Troglitazone prevents the rise in visceral adiposity and improves fatty liver associated with sulfonylurea therapy—A randomized controlled trial

Katoh, Shūichi; Hata, Shoichi; Matsushima, Masato; Ikemoto, Suguru; Inoue, Yasunori; Yokoyama, Jun′ichi; Tajima, Naoko

doi:10.1053/meta.2001.21691

Cited by 52 publications

(49 citation statements)

References 17 publications

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“…[75][76][77] More importantly, TGZ decreased the liver size and fat accumulation in the livers of patients with insulin resistance and type 2 diabetes or lipodystrophy syndrome, as determined by magnetic resonance imaging and computed tomography scans. 16,78 In addition, TGZ improved mitochondrial oxidation in insulin-resistant patients, 16 presumably through PPAR-␥ signaling, which is consistent with the stimulation of mitochondrial synthesis and function by PPAR-␥ coactivator-1␣. 5 The activation and induction of PPAR-␥ caused by TGZ is also observed with the antioxidant vitamin E 79 and anti-inflammatory drugs such as ibuprofen, 80,81 in the absence of cytotoxicity.…”

Section: Oxidative Stress and Mitochondrial Damagesupporting

confidence: 63%

Troglitazone and liver injury: In search of answers

Chojkier

2005

Hepatology

112

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Section: Oxidative Stress and Mitochondrial Damagesupporting

confidence: 63%

Troglitazone and liver injury: In search of answers

Chojkier

2005

Hepatology

112

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“…These data suggest that mechanisms of weight gain in subjects treated with troglitazone are not invariably associated with elevations in cardiovascular risk factors. This may result from the propensity of troglitazone to induce weight gain via fluid retention and/or accumulation of subcutaneous fat rather than increases in visceral adipose tissue (37,55). Alternatively, the beneficial effects of enhanced insulin sensitivity or PPAR-␥ activation may override the detrimental consequences of increased adipose accumulation on levels of CVRF.…”

Section: Diabetes Therapy and Cardiovascular Risk Factorsmentioning

confidence: 99%

Differential Effects of Metformin and Troglitazone on Cardiovascular Risk Factors in Patients With Type 2 Diabetes

et al. 2002

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OBJECTIVE -Traditional cardiovascular risk factors (CVRF) only partly explain the excessive risk of cardiovascular disease in patients with type 2 diabetes. There is now an increasing appreciation for many novel CVRF that occur largely as a result of insulin resistance and hyperinsulinemia. Therefore, we investigated whether diabetes medications that vary in their mechanism of action and ability to reduce insulin resistance may differ in their effects on both traditional and novel CVRF. RESEARCH DESIGN AND METHODS-We compared the addition of metformin or troglitazone therapy on CVRF in 22 subjects with type 2 diabetes who remained in poor glycemic control (with HbA 1c Ͼ8.5%) while taking glyburide 10 mg twice daily. Subjects were initially randomized to either metformin 850 mg once daily or troglitazone 200 mg once daily. Both medications were then titrated upward as needed to achieve fasting plasma glucose Ͻ120 mg/dl. Measures of glucose control, insulin resistance, and CVRF (blood pressure, lipids, plasminogen activator inhibitor-1, C-reactive protein, fibrinogen, and small dense LDL) were assessed both before and after therapy.RESULTS -After 4 months of treatment, both metformin and troglitazone led to similar decreases in fasting plasma glucose and HbA 1c . The reduction in insulin resistance determined by hyperinsulinemic-euglycemic clamp was nearly twofold greater with troglitazone than metformin. Metformin did not induce significant changes in blood pressure, LDL cholesterol, LDL size, HDL cholesterol, triglycerides, or plasminogen activator inhibitor-1. However, C-reactive protein did decrease by 33% (6 Ϯ 1 to 4 Ϯ 1 ng/l; P Ͻ 0.01). Troglitazone therapy was associated with increases in LDL size (26.21 Ϯ 0.22 to 26.56 Ϯ 0.25 nm; P ϭ 0.04) and HDL cholesterol (33 Ϯ 3 to 36 Ϯ 3 mg/dl; P ϭ 0.05) and decreases in triglycerides (197 Ϯ 19 to 155 Ϯ 23 mg/dl; P ϭ 0.07) and C-reactive protein by 60% (8 Ϯ 3 to 3 Ϯ 1 ng/l, P Ͻ 0.01).CONCLUSIONS -For patients with type 2 diabetes in whom maximal sulfonylurea therapy failed, the addition of the insulin sensitizer troglitazone seemed to have greater benefits on several traditional and novel CVRF than metformin therapy. These differences were not related to glycemic improvement but reflected, in part, the greater reduction in insulin resistance obtained with addition of troglitazone. These data suggest that medications that more effectively address this underlying metabolic defect may be more beneficial in reducing cardiovascular risk in type 2 diabetes.

