Supplementation with leucine does not prevent development of obesity in rats fed a high fat diet (258.5)

Abstract

Excess dietary fat consumption has been implicated in the development of obesity and diabetes. Obesity can be characterized by a disproportionate increase in fat mass. However, if muscle mass can be increased or maintained in obesity, this may facilitate weight loss. Historically, supplementation with the branched‐chain amino acid leucine has been shown to increase muscle protein synthesis via the protein kinase mTORC1. Recent studies suggest that supplementation with leucine also has the potential to reduce weight gain and fat deposition in high‐fat fed, obese mice. The objective of this study was to determine if long‐term dietary leucine supplementation prevents development of obesity in rats meal‐fed a high fat (60%) diet. Male, Sprague‐Dawley rats (n=30/dietary treatment) were meal‐fed (3 meals/day) either a control diet (C), control+leucine (CL), high‐fat (HF), or high‐fat+leucine (HFL) for 42 days. On day 42 rats were sacrificed at 0, 30 or 90 minutes postprandial. HF/HFL‐fed rats gained, 28 g more than rats fed C/CL diets (p<0.05). Insulin AUC was 35% higher in CL vs C and 13% higher in HFL vs HF. There was no difference in blood glucose values between treatment groups. Rats supplemented with leucine had significantly higher fat mass and significantly (p<0.05) lower muscle mass compared to their respective controls. However, preliminary data suggest that L and HFL activate translation initiation in muscle via 4E‐BP1 phosphorylation. Taken together, this study demonstrates that supplementation with leucine increases translation initiation, however this does not result in increased muscle mass. Supplementation with leucine does not prevent development of obesity in HF‐fed rats.Grant Funding Source: Supported by Arkansas Biosciences Institute.