EXPERIMENTAL STUDY Intralipid/heparin infusion suppresses serum leptin in humans

Background/aim: Our previous studies showed that administration of dexamethasone plus food increased serum leptin levels 100 % more than dexamethasone alone. We hypothesized that this increase in leptin from the meal could result directly from the provision of fuel metabolites rather than from the meal-induced rise in insulin. In the current study, we tested the effect of an i.v. lipid fuel source (Intralipid 20%/heparin) that would incur only a modest increase in insulin. This study was undertaken because the role of lipid in the regulation of human leptin levels has been controver-sial, with differing effects reported: stimulatory, inhibitory, or no effect at all. Methods: In order to evaluate how lipids affect serum leptin in humans, we administered the following to seven lean, healthy, fasting subjects: (i) Intralipid 20 % at 0.83 ml/kg.h plus heparin (800 IE/h) infused i.v. for 7 h (LIPID), (ii) LIPID with one initial pulse of insulin (0.09 U/kg) given s.c. (LIPIDþ INS), (iii) LIPID with dexamethasone (2 mg i.v. push) given at the start of the infusion (LIPIDþDEX), and (iv) LIPID with insulin plus dexamethasone (LIPIDþ INSþDEX). Control trials in another 14 subjects matched hormonal conditions but lacked the LIPID infusion. Blood levels were collected over 8 h for determination of free fatty acids (FFA), glucose, insulin, and lepti