Page last updated: 2024-11-02

pioglitazone and Hypertriglyceridemia

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.

Research Excerpts

ExcerptRelevanceReference
"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)."9.51Stratified 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."7.76Curcumin 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)."5.51Stratified 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."3.77Irbesartan 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."3.76Curcumin 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."2.47Macrovascular 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."1.43Postprandial 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."1.42Pioglitazone 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."1.38An unusual cause of delayed puberty: Berardinelli- Seip syndrome. ( Dhull, P; Kumar, KV; Patnaik, SK; Upreti, V, 2012)

Research

Studies (12)

TimeframeStudies, this research(%)All Research%
pre-19900 (0.00)18.7374
1990's1 (8.33)18.2507
2000's3 (25.00)29.6817
2010's7 (58.33)24.3611
2020's1 (8.33)2.80

Authors

AuthorsStudies
Brandon, R1
Jiang, Y1
Yeu, RQ1
Tweedie-Cullen, R1
Smallman, K1
Doherty, G1
Macaskill-Smith, KA1
Doran, RJ1
Clark, P1
Moffitt, A1
Merry, T1
Nehren, N1
King, F1
Hindmarsh, JH1
Leask, MP1
Merriman, TR1
Orr-Walker, B1
Shepherd, PR1
Paul, R1
Murphy, R1
Upreti, V1
Dhull, P1
Patnaik, SK1
Kumar, KV1
Wessels, B1
Ciapaite, J1
van den Broek, NM1
Houten, SM1
Nicolay, K1
Prompers, JJ1
Sykes, AP1
O'Connor-Semmes, R1
Dobbins, R1
Dorey, DJ1
Lorimer, JD1
Walker, S1
Wilkison, WO1
Kler, L1
Aslam, M1
Aggarwal, S1
Sharma, KK1
Galav, V1
Madhu, SV1
Abbasi, F1
Lamendola, C1
Leary, ET1
Reaven, GM1
Li, JM1
Li, YC1
Kong, LD1
Hu, QH1
Takai, S1
Jin, D1
Miyazaki, M1
Plutzky, J1
Barbaro, D1
Lapi, P1
Orsini, P1
Pasquini, C1
Ciaccio, S1
Shibata, T1
Matsui, K1
Nagao, K1
Shinkai, H1
Yonemori, F1
Wakitani, K1
Kane, JP1

Clinical Trials (1)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
A Double-blind, Randomized 12-week Study to Evaluate the Safety and Efficacy of GSK189075 Tablets vs Pioglitazone in Treatment Naive Subjects With Type 2 Diabetes Mellitus[NCT00500331]Phase 2334 participants (Actual)Interventional2007-01-23Completed
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Change From Baseline to Week 12 in Body Weight

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

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

Change From Baseline to Week 12 in Fasting Insulin

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

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

Change From Baseline to Week 12 in Fructosamine

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

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

Change From Baseline to Week 12 in Waist Circumference

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

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

Number of Participants With On-therapy Hypoglycemia

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Reviews

1 review available for pioglitazone and Hypertriglyceridemia

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

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

2011

Trials

2 trials available for pioglitazone and Hypertriglyceridemia

ArticleYear
Stratified glucose-lowering response to vildagliptin and pioglitazone by obesity and hypertriglyceridemia in a randomized crossover trial.
    Frontiers in endocrinology, 2022, Volume: 13

    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.
    Diabetes, obesity & metabolism, 2015, Volume: 17, Issue:1

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

2015

Other Studies

9 other studies available for pioglitazone and Hypertriglyceridemia

ArticleYear
An unusual cause of delayed puberty: Berardinelli- Seip syndrome.
    Journal of pediatric endocrinology & metabolism : JPEM, 2012, Volume: 25, Issue:11-12

    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.
    Diabetes, obesity & metabolism, 2015, Volume: 17, Issue:1

    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.
    PloS one, 2016, Volume: 11, Issue:1

    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.
    Diabetes, obesity & metabolism, 2009, Volume: 11, Issue:8

    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.
    Hepatology (Baltimore, Md.), 2010, Volume: 51, Issue:5

    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.
    Journal of pharmacological sciences, 2011, Volume: 116, Issue:3

    Topics: Adiponectin; Adipose Tissue; Angiotensin Receptor Antagonists; Animals; Antihypertensive Agents; Bip

2011
Pioglitazone treatment in Cushing's disease.
    Journal of endocrinological investigation, 2005, Volume: 28, Issue:4

    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.
    European journal of pharmacology, 1999, Jan-08, Volume: 364, Issue:2-3

    Topics: 3T3 Cells; Administration, Oral; Animals; Blood Glucose; Cell Differentiation; Chromans; Diabetes Me

1999
Does hypertriglyceridemia present an indication for pioglitazone therapy in diabetes?
    Diabetes technology & therapeutics, 2002, Volume: 4, Issue:2

    Topics: Diabetes Mellitus, Type 2; Drug Therapy, Combination; Humans; Hypertriglyceridemia; Hypoglycemic Age

2002