dose-Ranging Study of GSK189075 Versus Placebo In The Treatment of Type 2 Diabetes Mellitus in Treatment-Naïve Subjects[NCT00495469] | Phase 2 | 250 participants (Actual) | Interventional | 2007-08-17 | Completed | ||
Comparison of Metformin and Pioglitazone Effects on Serum YKL-40 Concentrations in Patients With Newly Diagnosed Type 2 Diabetes[NCT01963663] | 84 participants (Actual) | Interventional | 2012-11-30 | Completed | |||
Effects of a Pioglitazone/Metformin Fixed Combination in Comparison to Metformin in Combination With Glimepiride on Diabetic Dyslipidemia[NCT00770653] | Phase 3 | 305 participants (Actual) | Interventional | 2007-04-30 | Completed | ||
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 4 | 77 participants (Actual) | Interventional | 2008-11-30 | Completed | ||
[information is prepared from clinicaltrials.gov, extracted Sep-2024] |
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
Intervention | Percentage 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 |
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
Intervention | Kilograms (Mean) |
---|---|
Placebo + Pioglitazone With or Without Metformin | 1.50 |
Albiglutide 30 mg + Pioglitazone With or Without Metformin | -0.16 |
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
Intervention | Kilograms (Least Squares Mean) |
---|---|
Placebo + Pioglitazone With or Without Metformin | 0.45 |
Albiglutide 30 mg + Pioglitazone With or Without Metformin | 0.28 |
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
Intervention | Millimoles per liter (mmol/L) (Mean) |
---|---|
Placebo + Pioglitazone With or Without Metformin | 0.03 |
Albiglutide 30 mg + Pioglitazone With or Without Metformin | -1.26 |
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
Intervention | Millimoles per liter (mmol/L) (Least Squares Mean) |
---|---|
Placebo + Pioglitazone With or Without Metformin | 0.35 |
Albiglutide 30 mg + Pioglitazone With or Without Metformin | -1.28 |
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
Timeframe: From the start of study medication until the end of the treatment (up to Week 156)
Intervention | Weeks (Median) |
---|---|
Placebo + Pioglitazone With or Without Metformin | 52.86 |
Albiglutide 30 mg + Pioglitazone With or Without Metformin | NA |
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
Intervention | Percentage of HbA1c in the blood (Mean) | |
---|---|---|
Week 104, n= 29, 72 | Week 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 |
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
Intervention | Participants (Number) | ||
---|---|---|---|
HbA1c <6.5% | HbA1c <7% | HbA1c <7.5% | |
Albiglutide 30 mg + Pioglitazone With or Without Metformin | 20 | 32 | 44 |
Placebo + Pioglitazone With or Without Metformin | 7 | 12 | 17 |
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
Intervention | Participants (Number) | ||
---|---|---|---|
HbA1c <6.5% | HbA1c <7% | HbA1c <7.5% | |
Albiglutide 30 mg + Pioglitazone With or Without Metformin | 37 | 66 | 96 |
Placebo + Pioglitazone With or Without Metformin | 8 | 22 | 44 |
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
Intervention | Percentage of HbA1c in the blood (Least Squares Mean) |
---|---|
Albiglutide 30 mg + Metformin +/- Sulfonylurea | -0.67 |
Insulin Glargine 10 Units + Metformin +/- Sulfonylurea | -0.79 |
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
Intervention | Kilograms (Mean) |
---|---|
Albiglutide 30 mg + Metformin +/- Sulfonylurea | -3.47 |
Insulin Glargine 10 Units + Metformin +/- Sulfonylurea | 0.90 |
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
Intervention | Kilograms (Least Squares Mean) |
---|---|
Albiglutide 30 mg + Metformin +/- Sulfonylurea | -1.05 |
Insulin Glargine 10 Units + Metformin +/- Sulfonylurea | 1.56 |
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
Intervention | Millimoles per liter (mmol/L) (Mean) |
---|---|
Albiglutide 30 mg + Metformin +/- Sulfonylurea | -0.83 |
Insulin Glargine 10 Units + Metformin +/- Sulfonylurea | -2.19 |
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
Intervention | Millimoles per liter (mmol/L) (Least Squares Mean) |
---|---|
Albiglutide 30 mg + Metformin +/- Sulfonylurea | -0.87 |
Insulin Glargine 10 Units + Metformin +/- Sulfonylurea | -2.06 |
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
Intervention | Millimoles per hour per liter (mmol.h/L) (Mean) |
---|---|
Albiglutide 30 mg + Metformin +/- Sulfonylurea | 0.457 |
Insulin Glargine 10 Units + Metformin +/- Sulfonylurea | -1.657 |
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
Intervention | Percentage of HbA1c in the blood (Mean) |
---|---|
Albiglutide 30 mg + Metformin +/- Sulfonylurea | -0.83 |
Insulin Glargine 10 Units + Metformin +/- Sulfonylurea | -1.00 |
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
Timeframe: From the start of study medication until the end of the treatment (up to Week 156)
Intervention | Weeks (Median) |
---|---|
Albiglutide 30 mg + Metformin +/- Sulfonylurea | 107.57 |
Insulin Glargine 10 Units + Metformin +/- Sulfonylurea | NA |
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
Intervention | nanograms/milliliter (ng/mL) (Mean) | |||
---|---|---|---|---|
Week 8, Pre-dose, n=408 | Week 8, Post-dose, n=398 | Week 24, Pre-dose, n=416 | Week 24, Post-dose, n=401 | |
Albiglutide 30 mg + Metformin +/- Sulfonylurea | 1642.83 | 1911.35 | 2159.30 | 2748.15 |
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
