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NOVEL PHYSIOLOGICAL AND THERAPEUTIC IMPLICATIONS OF LEPTIN

Nuevas proyecciones fisiológicas, patológicas y terapéuticas de la leptina

Author
Goldenberg, Denisse; Departamento de Nutrición, Diabetes y Metabolismo. Escuela de Medicina. Pontificia Universidad Católica de Chile

Santos, José Luis; Departamento de Nutrición, Diabetes y Metabolismo. Escuela de Medicina. Pontificia Universidad Católica de Chile

Hodgson, María Isabel; Departamento de Nutrición, Diabetes y Metabolismo. Escuela de Medicina. Pontificia Universidad Católica de Chile

Cortés, Víctor A; Departamento de Nutrición, Diabetes y Metabolismo. Escuela de Medicina. Pontificia Universidad Católica de Chile

Full text
http://www.revistamedicadechile.cl/ojs/index.php/rmedica/article/view/2800
Abstract
The adipose tissue is an endocrine organ that produces a variety of protein hormones. One of them is leptin, which regulates several critical functions at the central nervous system such as caloric intake, basal energy expenditure, reproduction, glucose and lipid metabolism and osteogenesis. Acting at a local level, leptin modulates the immune system and promotes liver fibrogenesis. The most promising therapeutic implications of leptin will possibly be in type 1 diabetes mellitus (DM1). Its supplementation in animal models of DM1 prevents hyperglycemia and ketoacidosis. These actions depend on the activation of leptin receptors in the central nervous system and the suppression of glucagon signaling in the liver.
 
The adipose tissue is an endocrine organ that produces a variety of protein hormones. One of them is leptin, which regulates several critical functions at the central nervous system such as caloric intake, basal energy expenditure, reproduction, glucose and lipid metabolism and osteogenesis. Acting at a local level, leptin modulates the immune system and promotes liver fibrogenesis. The most promising therapeutic implications of leptin will possibly be in type 1 diabetes mellitus (DM1). Its supplementation in animal models of DM1 prevents hyperglycemia and ketoacidosis. These actions depend on the activation of leptin receptors in the central nervous system and the suppression of glucagon signaling in the liver.
 
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