pioglitazone has been researched along with Hypertriglyceridemia in 12 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.
Hypertriglyceridemia: A condition of elevated levels of TRIGLYCERIDES in the blood.
Excerpt | Relevance | Reference |
---|---|---|
"We hypothesized that people with type 2 diabetes who generally have high insulin resistance, such as people of Māori/Pacific ethnicity, and those with obesity and/or hypertriglyceridemia (OHTG), would have greater glucose-lowering by pioglitazone (an insulin sensitizer) versus vildagliptin (an insulin secretagogue)." | 9.51 | Stratified glucose-lowering response to vildagliptin and pioglitazone by obesity and hypertriglyceridemia in a randomized crossover trial. ( Brandon, R; Clark, P; Doherty, G; Doran, RJ; Hindmarsh, JH; Jiang, Y; King, F; Leask, MP; Macaskill-Smith, KA; Merriman, TR; Merry, T; Moffitt, A; Murphy, R; Nehren, N; Orr-Walker, B; Paul, R; Shepherd, PR; Smallman, K; Tweedie-Cullen, R; Yeu, RQ, 2022) |
" We investigated the effects of curcumin on fructose-induced hypertriglyceridemia and liver steatosis and explored its preventive mechanisms in rats." | 7.76 | Curcumin inhibits hepatic protein-tyrosine phosphatase 1B and prevents hypertriglyceridemia and hepatic steatosis in fructose-fed rats. ( Hu, QH; Kong, LD; Li, JM; Li, YC, 2010) |
"We hypothesized that people with type 2 diabetes who generally have high insulin resistance, such as people of Māori/Pacific ethnicity, and those with obesity and/or hypertriglyceridemia (OHTG), would have greater glucose-lowering by pioglitazone (an insulin sensitizer) versus vildagliptin (an insulin secretagogue)." | 5.51 | Stratified glucose-lowering response to vildagliptin and pioglitazone by obesity and hypertriglyceridemia in a randomized crossover trial. ( Brandon, R; Clark, P; Doherty, G; Doran, RJ; Hindmarsh, JH; Jiang, Y; King, F; Leask, MP; Macaskill-Smith, KA; Merriman, TR; Merry, T; Moffitt, A; Murphy, R; Nehren, N; Orr-Walker, B; Paul, R; Shepherd, PR; Smallman, K; Tweedie-Cullen, R; Yeu, RQ, 2022) |
" In this study, thirteen-week-old spontaneously hypertensive (SHR)/NDmcr-cp rats, representing a genetic model of metabolic syndrome, were treated daily with placebo, irbesartan (30 mg/kg), valsartan (10 mg/kg), or pioglitazone (10 mg/kg) for 4 weeks." | 3.77 | Irbesartan prevents metabolic syndrome in rats via activation of peroxisome proliferator-activated receptor γ. ( Jin, D; Miyazaki, M; Takai, S, 2011) |
" We investigated the effects of curcumin on fructose-induced hypertriglyceridemia and liver steatosis and explored its preventive mechanisms in rats." | 3.76 | Curcumin inhibits hepatic protein-tyrosine phosphatase 1B and prevents hypertriglyceridemia and hepatic steatosis in fructose-fed rats. ( Hu, QH; Kong, LD; Li, JM; Li, YC, 2010) |
"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) |
"Atorvastatin treatment (Group D) abolished PPHTg which became comparable to controls, pioglitazone treatment partially blunted PPHTg resulting in intermediate PPHTg." | 1.43 | Postprandial Hypertriglyceridemia Predicts Development of Insulin Resistance Glucose Intolerance and Type 2 Diabetes. ( Aggarwal, S; Aslam, M; Galav, V; Madhu, SV; Sharma, KK, 2016) |
"Pioglitazone treatment restored in vivo muscle oxidative capacity in diabetic rats to the level of lean controls." | 1.42 | Pioglitazone treatment restores in vivo muscle oxidative capacity in a rat model of diabetes. ( Ciapaite, J; Houten, SM; Nicolay, K; Prompers, JJ; van den Broek, NM; Wessels, B, 2015) |
"Berardinelli- Seip syndrome is an autosomal recessive disorder characterized by generalized lipoatrophy, extreme insulin resistance with dyslipidemia in childhood and development of diabetes in adolescence." | 1.38 | An unusual cause of delayed puberty: Berardinelli- Seip syndrome. ( Dhull, P; Kumar, KV; Patnaik, SK; Upreti, V, 2012) |
Timeframe | Studies, this research(%) | All Research% |
---|---|---|
pre-1990 | 0 (0.00) | 18.7374 |
1990's | 1 (8.33) | 18.2507 |
2000's | 3 (25.00) | 29.6817 |
2010's | 7 (58.33) | 24.3611 |
2020's | 1 (8.33) | 2.80 |
Authors | Studies |