Intervention | Participants (Number) | ||
---|---|---|---|
HbA1c <6.5% | HbA1c <7% | HbA1c <7.5% | |
Albiglutide 30 mg + Metformin +/- Sulfonylurea | 33 | 59 | 85 |
Insulin Glargine 10 Units + Metformin +/- Sulfonylurea | 18 | 46 | 71 |
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
Intervention | Participants (Number) | ||
---|---|---|---|
HbA1c <6.5% | HbA1c <7% | HbA1c <7.5% | |
Albiglutide 30 mg + Metformin +/- Sulfonylurea | 54 | 156 | 268 |
Insulin Glargine 10 Units + Metformin +/- Sulfonylurea | 25 | 78 | 135 |
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
Intervention | Percentage of HbA1c in the blood (Least Squares Mean) |
---|---|
Placebo | 0.15 |
Albiglutide 30 mg | -0.70 |
Albiglutide 50 mg | -0.89 |
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
Intervention | Kilograms (Mean) |
---|---|
Placebo | -2.91 |
Albiglutide 30 mg | -1.32 |
Albiglutide 50 mg | -2.24 |
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
Intervention | Kilograms (Least Squares Mean) |
---|---|
Placebo | -0.66 |
Albiglutide 30 mg | -0.39 |
Albiglutide 50 mg | -0.86 |
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
Intervention | Millimoles per liter (mmol/L) (Mean) |
---|---|
Placebo | -0.23 |
Albiglutide 30 mg | -1.31 |
Albiglutide 50 mg | -1.83 |
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
Intervention | Millimoles per liter (mmol/L) (Least Squares Mean) |
---|---|
Placebo | 1.00 |
Albiglutide 30 mg | -0.88 |
Albiglutide 50 mg | -1.38 |
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
Intervention | Nanomoles/Liter (nmol/L) (Least Squares Mean) |
---|---|
Placebo | -0.51 |
Albiglutide 30 mg | -1.74 |
Albiglutide 50 mg | -2.05 |
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
Intervention | Nanomoles/Liter (nmol/L) (Least Squares Mean) |
---|---|
Placebo | 0.05 |
Albiglutide 30 mg Weekly | 0.03 |
Albiglutide 50 mg Weekly | 0.08 |
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
Timeframe: From the start of study medication until the end of the treatment (up to Week 156)
Intervention | Weeks (Median) |
---|---|
Placebo | 49.71 |
Albiglutide 30 mg | 118.43 |
Albiglutide 50 mg | NA |
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
Intervention | nanograms/milliliter (ng/mL) (Mean) | |||
---|---|---|---|---|
Week 8 Pre-dose, n=85, 85 | Week 8 Post-dose, n=87, 80 | Week 24 Pre-dose, n=79, 74 | Week 24 Post-dose, n=81, 72 | |
Albiglutide 30 mg | 1582 | 1900 | 1912 | 2289 |
Albiglutide 50 mg | 1433 | 1759 | 3060 | 3484 |
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
Intervention | Percentage of HbA1c in the blood (Mean) | |
---|---|---|
Week 104, n=21, 39, 42 | Week 156, n=14, 30, 32 | |
Albiglutide 30 mg | -0.93 | -0.96 |
Albiglutide 50 mg | -1.18 | -1.07 |
Placebo | -0.40 | -0.61 |
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
Intervention | picomoles/Liter (pmol/L) (Least Squares Mean) | |
---|---|---|
4hr Ins AUC | 4hr Pro-Ins AUC | |
Albiglutide 30 mg | 2.9 | 1.9 |
Albiglutide 50 mg | 39.9 | -10.7 |
Placebo | 49.2 | 1.0 |
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
Intervention | Participants (Number) | ||
---|---|---|---|
Week 156, HbA1c <6.5% | Week 156, HbA1c <7.0% | Week 156, HbA1c <7.5% | |
Albiglutide 30 mg | 10 | 18 | 24 |
Albiglutide 50 mg | 11 | 19 | 29 |
Placebo | 6 | 8 | 13 |
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
Intervention | Participants (Number) | ||
---|---|---|---|
Week 52, HbA1c <6.5% | Week 52, HbA1c <7.0% | Week 52, HbA1c <7.5% | |
Albiglutide 30 mg | 25 | 49 | 59 |
Albiglutide 50 mg | 24 | 39 | 62 |
Placebo | 10 | 21 | 34 |
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
Intervention | Percentage of HbA1c in the blood (Least Squares Mean) |
---|---|
Placebo + Metformin + Glimepiride | 0.33 |
Pioglitazone + Metformin + Glimepiride | -0.80 |
Albiglutide + Metformin + Glimepiride | -0.55 |
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
Intervention | Kilograms (Least Squares Mean) |
---|---|
Placebo + Metformin + Glimepiride | -0.40 |
Pioglitazone + Metformin + Glimepiride | 4.43 |
Albiglutide + Metformin + Glimepiride | -0.42 |
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
Intervention | Millimoles per liter (mmol/L) (Least Squares Mean) |
---|---|
Placebo + Metformin + Glimepiride | 0.64 |
Pioglitazone + Metformin + Glimepiride | -1.74 |
Albiglutide + Metformin + Glimepiride | -0.69 |
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
Timeframe: From the start of study medication until the end of the treatment (up to Week 156)
Intervention | Weeks (Median) |
---|---|
Placebo + Metformin + Glimepiride | 49.57 |
Pioglitazone + Metformin + Glimepiride | NA |
Albiglutide + Metformin + Glimepiride | 137.71 |
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
Intervention | Kilograms (Mean) | |
---|---|---|
Week 104, n=12, 130, 104 | Week 156, n=9, 90, 71 | |
Albiglutide + Metformin + Glimepiride | -0.90 | -1.53 |
Pioglitazone + Metformin + Glimepiride | 6.28 | 6.52 |
Placebo + Metformin + Glimepiride | -2.16 | -4.47 |
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
Intervention | Millimoles per liter (mmol/L) (Mean) | |
---|---|---|
Week 104, n=12, 128, 103 | Week 156, n=9, 88, 71 | |
Albiglutide + Metformin + Glimepiride | -0.99 | -0.88 |
Pioglitazone + Metformin + Glimepiride | -1.98 | -1.94 |
Placebo + Metformin + Glimepiride | 0.43 | -0.50 |
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
