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Abstract & Commentary
Synopsis: Decreased intake of dietary fat and increased physical activity reduced plasma leptin concentrations beyond the reduction expected as a result of changes in fat mass.
Source: Reseland JE, et al. Am J Clin Nutr. 2001;73:240-245.
Leptin is a peptide hormone expressed and secreted in proportion to adipocyte size and number and circulates in plasma in a concentration highly correlated with body fat mass. Administration of leptin to animals has indicated that it participates in the regulation of food intake and energy expenditure. Because there is a large variation in leptin concentration in individuals with similar body composition, Reseland and colleagues and Considine and colleagues1 believe that factors other than fat cell mass and number must be important in determining plasma leptin concentrations.
The objective of this study was to determine whether changes in dietary energy sources and exercise-mediated energy expenditure, alone or in combination, affect plasma leptin concentrations. In a randomized trial, 1186 men with metabolic syndrome (insulin resistance) were divided into 4 groups: diet, exercise, combination of diet and exercise, and control. Data on dietary intake, physical fitness, and demographics were collected, and plasma leptin concentrations were measured before and after a 1-year intervention period.
Plasma leptin concentrations, body mass index, and fat mass decreased in association with long-term reductions in food intake as well as increased physical activity. By adjusting for either body mass index or fat mass, they observed a highly significant reduction in plasma leptin concentration after both the diet and exercise interventions. There was no interaction between interventions, suggesting a direct and additive effect of changes in diet and physical activity on plasma leptin concentrations. Reseland et al concluded that decreased intake of dietary fat and increased physical activity reduced plasma leptin concentrations beyond the reduction expected as a result of changes in fat mass.
Comment by Ralph R. Hall, MD, FACP
Obese individuals have increased concentrations of serum leptin and a concomitant decreased sensitivity to leptin. This is similar to the findings with serum insulin levels in obesity. As with insulin, administration of leptin may result in increased signaling to the central nervous system and pituitary. Thereby, reductions in food intake, body fat mass, and body weight in obese patients may result from treatment with recombinant leptin.
Leptin treatment of a young obese girl with a mutated ob gene with congenital leptin deficiency produced a reduction in body fat and a dramatic reduction in appetite, food seeking behavior, food intake, and body weight.2 Additional trials in obese adults have also been encouraging.3
There are other effects of leptin, such as Heptulla and colleagues’ study on the effects on pituitary growth hormone release and other studies noting the relationship to LH, FSH, ACTH, and cortisol levels which will merit following.4 However, in the meantime, the studies of Reseland et al demonstrate that just as with insulin resistance, exercise and diet can increase the sensitivity to serum leptin. This seems to be a more desirable approach than the administration of recombinant leptin which is likely to be an extremely expensive effort.
1. Considine RV, et al. N Engl J Med. 1996;334:292-295.
2. Farooqi IS, et al. N Engl J Med. 1999;341:879-884.
3. Heymsfield SB, et al. JAMA. 1999;282:1568-1575.
4. Heptulla R, et al. J Clin Endocrinol Metab. 2001;86: 90-96.