Targeting Abdominal Obesity

Pharmacotherapy for the Prevention of Type 2 Diabetes

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This improvement may not be related to any loss of intra-abdominal adipose tissue and may instead be related to the subcutaneous fat gain of patients treated with pioglitazone. However, this hypothesis remains to be tested. The TRIPOD (Troglitazone in Prevention of Diabetes) study has also tested the effectiveness of a PPAR-γ agonist, troglitazone, in reducing type 2 diabetes incidence (22). The study sample included high-risk Hispanic women with previous gestational diabetes who were randomized to troglitazone (n=133) and a placebo (n=133). In the median follow-up of 30 months, diabetes incidence was 12.1% in women on placebo and 5.4% in women treated with troglitazone, suggesting that treatment with troglitazone could significantly reduce type 2 diabetes onset in this population. It is important to point out, however, that troglitazone was withdrawn from the market in 2000 because of liver toxicity. In the DREAM trial (Diabetes REduction Assessment with ramipril and rosiglitazone Medication), 5,269 men and women aged 30 years or more with impaired fasting glucose or IGT without prior cardiovascular disease were randomized to receive 8 mg/day of rosiglitazone or a placebo. Rosiglitazone substantially (6%) reduced the risk of developing diabetes over the 4 year follow-up. Waist circumference did not change after treatment with rosiglitazone or the placebo. Interestingly, rosiglitazone treatment significantly increased hip circumference whereas the placebo did not. Rosiglitazone therefore reduced waist-to-hip ratio significantly, suggesting that rosiglitazone treatment can also cause an increase in subcutaneous adipose tissue. In light of this, it is reasonable to believe that rosiglitazone improves cardiometabolic risk profile by 1) creating an anti-atherogenic and anti-diabetogenic energy sink, i.e., subcutaneous fat and 2) mobilizing intra-abdominal adipose tissue.

Reference

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22. Buchanan TA, Xiang AH, Peters RK, et al. Preservation of pancreatic beta-cell function and prevention of type 2 diabetes by pharmacological treatment of insulin resistance in high-risk hispanic women. Diabetes 2002; 51: 2796-803.

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