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“…Unlike the previous results (11,17), this study found no significant reduction in the visceral fat mass. This finding can be partially explained by the fact that treatment with sulfonylureas might increase the visceral fat mass (18). In the present study, the combination treatments of sulfonylurea (nZ31) or sulfonylurea/metformin (nZ48) resulted in an increase in VFT (1.79G3.70 or 0.68G4.08 mm respectively) after 3 months, while the combination treatment with only metformin (nZ77) reduced the VFT (K0.93G 4.02 mm, P for trend Z0.068).…”

Section: Discussionmentioning

confidence: 99%

The increase in abdominal subcutaneous fat depot is an independent factor to determine the glycemic control after rosiglitazone treatment

Kim¹,

Hur²,

Kim³

et al. 2007

eur j endocrinol

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Objective: The goal was to investigate the interrelationships between the hypoglycemic effects of rosiglitazone and the changes in the regional adiposity of type 2 diabetic patients. Design and methods: We added rosiglitazone (4 mg/day) to 173 diabetic patients (111 males and 62 females) already taking a stable dose of conventional antidiabetic medications except for thiazolidinediones. The abdominal fat distribution was assessed by ultrasonography at baseline and 12 weeks later. Using ultrasonographic images, the s.c. and visceral fat thickness (SFT and VFT respectively) were measured. Results: Rosiglitazone treatment for 3 months improved the glycemic control. However, the response to rosiglitazone was no more than 36.4%; the deterioration of the glycemic control was found in 16.8% of subjects. In addition, rosiglitazone treatment significantly increased the body fat mass, especially the s.c. fat. However that did not alter the visceral fat content. The percentage changes in fasting plasma glucose (FPG) and glycated hemoglobin (HbA1c) concentrations after treatment were inversely correlated with the increase in SFT (rZK0.327 and K0.353, P!0.001 respectively) and/or body weight (rZK0.316 and K0.327, P!0.001 respectively). Multiple regression analysis revealed that the improvement in the FPG after rosiglitazone treatment was correlated with the baseline FPG (P!0.001) and the change in the SFT (PZ0.019), and the reduction in the HbA1c was related with the baseline FPG (PZ0.003) and HbA1c (P!0.001) and the changes in the SFT (PZ0.010) or VFT (PZ0.013). Conclusions: The increase in the s.c. fat depot after rosiglitazone treatment may be an independent factor that determines the hypoglycemic efficacy.

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Troglitazone prevents the rise in visceral adiposity and improves fatty liver associated with sulfonylurea therapy—A randomized controlled trial

Cited by 52 publications

References 17 publications

Troglitazone and liver injury: In search of answers

Troglitazone and liver injury: In search of answers

Differential Effects of Metformin and Troglitazone on Cardiovascular Risk Factors in Patients With Type 2 Diabetes

The increase in abdominal subcutaneous fat depot is an independent factor to determine the glycemic control after rosiglitazone treatment

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