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• _3 wasQuotedFrom 16020439 provenance.
• _3 value "chronic exercise without reductions in body weight does not affect plasma adiponectin levels in insulin-resistant populations (50). Thus the exercise-mediated enhancement of insulin action appears to be independent of changes in plasma adiponectin (116). However, the level of weight loss may be an important determinant of changes in plasma adiponectin levels. A 6-mo dietary intervention in conjunction with an exercise program that resulted in a 3% decrease in body fat (13% decrease in total fat mass) did not have an effect on plasma adiponectin levels (92). However, other lifestyle modification programs that resulted in greater weight loss increased plasma adiponectin and insulin sensitivity (23). The current evidence would suggest that exercise-induced improvements in insulin action occur independently of changes in plasma adiponectin. Additionally, the observation that the effects of exercise and weight loss on insulin action are additive may indicate that each modality mediates its effects through distinct pathways(17). Leptin. In the early 1990s it was discovered that defects in the ob gene lead to obesity in the ob/ob mouse (120). Leptin is a product of the ob gene and circulates as a 16-kDa protein (120). Expression and secretion of leptin occurs primarily in white adipose tissue (13, 31, 33, 59); however, additional physiological sites of production have been established such as the stomach (6), brain (22, 111), placenta (67), skeletal muscle (109), bone (91), and arterial endothelium (85). Plasma leptin exhibits a circadian rhythm with the highest concentrations occurring near midnight and lowest concentrations near midmorning (8, 31, 34, 52). The diurnal rhythm of leptin secretion is hormonally (growth hormone, insulin, cortisol) influenced (2, 108), is dependent on gender (3, 93) and energy availability (3, 16, 41, 108), and may be altered by meal timing (95) and composition (9, 38). Similar to adiponectin, leptin directly, or indirectly through hypothalamic-mediated responses, activates AMPK in skeletal muscle, thus increasing fatty acid oxidation and glucose uptake (72, 73)." provenance.