Galia Gat-Yablonski1, Moshe Phillip. 1. Institute for Endocrinology and Diabetes, National Center for Childhood Diabetes, Schneider Children's Medical Center of Israel, Israel.
Abstract
PURPOSE OF REVIEW: Leptin, first identified as the product of the ob gene in leptin-deficient obese (ob/ob) mice, was originally described as a circulating hormone involved in feeding behavior and energy homeostasis. It was later found to be a pleiotropic hormone involved in the regulation of a variety of physiological processes. This review summarizes our recent understanding of the role of leptin as a linear growth-stimulating factor. RECENT FINDINGS: Leptin was found to have mitogenic effects on numerous cell types in vivo and in vitro, including several cancer cells, cells of the immune system, as well as chondrocytes of the epiphyseal growth plate. SUMMARY: Leptin stimulates linear growth by regulating the energy balance of the organism and by stimulating the production and secretion of growth hormone from the hypothalamus; at the same time, it is involved with bone remodeling and has a direct effect on the chondrocytes of the growth plate.
PURPOSE OF REVIEW: Leptin, first identified as the product of the ob gene in leptin-deficient obese (ob/ob) mice, was originally described as a circulating hormone involved in feeding behavior and energy homeostasis. It was later found to be a pleiotropic hormone involved in the regulation of a variety of physiological processes. This review summarizes our recent understanding of the role of leptin as a linear growth-stimulating factor. RECENT FINDINGS:Leptin was found to have mitogenic effects on numerous cell types in vivo and in vitro, including several cancer cells, cells of the immune system, as well as chondrocytes of the epiphyseal growth plate. SUMMARY:Leptin stimulates linear growth by regulating the energy balance of the organism and by stimulating the production and secretion of growth hormone from the hypothalamus; at the same time, it is involved with bone remodeling and has a direct effect on the chondrocytes of the growth plate.
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