Intervention | Percentage of HbA1c in the blood (Mean) | |
---|---|---|
Week 104, n=12, 130, 104 | Week 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 |
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
Intervention | Participants (Number) | ||
---|---|---|---|
HbA1c <6.5% | HbA1c <7.0% | HbA1c <7.5% | |
Albiglutide + Metformin + Glimepiride | 16 | 26 | 45 |
Pioglitazone + Metformin + Glimepiride | 23 | 44 | 68 |
Placebo + Metformin + Glimepiride | 1 | 3 | 5 |
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
Intervention | Participants (Number) | ||
---|---|---|---|
HbA1c <6.5% | HbA1c <7.0% | HbA1c <7.5% | |
Albiglutide + Metformin + Glimepiride | 27 | 79 | 126 |
Pioglitazone + Metformin + Glimepiride | 37 | 94 | 150 |
Placebo + Metformin + Glimepiride | 4 | 10 | 19 |
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
Intervention | Percentage of HbA1c in the blood (Least Squares Mean) |
---|---|
Placebo Plus Metformin | 0.27 |
Sitagliptin 100 mg Plus Metformin | -0.28 |
Glimepiride 2 mg Plus Metformin | -0.36 |
Albiglutide 30 mg Plus Metformin | -0.63 |
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
Intervention | Kilograms (Least Squares Mean) |
---|---|
Placebo Plus Metformin | -1.00 |
Sitagliptin 100 mg Plus Metformin | -0.86 |
Glimepiride 2 mg Plus Metformin | 1.17 |
Albiglutide 30 mg Plus Metformin | -1.21 |
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
Intervention | Kilograms (Mean) |
---|---|
Placebo Plus Metformin | -3.61 |
Sitagliptin 100 mg Plus Metformin | -2.05 |
Glimepiride 2 mg Plus Metformin | 0.98 |
Albiglutide 30 mg Plus Metformin | -2.31 |
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
Intervention | Millimoles per liter (mmol/L) (Least Squares Mean) |
---|---|
Placebo Plus Metformin | 0.55 |
Sitagliptin 100 mg Plus Metformin | -0.12 |
Glimepiride 2 mg Plus Metformin | -0.41 |
Albiglutide 30 mg Plus Metformin | -0.98 |
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
Intervention | Millimoles 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 |
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
Intervention | Percentage 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 |
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
Timeframe: From the start of study medication until the end of the treatment (up to Week 156)
Intervention | Weeks (Median) |
---|---|
Placebo Plus Metformin | 67.71 |
Sitagliptin 100 mg Plus Metformin | NA |
Glimepiride 2 mg Plus Metformin | NA |
Albiglutide 30 mg Plus Metformin | NA |
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
Intervention | Participants (Number) | ||
---|---|---|---|
HbA1c <6.5% | HbA1c <7.0% | HbA1c <7.5% | |
Albiglutide 30 mg Plus Metformin | 50 | 113 | 172 |
Glimepiride 2 mg Plus Metformin | 40 | 94 | 147 |
Placebo Plus Metformin | 7 | 15 | 27 |
Sitagliptin 100 mg Plus Metformin | 45 | 94 | 132 |
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
Intervention | Participants (Number) | ||
---|---|---|---|
HbA1c <6.5% | HbA1c <7.0% | HbA1c <7.5% | |
Albiglutide 30 mg Plus Metformin | 31 | 69 | 90 |
Glimepiride 2 mg Plus Metformin | 15 | 44 | 69 |
Placebo Plus Metformin | 4 | 7 | 13 |
Sitagliptin 100 mg Plus Metformin | 23 | 44 | 69 |
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
Intervention | percentage of hemoglobin (Least Squares Mean) |
---|---|
Placebo | -0.34 |
Lixisenatide | -0.90 |
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) |
---|---|
Placebo | 6.98 |
Lixisenatide | 6.72 |
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
Intervention | kilogram (Least Squares Mean) |
---|---|
Placebo | 0.21 |
Lixisenatide | -0.21 |
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 | mmol/L (Least Squares Mean) |
---|---|
Placebo | -0.32 |
Lixisenatide | -1.16 |
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 | pmol/L (Least Squares Mean) |
---|---|
Placebo | -1.01 |
Lixisenatide | -10.36 |
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
Intervention | percentage of participants (Number) |
---|---|
Placebo | 11.3 |
Lixisenatide | 3.8 |
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
Intervention | percentage of participants (Number) |
---|---|
Placebo | 5.1 |
Lixisenatide | 9.2 |
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
Intervention | percentage of participants (Number) |
---|---|
Placebo | 26.4 |
Lixisenatide | 52.3 |
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
Intervention | percentage of participants (Number) |
---|---|
Placebo | 10.1 |
Lixisenatide | 28.9 |
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
Intervention | participants (Number) | |
---|---|---|
Symptomatic Hypoglycemia | Severe Symptomatic Hypoglycemia | |
Lixisenatide | 23 | 0 |
Placebo | 7 | 0 |
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.
Intervention | participants (Number) |
---|---|
Pioglitazone | 1 |
Placebo | 3 |
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.
Intervention | percent (Least Squares Mean) |
---|---|
Pioglitazone | -0.69 |
Placebo | -0.14 |
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.
Intervention | percent (Least Squares Mean) |
---|---|
Pioglitazone | -0.14 |
Placebo | 0.04 |
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.
Intervention | mg/dL (Least Squares Mean) | |
---|---|---|
Baseline to Month 12 (n=57; n=61) | Month 12 to Month 18 (n=54; n=57) | |
Pioglitazone | -2.8 | 0.4 |
Placebo | 6.0 | -1.0 |
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.
