Differential effects of rosiglitazone and metformin on postprandial lipemia in patients with HIV-lipodystrophy
Arteriosclerosis, Thrombosis, and Vascular Biology , Volume 31 - Issue 1 p. 228- 233
Objective- To compare the effects of rosiglitazone (8 mg/d, n=19) and metformin (2 g/d, n=18) on postprandial lipemia in patients with HIV-lipodystrophy. Methods and results- Lipodystrophy in HIV is associated with insulin resistance and disturbed postprandial triglyceride and free fatty acid (FFA) metabolism. We conducted an open randomized 6-month study with standardized 10-h oral fat-loading tests at baseline and after treatment. Rosiglitazone (-34%) and metformin (-37%) reduced homeostasis model assessment similarly (P<0.05). Rosiglitazone did not change the area under the curve for FFA and triglyceride; however, it did reduce the area under the curve for hydroxybutyric acid (a marker of hepatic FFA oxidation) by 25% (P<0.05). Rosiglitazone increased the area under the curve for remnantlike particle cholesterol by 40% (P<0.01) compared with baseline. Metformin did not change any of the postprandial measurements. Conclusion- Rosiglitazone improved insulin sensitivity and decreased postprandial hydroxybutyric acid levels in patients with HIV-lipodystrophy, suggesting improved FFA handling. Despite metabolic improvements, rosiglitazone caused a marked increase in postprandial remnantlike particle cholesterol, which may adversely affect cardiovascular risk. Metformin did not affect postprandial lipemia and could be used to treat insulin resistance in this population.
|HIV, adipose tissue, atherosclerosis, insulin resistance, postprandial, triglycerides|
|Arteriosclerosis, Thrombosis, and Vascular Biology|
|Organisation||Erasmus MC: University Medical Center Rotterdam|
van Wijk, J.P.H, Hoepelman, I.M, de Koning, E.J.P, Dallinga-Thie, G.M, Rabelink, T.J, & Castro Cabezas, M. (2011). Differential effects of rosiglitazone and metformin on postprandial lipemia in patients with HIV-lipodystrophy. Arteriosclerosis, Thrombosis, and Vascular Biology, 31(1), 228–233. doi:10.1161/ATVBAHA.110.216192