View article

Methods: 32 obese and nondiabetic adult volunteers were randomized to receive either extended release nicotinic acid (Niaspan) 2000 mg daily for 16 weeks or fenofibrate 200 mg daily for 8 weeks or placebo for 8 weeks. A euglycemic-hyperinsulinemic clamp procedure and stable isotopically labeled tracer infusions were used to assess insulin action, and magnetic resonance spectroscopy was used to determine IHTG content before and after treatment.

Results: 29 subjects completed both pre-and post-intervention studies. The entire cohort had a median IHTG content of 24%(range 10− 45%); IHTG content, body mass index, percent body fat and visceral adipose tissue volume were similar in the three study arms. Basal plasma FFA concentration changed by− 2%, 33% and− 3% in fenofibrate, Niaspan and placebo groups, respectively. The sensitivity of adipose tissue to insulin mediated suppression of lipolytic activity changed by 4%,− 24% and− 9% in fenofibrate, Niaspan and placebo groups, respectively. None of these changes reached statistical significance and there was no change in IHTG content in all study arms. Treatment with fenofibrate resulted in a 30% reduction in triglyceride and treatment with long-acting nicotinic acid resulted in a 12% increase in HDL cholesterol. Conclusion: Treatment with fenofibrate and long-acting nicotinic acid improves lipid profiles but do not decrease IHTG content or improve insulin ability to suppress fatty acid release from adipose tissue. These findings demonstrate that the beneficial effect of fenofibrate and longacting nicotinic acid on plasma lipids is not due to effects on adipose tissue lipolytic activity …