Adipose tissue as an endocrine organ
Bhatt, Janardan (2006) Adipose tissue as an endocrine organ. Journal of Applied Basic Medical Sciences, 8 (1). pp. 134-141. ISSN ISSN-0972-4729
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Leptin inhibits feeding by binding to long LRb receptor in brain, leading to activation of the JAK-STAT pathway. The leptin signal is terminated by induction of SOCS3 and PTP1B activity. Importance of these molecules have been confirmed in knockout mice. Ablation of LRb and STAT3 in neurons causes hyperphagia ,obesity and neuroendocrine deficits, while the loss of SOCS3 or PTP1B prevent obesity. Adiponectin is associated with improvement in insulin sensitivity , decrease lipids by enhancing oxidation and protection against atherosclerosis. Adiponectin is increased by thiazolidinediones and likely mediates the anti diabetic effects of these drugs. Resistin exerts an opposite effect to adiponectin by inhibiting insulin action in rodents, but their role in human is uncertain. The recent breakthroughs in our understanding of energy balance, especially the discovery of adipocyte hormones, into the role of adipose tissue in health and disease. Adipose tissue is a versatile organ system necessary for survival. However, dysregulation of adipose signaling in the brain and peripheral organs clearly leads to major metabolic abnormalities, particularly obesity, insulin resistance, diabetes and dyslipidemia. Leptin, adiponectin and to some extent resistin offer potential mechanisms to explain how adipose tissue is able to modulate glucose and lipid metabolism under various physiologic and pathologic states. While rodents have provided useful models for studying these processes, it is essential to examine the effects of adipocyte hormones by direct administration in humans where possible. Adipocyte hormones could become important markers of disease prevention as well as potential therapeutic targets for obesity and related diseases.
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