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a Institute for Aging Research, Department of Medicine, Albert Einstein College of Medicine, Bronx, New York
b Diabetes Research and Training Center, Department of Medicine, Albert Einstein College of Medicine, Bronx, New York
c Division of Pediatric Endocrinology, Children's Hospital at Montefiore, Bronx, New York
Nir Barzilai, Institute for Aging Research, Belfer Building 701, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461 E-mail: barzilai{at}aecom.yu.edu.
Decision Editor: Andrzej Bartke, PhD
Leptin has been shown to modulate total body fat and visceral fat distribution and to enhance insulin action in young rats. We hypothesize that failure of leptin action may contribute to the increase in visceral fat and insulin resistance in aging. By chronic subcutaneous infusion of leptin over 7 days, we increased leptin levels in young rats to match the levels in aging ad libitum fed rats. Leptin induced an 
50% decrease in food intake compared with saline controls, an 50% decrease in visceral fat, and improved hepatic (fourfold) and peripheral (30%) insulin action (euglycemic hyperinsulinemic clamp technique) compared with the pair-fed group (p < .001). Although the plasma leptin level was doubled in aging rats, leptin failed to produce a significant change in food intake, in fat mass and its distribution, and in hepatic and peripheral insulin action. Increasing plasma leptin levels failed to suppress leptin gene expression in aging rats as compared with the 50% suppression seen in young rats (p < .01). We propose that leptin resistance may play a causative role in the metabolic decline seen with aging.
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