1593-P: GI Exposure Is Required for the Leptin Lowering Effect of Ethanol Treatment

by sugaradmin



Introduction and Objective: Hypoleptinemia is a potent orexigenic signal. Ethanol (EtOH) consumption is associated with weight gain in humans, and acute ethanol treatment leads to reductions in leptin levels in both fasted humans and rats. The objective of this study was to determine whether the route of administration or treatment in the fed or fasted state influences the leptin lowering effect of EtOH.Methods: Three separate groups of male Sprague Dawley rats were exposed to either oral or intravenous (IV) treatment with EtOH (2g/kg via oral gavage/0.067 g/kg/min IV for 30 min; n=7/group) on three consecutive days. Each rat served as its own control and received saline treatment either 7 d prior to or 7 d following exposure to EtOH. Two groups were fasted overnight prior to treatment. Plasma leptin levels were measured each day at baseline and 3 h following EtOH treatment. Data are expressed as mean + SEM. A two-way ANOVA was used to test the effect of treatment on leptin levels (saline vs. EtOH).Results: Baseline leptin levels in the oral/fasted and IV/fasted groups were 3.7 + 0.7 and 2.3 + 0.8 ng/mL, respectively, and were 6.9 + 1.2 ng/mL in the IV/fed group. There was a significant main effect of treatment in the oral/fasted group (p=0.005) where the average daily change in leptin levels 3 h post EtOH treatment was -0.72 + 0.21 ng/mL. There was no effect of treatment on leptin in the IV/fed or IV/fasted groups (p=0.86 and p=0.25, respectively). In the IV groups, average daily changes in leptin levels 3 h following saline vs leptin treatment were -1.7 + 0.4 vs -1.3 + 0.3 ng/mL in the fed group, and -0.4 + 0.5 vs -0.3 + 0.2 ng/mL in the fasted group.Conclusion: Although we were able to replicate previous work indicating a modest reduction in leptin levels following acute EtOH treatment in fasted rats, our results do not support a cumulative leptin-lowering effect of recurrent EtOH treatment. Surprisingly, IV EtOH treatment in either the fed or fasted state had no impact on leptin levels. This suggests that the leptin-lowering effects of EtOH requires oral ingestion and exposure of the GI system to EtOH.

Disclosure

A. Narez: None. A. Bui: None. L. DePrimo: None. S. Junot: None. C.R. Meaux: None. D. McDougal: None.

Funding

NIH (R01DK131165)



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