Intervention | participants (Number) | |
---|---|---|
Double-Blind Period (n=76; n=75) | Follow-up Period (n=63; n=59) | |
Pioglitazone | 1 | 0 |
Placebo | 7 | 1 |
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
Intervention | Percentage 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 |
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)
Intervention | Percentage of filtered glucose molecules (Mean) |
---|---|
Placebo | -1.09 |
GSK189075 50 mg | 27.96 |
GSK189075 100 mg | 40.43 |
GSK189075 250 mg | 38.98 |
GSK189075 500 mg | 42.41 |
GSK189075 1000 mg | 52.39 |
Pioglitazone 30 mg | -0.99 |
"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)
Intervention | Nanomol*hour per Liter (nmol*hr/L) (Mean) |
---|---|
Placebo | -0.140 |
GSK189075 50 mg | 0.654 |
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 |
"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)
Intervention | Picomol*hour per Liter (pmol*hr/L) (Mean) |
---|---|
Placebo | -5.3 |
GSK189075 50 mg | 162.4 |
GSK189075 100 mg | -70.9 |
GSK189075 250 mg | 66.6 |
GSK189075 500 mg | -173.9 |
GSK189075 1000 mg | -97.8 |
Pioglitazone 30 mg | 10.0 |
"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)
Intervention | Millimol*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 |
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
Intervention | Kilograms (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 mg | 0.96 |
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
Intervention | Picomol per Liter (pmol/L) (Mean) |
---|---|
Placebo | -30.6 |
GSK189075 50 mg | 0.3 |
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 |
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
Intervention | Micromol per Liter (mcmol/L) (Mean) |
---|---|
Placebo | 5.7 |
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 |
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
Intervention | Centimeters (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 mg | 1.3 |
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
Intervention | Participants (Count of Participants) |
---|---|
Placebo | 1 |
GSK189075 50 mg | 1 |
GSK189075 100 mg | 0 |
GSK189075 250 mg | 0 |
GSK189075 500 mg | 1 |
GSK189075 1000 mg | 0 |
Pioglitazone 30 mg | 0 |
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
Intervention | Percentage of hemoglobin (Mean) | |
---|---|---|
Week 4 | Week 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 |
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
Intervention | Millimoles per Liter (mmol/L) (Mean) | ||
---|---|---|---|
Week 4 | Week 8 | Week 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 |
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
Intervention | Participants (Count of Participants) | ||||||
---|---|---|---|---|---|---|---|
HbA1c <= 6.5% | HbA1c <7.0% | FPG <7 mmo/L | FPG <7.8 mmol/L | FPG <5.5 mmol/L | Decrease from Baseline of HbA1c >= 0.7% | Decrease from Baseline of FPG ≥1.7 mmol/L | |
GSK189075 100 mg | 8 | 18 | 20 | 26 | 2 | 27 | 19 |
GSK189075 1000 mg | 17 | 29 | 22 | 34 | 3 | 39 | 30 |
GSK189075 250 mg | 11 | 22 | 18 | 27 | 5 | 33 | 21 |
GSK189075 50 mg | 10 | 20 | 16 | 24 | 4 | 33 | 15 |
GSK189075 500 mg | 17 | 28 | 22 | 33 | 4 | 36 | 24 |
Pioglitazone 30 mg | 8 | 21 | 21 | 31 | 2 | 28 | 23 |
Placebo | 3 | 9 | 4 | 13 | 0 | 16 | 8 |
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
Intervention | Participants (Count of Participants) | |
---|---|---|
Low Hemoglobin | Low Hematocrit | |
GSK189075 100 mg | 0 | 0 |
GSK189075 1000 mg | 0 | 0 |
GSK189075 250 mg | 0 | 0 |
GSK189075 50 mg | 0 | 0 |
GSK189075 500 mg | 0 | 0 |
Pioglitazone 30 mg | 0 | 0 |
Placebo | 1 | 1 |
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
Intervention | Participants (Count of Participants) | |||||
---|---|---|---|---|---|---|
High SBP | Low SBP | High DBP | Low DBP | High heart rate | Low heart rate | |
GSK189075 100 mg | 2 | 1 | 0 | 2 | 0 | 0 |
GSK189075 1000 mg | 1 | 2 | 2 | 1 | 0 | 1 |
GSK189075 250 mg | 0 | 2 | 0 | 0 | 0 | 0 |
GSK189075 50 mg | 0 | 0 | 0 | 1 | 1 | 0 |
GSK189075 500 mg | 0 | 2 | 0 | 0 | 0 | 1 |
Pioglitazone 30 mg | 0 | 0 | 0 | 3 | 0 | 0 |
Placebo | 3 | 0 | 1 | 0 | 0 | 0 |
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)
Intervention | Participants (Count of Participants) | |||
---|---|---|---|---|
PR interval > 300 msec | QRS Duration > 200 msec | QTc(Bazett) > 500 msec | QTc(Fridericia) > 500 msec | |
GSK189075 100 mg | 0 | 0 | 0 | 0 |
GSK189075 1000 mg | 0 | 0 | 0 | 0 |
GSK189075 250 mg | 0 | 0 | 0 | 0 |
GSK189075 50 mg | 0 | 0 | 0 | 0 |
GSK189075 500 mg | 0 | 0 | 0 | 0 |
Pioglitazone 30 mg | 0 | 0 | 0 | 0 |
Placebo | 0 | 0 | 0 | 0 |
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
Intervention | Participants (Count of Participants) | |
---|---|---|
