Abstract
Growth hormone (GH) secretion is impaired in obese children and adults but the physiologic mechanisms for obesity-induced hyposomatotropism remain unclear. Metabolic disturbances that result from obesity and a central accumulation of body fat, such as increased circulating insulin and free-fatty acid concentrations, reduce growth hormone secretion at the level of the pituitary and perhaps the hypothalamus. Leptin is a logical choice as a humoral signal to relay information regarding the body composition and the fat distribution to the hypothalamus and pituitary. Leptin is secreted directly from the adipocytes and leptin receptors are located in the pituitary and the hypothalamus including growth hormone' releasing hormone neurons. Serum leptin concentrations are inversely related to basal and growth hormone releasing hormone-stimulated GH secretion and inversely related to pituitary GH expression. However, correlational studies do not prove causality and the evidence is not yet convincing enough to conclude that leptin plays a role in the modulation of the neuroendocrine GH axis in obesity.
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