Leptin participates in the regulation of glucocorticoid and growth hormone axes

An adipocyte factor transducing the quantity of adipose to a hormonal message that targets the hypothalamus has been postulated for many years. Recently, a gene that encodes such a protein (named leptin) was identified. These findings indicate that adipose tissue performs important biological functions beyond storage of fat. In fact, data indicate that adipose tissue functions very much like other endocrine tissues, releasing a hormone into the circulatory system to relay a message to its target. Although there may be more than one target tissue for leptin, the best accepted component of any leptin endocrine axis is the hypothalamus. Because this integrative center is fundamental to many neuroendocrine axes, classical endocrine feedback circuits must now be extended to include leptin. Leptin deficiency is extremely rare and has been only reported in a mutant moi-bid obese mouse strain and in two children who also sr(suffer from extreme obesity. Most types of human and murine obesity are accompanied by elevated leptin levels, and the concentrations of this hormone correlate well with degree of adiposity. Thus, it is thought that leptin may serve as a fuel gauge for the hypothalamus. When sufficient fuel is present or when lipid is being synthesized and stored in adipose, leptin levels rise and reduce further Seeding behavior In addition, a signal of abundant fuel reserve also serves as a message that energy can be expended for anabolism of protein and other biological processes such as growth, repair, and reproduction. Our delta, together with those reported by others, indicate that leptin inhibits the hypothalamic-pituitary-adrenal axis (HPAA) and thus antagonizes the catabolic glucocorticoids. A review of available data also supports that leptin stimulates the hypothalamic-growth hormone axis and hence promotes protein synthesis. Energy,must be expended to support this anabolic state, and data indicate the energy is derived from metabolism of adipose reserve. Such loss of lipid would lend to decrease plasma leptin levels and thereby signal a state for replenishment of adipose stores. (C) Elsevier Science Inc 1998.