AE | SAE | |
GSK189075 100 mg | 17 | 0 |
GSK189075 1000 mg | 22 | 0 |
GSK189075 250 mg | 19 | 0 |
GSK189075 50 mg | 18 | 0 |
GSK189075 500 mg | 18 | 0 |
Pioglitazone 30 mg | 22 | 0 |
Placebo | 18 | 0 |
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
Intervention | Percent change (Median) | |||||||||||
---|---|---|---|---|---|---|---|---|---|---|---|---|
TG: Week 4 | TG: Week 8 | TG: Week 12 | TC: Week 4 | TC: Week 8 | TC: Week 12 | LDL-C: Week 4 | LDL-C: Week 8 | LDL-C: Week 12 | HDL-C: Week 4 | HDL-C: Week 8 | HDL-C: Week 12 | |
GSK189075 100 mg | 6.32 | 0.59 | 10.92 | 1.62 | 3.64 | 5.45 | 0.37 | 3.62 | 3.57 | 3.69 | 5.00 | 4.96 |
GSK189075 1000 mg | -4.62 | -7.30 | -9.97 | 2.39 | 0.00 | 2.77 | 7.02 | 4.44 | 14.89 | 0.00 | 0.00 | 4.27 |
GSK189075 250 mg | -13.42 | -10.01 | -4.71 | 4.13 | 4.49 | 3.97 | 6.91 | 8.96 | 3.93 | 5.13 | 3.09 | 6.70 |
GSK189075 50 mg | -3.45 | -9.09 | -10.91 | 1.85 | 3.49 | 3.39 | 0.83 | 8.67 | 6.69 | 5.43 | 6.20 | 5.56 |
GSK189075 500 mg | -13.04 | -13.35 | -15.28 | 4.43 | 5.31 | 9.82 | 10.03 | 7.57 | 11.43 | 5.69 | 7.14 | 11.93 |
Pioglitazone 30mg | -7.22 | -0.79 | -7.19 | 2.29 | 1.06 | -2.05 | 0.00 | -2.24 | 1.18 | 9.18 | 8.20 | 10.00 |
Placebo | -8.35 | -1.66 | 3.32 | 0.47 | 0.82 | 4.75 | 0.82 | 3.17 | 3.17 | -1.97 | 0.00 | 0.00 |
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
Intervention | Percentage (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 |
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
Intervention | kilograms (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 QD | 0.00 |
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
Intervention | millimoles 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 |
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
Intervention | micromoles 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 |
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
Intervention | mmol/L (Least Squares Mean) |
---|---|
Placebo | -0.02 |
GSK189075 100 mg QD | 0.00 |
GSK189075 250 mg QD | 0.02 |
GSK189075 500 mg QD | 0.06 |
GSK189075 1000 mg QD | 0.05 |
GSK189075 250 mg BID | 0.04 |
Pioglitazone 30 mg QD | 0.09 |
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
Intervention | Ratio (Least Squares Mean) |
---|---|
Placebo | 0.06 |
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 BID | 0.10 |
Pioglitazone 30 mg QD | -0.07 |
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
Intervention | mmol/L (Least Squares Mean) |
---|---|
Placebo | -0.02 |
GSK189075 100 mg QD | -0.17 |
GSK189075 250 mg QD | -0.03 |
GSK189075 500 mg QD | 0.08 |
GSK189075 1000 mg QD | -0.04 |
GSK189075 250 mg BID | 0.23 |
Pioglitazone 30 mg QD | 0.07 |
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
Intervention | mmol/L (Least Squares Mean) |
---|---|
Placebo | -0.03 |
GSK189075 100 mg QD | -0.08 |
GSK189075 250 mg QD | -0.12 |
GSK189075 500 mg QD | 0.10 |
GSK189075 1000 mg QD | -0.02 |
GSK189075 250 mg BID | 0.22 |
Pioglitazone 30 mg QD | 0.00 |
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
Intervention | Ratio (Least Squares Mean) |
---|---|
Placebo | 0.14 |
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 BID | 0.01 |
Pioglitazone 30 mg QD | -0.26 |
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
Intervention | mmol/L (Least Squares Mean) |
---|---|
Placebo | -0.01 |
GSK189075 100 mg QD | 0.19 |
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 |
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
Intervention | Participants (Count of Participants) |
---|---|
Placebo | 9 |
GSK189075 100 mg QD | 12 |
GSK189075 250 mg QD | 11 |
GSK189075 500 mg QD | 7 |
GSK189075 1000 mg QD | 14 |
GSK189075 250 mg BID | 7 |
Pioglitazone 30 mg QD | 8 |
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
Intervention | Participants (Count of Participants) |
---|---|
Placebo | 0 |
GSK189075 100 mg QD | 1 |
GSK189075 250 mg QD | 0 |
GSK189075 500 mg QD | 2 |
GSK189075 1000 mg QD | 1 |
GSK189075 250 mg BID | 1 |
Pioglitazone 30 mg QD | 0 |
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
Intervention | Percentage (Mean) | |
---|---|---|
Week 4 | Week 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 |
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
Intervention | Participants (Count of Participants) | ||
---|---|---|---|
Responders (<7 mmol/L) | Responders (<7.8 mmol/L) | Responders (reduction >=1.7 mmol/L) | |
GSK189075 100 mg QD | 10 | 20 | 9 |
GSK189075 1000 mg QD | 12 | 21 | 14 |
GSK189075 250 mg BID | 14 | 22 | 19 |
GSK189075 250 mg QD | 14 | 19 | 13 |
GSK189075 500 mg QD | 11 | 17 | 11 |
Pioglitazone 30 mg QD | 13 | 15 | 17 |
Placebo | 6 | 13 | 5 |
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
Intervention | Participants (Count of Participants) | ||
---|---|---|---|
