Evidence supporting an adipo-leptin-growth hormone axis in obesity-relatedhyposomatotropism

Growth hormone (GH) secretion is impaired in obese children and adults but the physiologic mechanisms for obesity induced hyposomatotropism remain unc lear. Metabolic disturbances that result from obesity and a central accumul ation of body fat, such as increased circulating insulin and free-fatty aci d concentrations, reduce growth hormone secretion at the level of the pitui tary and perhaps the hypothalamus. Leptin is a logical choice as a humoral signal to relay information regarding the body composition and the fat dist ribution to the hypothalamus and pituitary. Leptin is secreted directly fro m the adipocytes and leptin receptors are located in the pituitary and the hypothalamus including growth hormone-releasing hormone neurons. Serum lept in concentrations are inversely related to basal and growth hormone releasi ng hormone-stimulated GH secretion and inversely related to pituitary GH ex pression. However, correlational studies do not prove causality and the evi dence is not yet convincing enough to conclude that leptin plays a role in the modulation of the neuroendocrine GH axis in obesity.