Plasma Leptin and Exercise
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Plasma Leptin and Exercise Recent Findings Matthew W. Hulver1 and Joseph A. Houmard2 1 2
Department of Physiology, East Carolina University, Greenville, North Carolina, USA Human Performance Laboratory, East Carolina University, Greenville, North Carolina, USA
Abstract
It is established that plasma leptin is associated with satiety and that leptin stimulates lipid metabolism, and increases energy expenditure. These effects implicate leptin as a major regulator of energy homeostasis, which may serve to limit excess energy storage. As plasma leptin concentrations are tightly coupled with fat mass in humans, decreases in adipose mass with weight loss coincide with decreased concentrations of circulating leptin. However, due to many confounding factors, the effects of exercise on circulating leptin are less clear. The data from investigations examining single exercise bouts suggest that serum leptin concentrations are unaltered by short duration (41 minutes or less), non-exhaustive exercise, but may be affected by short duration, exhaustive exercise. More convincingly, studies investigating long duration exercise bouts indicate that serum leptin concentrations are reduced with exercise durations ranging from one to multiple hours. These findings raise speculation that exercise-associated reductions in leptin may be due to alterations in nutrient availability or nutrient flux at the level of the adipocytes, the primary site of leptin production and secretion. Thus, one purpose of this review is to discuss the effects of exercise on circulating leptin concentrations with special emphasis on studies that have examined single exercise bouts that are associated with high levels of energy expenditure and energy deficit. In addition, a ‘nutrient sensing pathway’ (the hexosamine biosynthetic pathway), which regulates leptin gene expression, will be discussed as a possible mechanism by which exercise-induced energy deficit may modulate serum leptin concentrations.
Since the cloning of the obese gene in 1994 by Zhang et al.,[1] much work has been devoted to elucidating the biology and physiological role of leptin. To date, it is known that plasma leptin concentrations are associated with satiety[2-5] and that leptin stimulates the oxidation of lipids[6-8] and increases energy expenditure.[9-13] These effects suggest that leptin plays a major role in energy homeostasis and serves to limit excessive energy storage in adipose tissue of mammals. Counter intuitive to these findings, human obesity is accompanied by
hyperleptinaemia,[14-18] which is indicative of either a state of reduced leptin clearance and/or excess leptin secretion with obesity. The cause of hyperleptinaemia with obesity in humans has yet to be clearly elucidated. In an attempt to treat hyperleptinaemia, interventions such as weight loss[19-22] and exercise[22-49] have been investigated. As plasma leptin concentrations are tightly coupled with fat mass in humans,[9,17,20,30,50] decreases i
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