Responders (<=6.5%) | Responders (<7%) | Responders (reduction>=0.7%) | |
GSK189075 100 mg QD | 5 | 11 | 13 |
GSK189075 1000 mg QD | 7 | 13 | 18 |
GSK189075 250 mg BID | 6 | 15 | 21 |
GSK189075 250 mg QD | 4 | 12 | 18 |
GSK189075 500 mg QD | 4 | 10 | 13 |
Pioglitazone 30 mg QD | 4 | 11 | 13 |
Placebo | 3 | 7 | 9 |
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
Intervention | Participants (Count of Participants) | |||||||||||||
---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
Albumin, low | Alkaline phosphatase, high | Alanine aminotransferase, high | Aspartate aminotransferase, high | Total bilirubin, high | Calcium, low | carbon dioxide content/Bicarbonate, low | Glucose, high | Potassium, high | Potassium, low | Sodium, high | Phosphorus, high | Total protein, high | Total protein, low | |
GSK189075 100 mg QD | 1 | 1 | 1 | 1 | 1 | 1 | 2 | 0 | 0 | 1 | 1 | 0 | 1 | 1 |
GSK189075 1000 mg QD | 0 | 0 | 0 | 0 | 1 | 0 | 1 | 0 | 2 | 0 | 0 | 0 | 0 | 0 |
GSK189075 250 mg BID | 0 | 0 | 0 | 0 | 1 | 2 | 1 | 0 | 1 | 0 | 0 | 0 | 0 | 0 |
GSK189075 250 mg QD | 0 | 0 | 0 | 0 | 0 | 3 | 0 | 0 | 1 | 0 | 0 | 0 | 0 | 0 |
GSK189075 500 mg QD | 0 | 0 | 0 | 0 | 0 | 0 | 1 | 0 | 0 | 0 | 0 | 1 | 0 | 0 |
Pioglitazone 30 mg QD | 0 | 0 | 0 | 0 | 2 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 0 |
Placebo | 0 | 0 | 0 | 0 | 1 | 0 | 0 | 1 | 0 | 0 | 0 | 0 | 0 | 0 |
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
Intervention | Participants (Count of Participants) | ||||||
---|---|---|---|---|---|---|---|
Hemoglobin, high | Hemoglobin, low | Hematocrit, high | Hematocrit, low | Platelet count, high | Platelet count, low | White blood cell count, low | |
GSK189075 100 mg QD | 0 | 0 | 0 | 2 | 0 | 0 | 0 |
GSK189075 1000 mg QD | 2 | 0 | 2 | 0 | 0 | 1 | 1 |
GSK189075 250 mg BID | 0 | 0 | 0 | 0 | 2 | 0 | 0 |
GSK189075 250 mg QD | 0 | 0 | 0 | 0 | 0 | 0 | 0 |
GSK189075 500 mg QD | 1 | 0 | 1 | 0 | 0 | 0 | 0 |
Pioglitazone 30 mg QD | 0 | 1 | 0 | 0 | 0 | 0 | 1 |
Placebo | 1 | 2 | 1 | 1 | 0 | 1 | 0 |
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
Intervention | Participants (Count of Participants) | |
---|---|---|
Any AEs | Any SAEs | |
GSK189075 100 mg QD | 15 | 1 |
GSK189075 1000 mg QD | 21 | 0 |
GSK189075 250 mg BID | 20 | 1 |
GSK189075 250 mg QD | 20 | 0 |
GSK189075 500 mg QD | 11 | 0 |
Pioglitazone 30 mg QD | 12 | 0 |
Placebo | 8 | 0 |
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
Intervention | Participants (Count of Participants) | |||||
---|---|---|---|---|---|---|
SBP, supine, low | DBP, supine, high | HR, supine, low | Orthostatic SBP, standing, low | Orthostatic DBP, standing, low | Orthostatic HR, standing, high | |
GSK189075 100 mg QD | 2 | 0 | 0 | 0 | 1 | 5 |
GSK189075 1000 mg QD | 2 | 0 | 1 | 0 | 0 | 5 |
GSK189075 250 mg BID | 2 | 1 | 0 | 1 | 1 | 7 |
GSK189075 250 mg QD | 0 | 0 | 0 | 3 | 3 | 6 |
GSK189075 500 mg QD | 3 | 0 | 0 | 4 | 2 | 5 |
Pioglitazone 30 mg QD | 3 | 0 | 1 | 0 | 1 | 5 |
Placebo | 1 | 0 | 1 | 1 | 1 | 4 |
The change between Adiponectin collected at week 24 or final visit and Adiponectin collected at baseline. (NCT00770653)
Timeframe: Baseline and Week 24.
Intervention | μg/mL (Least Squares Mean) |
---|---|
Pioglitazone 15 mg and Metformin 850 mg BID | 6.79 |
Glimepiride 2 mg and Metformin 850 mg BID | 0.72 |
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.
Intervention | mmHg (Least Squares Mean) |
---|---|
Pioglitazone 15 mg and Metformin 850 mg BID | -1.3 |
Glimepiride 2 mg and Metformin 850 mg BID | -0.1 |
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.
Intervention | ng/mL (Least Squares Mean) |
---|---|
Pioglitazone 15 mg and Metformin 850 mg BID | -3.7 |
Glimepiride 2 mg and Metformin 850 mg BID | -0.5 |
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.
Intervention | percent (Mean) |
---|---|
Pioglitazone 15 mg and Metformin 850 mg BID | 1.3 |
Glimepiride 2 mg and Metformin 850 mg BID | -0.4 |
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.
Intervention | percent (Mean) |
---|---|
Pioglitazone 15 mg and Metformin 850 mg BID | 2.4 |
Glimepiride 2 mg and Metformin 850 mg BID | -0.5 |
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.
Intervention | percent (Mean) |
---|---|
Pioglitazone 15 mg and Metformin 850 mg BID | 3.2 |
Glimepiride 2 mg and Metformin 850 mg BID | -1.1 |
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.
Intervention | percent (Mean) |
---|---|
Pioglitazone 15 mg and Metformin 850 mg BID | 2.7 |
Glimepiride 2 mg and Metformin 850 mg BID | -1.3 |
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.
Intervention | percent (Mean) |
---|---|
Pioglitazone 15 mg and Metformin 850 mg BID | 3.3 |
Glimepiride 2 mg and Metformin 850 mg BID | -.15 |
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.