---|---|
Brandon, R | 1 |
Jiang, Y | 1 |
Yeu, RQ | 1 |
Tweedie-Cullen, R | 1 |
Smallman, K | 1 |
Doherty, G | 1 |
Macaskill-Smith, KA | 1 |
Doran, RJ | 1 |
Clark, P | 1 |
Moffitt, A | 1 |
Merry, T | 1 |
Nehren, N | 1 |
King, F | 1 |
Hindmarsh, JH | 1 |
Leask, MP | 1 |
Merriman, TR | 1 |
Orr-Walker, B | 1 |
Shepherd, PR | 1 |
Paul, R | 1 |
Murphy, R | 1 |
Upreti, V | 1 |
Dhull, P | 1 |
Patnaik, SK | 1 |
Kumar, KV | 1 |
Wessels, B | 1 |
Ciapaite, J | 1 |
van den Broek, NM | 1 |
Houten, SM | 1 |
Nicolay, K | 1 |
Prompers, JJ | 1 |
Sykes, AP | 1 |
O'Connor-Semmes, R | 1 |
Dobbins, R | 1 |
Dorey, DJ | 1 |
Lorimer, JD | 1 |
Walker, S | 1 |
Wilkison, WO | 1 |
Kler, L | 1 |
Aslam, M | 1 |
Aggarwal, S | 1 |
Sharma, KK | 1 |
Galav, V | 1 |
Madhu, SV | 1 |
Abbasi, F | 1 |
Lamendola, C | 1 |
Leary, ET | 1 |
Reaven, GM | 1 |
Li, JM | 1 |
Li, YC | 1 |
Kong, LD | 1 |
Hu, QH | 1 |
Takai, S | 1 |
Jin, D | 1 |
Miyazaki, M | 1 |
Plutzky, J | 1 |
Barbaro, D | 1 |
Lapi, P | 1 |
Orsini, P | 1 |
Pasquini, C | 1 |
Ciaccio, S | 1 |
Shibata, T | 1 |
Matsui, K | 1 |
Nagao, K | 1 |
Shinkai, H | 1 |
Yonemori, F | 1 |
Wakitani, K | 1 |
Kane, JP | 1 |
Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
---|---|---|---|---|---|---|---|
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 | ||
[information is prepared from clinicaltrials.gov, extracted Sep-2024] |
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 |
1 review available for pioglitazone and Hypertriglyceridemia
Article | Year |
---|---|
Macrovascular effects and safety issues of therapies for type 2 diabetes.
Topics: Atherosclerosis; Diabetes Mellitus, Type 2; Diabetic Angiopathies; Diabetic Retinopathy; Disease Pro | 2011 |
2 trials available for pioglitazone and Hypertriglyceridemia
Article | Year |
---|---|
Stratified glucose-lowering response to vildagliptin and pioglitazone by obesity and hypertriglyceridemia in a randomized crossover trial.
Topics: Adult; Cross-Over Studies; Diabetes Mellitus, Type 2; Dipeptidyl-Peptidase IV Inhibitors; Glucose; G | 2022 |
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 |
9 other studies available for pioglitazone and Hypertriglyceridemia
Article | Year |
---|---|
An unusual cause of delayed puberty: Berardinelli- Seip syndrome.
Topics: Administration, Cutaneous; Adolescent; Atorvastatin; Combined Modality Therapy; Diet, Fat-Restricted | 2012 |
Pioglitazone treatment restores in vivo muscle oxidative capacity in a rat model of diabetes.
Topics: Animals; Biomarkers; Carnitine; Diabetes Mellitus, Type 2; Hypertriglyceridemia; Hypoglycemic Agents | 2015 |
Postprandial Hypertriglyceridemia Predicts Development of Insulin Resistance Glucose Intolerance and Type 2 Diabetes.
Topics: Animals; Atorvastatin; Blood Glucose; Body Weight; Causality; Diabetes Mellitus, Type 2; Dietary Fat | 2016 |
Pioglitazone decreases postprandial accumulation of remnant lipoproteins in insulin-resistant smokers.
Topics: Cardiovascular Diseases; Cholesterol; Fasting; Female; Humans; Hypertriglyceridemia; Hypoglycemic Ag | 2009 |
Curcumin inhibits hepatic protein-tyrosine phosphatase 1B and prevents hypertriglyceridemia and hepatic steatosis in fructose-fed rats.
Topics: Animals; Curcumin; Dietary Carbohydrates; Extracellular Signal-Regulated MAP Kinases; Fatty Liver; F | 2010 |
Irbesartan prevents metabolic syndrome in rats via activation of peroxisome proliferator-activated receptor γ.
Topics: Adiponectin; Adipose Tissue; Angiotensin Receptor Antagonists; Animals; Antihypertensive Agents; Bip | 2011 |
Pioglitazone treatment in Cushing's disease.
Topics: Adrenocorticotropic Hormone; Aged; Comorbidity; Diabetes Mellitus; Female; Humans; Hydrocortisone; H | 2005 |
Pharmacological profiles of a novel oral antidiabetic agent, JTT-501, an isoxazolidinedione derivative.
Topics: 3T3 Cells; Administration, Oral; Animals; Blood Glucose; Cell Differentiation; Chromans; Diabetes Me | 1999 |
Does hypertriglyceridemia present an indication for pioglitazone therapy in diabetes?
Topics: Diabetes Mellitus, Type 2; Drug Therapy, Combination; Humans; Hypertriglyceridemia; Hypoglycemic Age | 2002 |