Leptin is a 16 kDa peptide that is secreted from white adipose tissue in proportion to the size of the fat mass in humans and other mammals. Leptin binds to receptors in the hypothalamus and decreases food intake and increases energy expenditure by inhibiting the release of the orexigenic peptides neuropeptide Y and agouti related peptide, and by stimulating the release of the anorexigenic peptides proopiomelanocortin and corticotrophin-releasing hormone. As the size and number of adipocytes increases, leptin acts to suppress the need for further fat accumulation. This is one of the mechanisms the body has to prevent large fluctuation is body weight despite large fluctuations in food intake or exercise levels. Evidence from studies suggests that long-term changes in lifestyle habits that cause weight loss which are effective in reducing levels of body fat, will result in a decrease in circulating levels of leptin.
For example, researchers1 created diet and exercise programmes for 186 men with metabolic syndrome in order to assess if changes in dietary energy intake or exercise-mediated energy expenditure was able to affect plasma leptin concentrations. Dietary advice included increased consumption of fish and fish products, increased vegetables, increased fibre-rich food and the incorporation of foods containing complex carbohydrates. Subjects were also advised to reduce levels of saturated fat and cholesterol. The exercise programme involved aerobic type exercise 3 times per week for 60 minutes each session. All subjects followed a diet, diet plus exercise or exercise only programme for one year. All subjects in the treatment groups lost fat mass and had beneficial changes to their body mass index. Interestingly the diet only group lost more fat (kg) than the diet plus exercise group.
Changes in the plasma leptin concentrations showed positive correlation with the body mass index after both dietary and exercise treatments. However, changed in plasma leptin concentrations were correlated with changes in percentage body fat after exercise treatment but not after dietary treatment. Reductions in total energy intake and fat intake correlated with changes in leptin levels after dietary treatment, and reductions in carbohydrate and total energy intake correlated with plasma leptin levels after exercise treatment. The changes in leptin levels was additive, suggesting that diet and exercise both have direct affects on plasma leptin concentrations. The authors concluded that reductions in plasma leptin concentrations were more than would be expected from loss of the associated fat mass. These results support previous studies that show that leptin levels are reduced as fat mass decreases.
RdB