Intervention | percent (Mean) |
---|---|
Pioglitazone 15 mg and Metformin 850 mg BID | 2.5 |
Glimepiride 2 mg and Metformin 850 mg BID | -1.3 |
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.
Intervention | percent (Mean) |
---|---|
Pioglitazone 15 mg and Metformin 850 mg BID | 3.1 |
Glimepiride 2 mg and Metformin 850 mg BID | -1.4 |
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.
Intervention | percent (Mean) |
---|---|
Pioglitazone 15 mg and Metformin 850 mg BID | 2.7 |
Glimepiride 2 mg and Metformin 850 mg BID | -1.3 |
The change between Fasting Glucose collected at week 24 or final visit and Fasting Glucose collected at baseline. (NCT00770653)
Timeframe: Baseline and Week 24.
Intervention | mg/dL (Least Squares Mean) |
---|---|
Pioglitazone 15 mg and Metformin 850 mg BID | -21.6 |
Glimepiride 2 mg and Metformin 850 mg BID | -21.1 |
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.
Intervention | pmol/L (Least Squares Mean) |
---|---|
Pioglitazone 15 mg and Metformin 850 mg BID | -5.18 |
Glimepiride 2 mg and Metformin 850 mg BID | -0.11 |
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.
Intervention | mg/dL (Least Squares Mean) |
---|---|
Pioglitazone 15 mg and Metformin 850 mg BID | -0.83 |
Glimepiride 2 mg and Metformin 850 mg BID | -0.95 |
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.
Intervention | mg/L (Mean) |
---|---|
Pioglitazone 15 mg and Metformin 850 mg BID | -0.87 |
Glimepiride 2 mg and Metformin 850 mg BID | 0.00 |
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.
Intervention | mg/L (Least Squares Mean) |
---|---|
Pioglitazone 15 mg and Metformin 850 mg BID | -0.21 |
Glimepiride 2 mg and Metformin 850 mg BID | -0.04 |
The change between HDL-Cholesterol collected at week 24 or final visit and HDL-Cholesterol collected at baseline. (NCT00770653)
Timeframe: Baseline and Week 24.
Intervention | mg/dL (Least Squares Mean) |
---|---|
Pioglitazone 15 mg and Metformin 850 mg BID | 3.3 |
Glimepiride 2 mg and Metformin 850 mg BID | -0.4 |
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.
Intervention | mg/dL (Least Squares Mean) |
---|---|
Pioglitazone 15 mg and Metformin 850 mg BID | 0.1 |
Glimepiride 2 mg and Metformin 850 mg BID | 0.3 |
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.
Intervention | mg/dL (Least Squares Mean) |
---|---|
Pioglitazone 15 mg and Metformin 850 mg BID | 9.7 |
Glimepiride 2 mg and Metformin 850 mg BID | 11.2 |
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.
Intervention | mg/dL (Least Squares Mean) |
---|---|
Pioglitazone 15 mg and Metformin 850 mg BID | 6.2 |
Glimepiride 2 mg and Metformin 850 mg BID | 6.1 |
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.
Intervention | ng/mL (Least Squares Mean) |
---|---|
Pioglitazone 15 mg and Metformin 850 mg BID | 31.4 |
Glimepiride 2 mg and Metformin 850 mg BID | 51.6 |
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.
Intervention | nmol/L (Least Squares Mean) |
---|---|
Pioglitazone 15 mg and Metformin 850 mg BID | -2.7 |
Glimepiride 2 mg and Metformin 850 mg BID | 32.5 |
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.
Intervention | sec (Least Squares Mean) |
---|---|
Pioglitazone 15 mg and Metformin 850 mg BID | -30.3 |
Glimepiride 2 mg and Metformin 850 mg BID | -1.0 |
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.
Intervention | pg/mL (Least Squares Mean) |
---|---|
Pioglitazone 15 mg and Metformin 850 mg BID | -40.7 |
Glimepiride 2 mg and Metformin 850 mg BID | 102.4 |
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.
Intervention | ng/mL (Least Squares Mean) |
---|---|
Pioglitazone 15 mg and Metformin 850 mg BID | -13.0 |
Glimepiride 2 mg and Metformin 850 mg BID | -3.2 |
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.
Intervention | ng/mL (Least Squares Mean) |
---|---|
Pioglitazone 15 mg and Metformin 850 mg BID | 11.6 |
Glimepiride 2 mg and Metformin 850 mg BID | 3.3 |
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.
Intervention | mmHg (Least Squares Mean) |
---|---|
Pioglitazone 15 mg and Metformin 850 mg BID | -2.5 |
Glimepiride 2 mg and Metformin 850 mg BID | 0.5 |
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.
Intervention | pg/mL (Least Squares Mean) |
---|---|
Pioglitazone 15 mg and Metformin 850 mg BID | -216.4 |
Glimepiride 2 mg and Metformin 850 mg BID | 527.8 |
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.
Intervention | mg/dL (Least Squares Mean) |
---|---|
Pioglitazone 15 mg and Metformin 850 mg BID | -40.9 |
Glimepiride 2 mg and Metformin 850 mg BID | -16.7 |
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.
Intervention | percent (Least Squares Mean) |
---|---|
Pioglitazone 15 mg and Metformin 850 mg BID | -19.5 |
Glimepiride 2 mg and Metformin 850 mg BID | 1.4 |
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.
Intervention | participants (Number) |
---|---|
Pioglitazone 15 mg and Metformin 850 mg BID | 136 |
Glimepiride 2 mg and Metformin 850 mg BID | 137 |
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.
