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The fall in leptin concentration is a major determinant of the metabolic adaptation induced by caloric restriction independently of the changes in leptin circadian rhythms.
Lecoultre, V, Ravussin, E, Redman, LM
The Journal of clinical endocrinology and metabolism. 2011;96(9):E1512-6
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Plain language summary
Weight loss induced by caloric restriction (CR) is associated with a drop in energy expenditure (EE) beyond that expected for the changes in body composition, often blunting weight loss and predisposing individuals to weight regain. Recent evidence has identified leptin to be associated with this exaggerated decrease in EE. The aim of this trial was to explore the changes in leptin over a 24-hour period in response to caloric restriction, and explore its association with metabolic adaptation. Forty-eight participants were assigned to one of four groups for six months: control, CR, CR with exercise and a low calorie diet. This study indicates that the decline in 24-hour leptin in response to CR is a significant determinant of metabolic adaptation. Based on this study, the authors conclude that this decrease in leptin may underlie the additional reduction in EE observed in individuals following diet-induced weight loss.
Abstract
CONTEXT Leptin is involved in the hormonal regulation of the reproductive, somatotropic, thyroid, and autonomic axes and ultimately in the regulation of energy balance. In parallel to the metabolic adaptation observed in response to caloric restriction (CR), plasma leptin concentrations are substantially decreased, suggesting a role for this hormone in the drop in energy expenditure beyond that predicted by the changes in body composition (metabolic adaptation). AIM: The aim of the study was to explore the changes in 24-h leptin circadian rhythm in response to CR and to investigate the relationship between these changes and metabolic adaptation. DESIGN In a randomized, controlled trial (Comprehensive Assessment of Long-Term Effects of Reducing Intake of Energy), 48 subjects were assigned to a control group or one of three CR groups for 6 months. Leptin concentration was assessed every 30 min for 24 h, and leptin circadian variations were fitted by Cosinor analysis. Sedentary energy expenditure and urinary catecholamine excretion were measured for 24 h in a metabolic chamber. RESULTS Six months of CR decreased body weight by -11.4 ± 0.6% (mean ± sem; P < 0.001). Mean 24-h circulating leptin concentration decreased by -44 ± 3% (P < 0.001), whereas leptin diurnal amplitude slightly increased over the 6 months of CR. CR caused a metabolic adaptation of -126 ± 25 kcal/d (P <0.001) and a significant decrease in urinary norepinephrine (-13 ± 3%) and T(3) concentrations (10 ± 2%). The metabolic adaptation was significantly and independently related to the changes in 24-h leptin (r(2) = 0 .22, P < 0.01) but not to the changes in leptin amplitude. CONCLUSION Our results confirm an important role for leptin as an independent determinant of the metabolic adaptation in response to CR.