Intervention | mg/dL (Least Squares Mean) |
---|---|
Pioglitazone 15 mg and Metformin 850 mg BID | 3.2 |
Glimepiride 2 mg and Metformin 850 mg BID | -0.3 |
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
Intervention | mmol/l (Mean) | |
---|---|---|
Baseline FSG | 3rd Month FSG | |
Metformin ( 002 Group) | 6.2 | 6.5 |
Pioglitazone (001 Group) | 6.9 | 5.4 |
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
Intervention | μU/ml (Mean) | |
---|---|---|
Baseline FSI | 3rd month FSI | |
Metformin ( 002 Group) | 13.0 | 13.9 |
Pioglitazone (001 Group) | 16.2 | 12.3 |
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
Intervention | percentage (Mean) | |
---|---|---|
Baseline HbA1c | 3rd month HbA1c | |
Metformin ( 002 Group) | 7.8 | 7.0 |
Pioglitazone (001 Group) | 7.3 | 6.7 |
"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
Intervention | percentage (Mean) | |||
---|---|---|---|---|
Baseline HOMA percent beta cells function | 3rd month HOMA percent beta cells function | Baseline HOMA percent sensitivity | 3rd month HOMA percent sensitivity | |
Metformin ( 002 Group) | 109.3 | 116.0 | 76.2 | 67.2 |
Pioglitazone (001 Group) | 118.9 | 132.3 | 51.1 | 69.3 |
"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
Intervention | Score on a scale ( SI unit) (Mean) | |||
---|---|---|---|---|
Baseline QUICKI | 3rd month QUICKI | Baseline HOMA IR | 3rd month HOMA IR | |
Metformin ( 002 Group) | 0.57 | 0.54 | 3.7 | 4.3 |
Pioglitazone (001 Group) | 0.52 | 0.59 | 5.1 | 2.9 |
"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
Intervention | mg/dl (Mean) | |||||||
---|---|---|---|---|---|---|---|---|
Baseline TC | 3rd month TC | Baseline TG | 3rd month TG | Baseline HDL | 3rd month HDL | Baseline LDL | 3rd month LDL | |
Metformin (002 Group) | 193.0 | 177.0 | 166.0 | 175.0 | 34.4 | 34.7 | 125.6 | 112.0 |
Pioglitazone (001 Group) | 182.0 | 178 | 183 | 195 | 33 | 33.2 | 112.8 | 105.5 |
12 reviews available for pioglitazone and Hyperglycemia, Postprandial
Article | Year |
---|---|
Diabetes, stroke, and neuroresilience: looking beyond hyperglycemia.
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.
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?
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.
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].
Topics: Delayed-Action Preparations; Diabetes Mellitus, Type 2; Dipeptidyl-Peptidase IV Inhibitors; Drug Adm | 2014 |
Initiating insulin in patients with type 2 diabetes.
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.
Topics: Atherosclerosis; Diabetes Mellitus, Type 2; Diabetic Angiopathies; Diabetic Retinopathy; Disease Pro | 2011 |
[Syndrome X].
Topics: Animals; Bezafibrate; Biguanides; Fatty Acids, Nonesterified; Humans; Hyperglycemia; Hyperinsulinism | 2002 |
[Thiazolidinediones: effect of the pioglitazone on hyperglycemia, dyslipidemia and cardiovascular risk].
Topics: Cardiovascular Diseases; Humans; Hyperglycemia; Hyperlipidemias; Hypoglycemic Agents; Pioglitazone; | 2003 |
Peroxisome proliferator-activated receptor-gamma agonists in atherosclerosis: current evidence and future directions.
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)].
Topics: Acarbose; Cyclohexanes; Fasting; Glucose Intolerance; Glycation End Products, Advanced; Humans; Hype | 2005 |
[Hypoglycemic agents to improve insulin resistance].
Topics: Adipocytes; Animals; Cell Differentiation; Chromans; Diabetes Mellitus, Type 2; Disease Models, Anim | 2000 |
19 trials available for pioglitazone and Hyperglycemia, Postprandial
Article | Year |
---|---|
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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).
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).
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).
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).
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
Topics: Adiponectin; Blood Glucose; Diabetes Mellitus, Type 2; Double-Blind Method; Drug Administration Sche | 2007 |
56 other studies available for pioglitazone and Hyperglycemia, Postprandial
Article | Year |
---|---|
Synthesis and biological activity of metabolites of the antidiabetic, antihyperglycemic agent pioglitazone.
Topics: Animals; Dogs; Half-Life; Humans; Hyperglycemia; Hypoglycemic Agents; Insulin Resistance; Magnetic R | 1996 |
Discovery of a novel selective PPARgamma modulator from (-)-Cercosporamide derivatives.
Topics: Animals; Benzofurans; Crystallography, X-Ray; Diabetes Mellitus; Glucose; Humans; Hyperglycemia; Hyp | 2010 |
Development of a new class of benzoylpyrrole-based PPARα/γ activators.
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-
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.
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.
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.
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.
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?
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
Topics: Animals; Blood Glucose; Diabetes Mellitus; Glucose; Glycated Hemoglobin; Glycated Serum Albumin; Gly | 2008 |
TZDs reduce mitochondrial ROS production and enhance mitochondrial biogenesis.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
Topics: Alloxan; Animals; Antioxidants; Diabetes Mellitus, Experimental; Glutathione; Glutathione Peroxidase | 2005 |
PPARgamma agonists exert antifibrotic effects in renal tubular cells exposed to high glucose.
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.
Topics: Animals; Antineoplastic Agents; Carcinoma, Non-Small-Cell Lung; Drug Resistance, Neoplasm; Enzyme In | 2005 |
PPARgamma agonists: a new strategy for antithrombotic therapy.
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.
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.
Topics: Adult; Aged; Antipsychotic Agents; Blood Glucose; Female; Homeostasis; Humans; Hyperglycemia; Hypogl | 2007 |
Prevention and noninvasive management of coronary atherosclerosis in patients with diabetes.
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.
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.
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.
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.
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].
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.
Topics: Animals; Blood Glucose; Body Weight; Hyperglycemia; Hypoglycemic Agents; Insulin; Insulin Resistance | 1990 |