Hypothalamic Alterations in ObesitySimone van de Sande-Lee1,2* and Licio A Velloso2
- Corresponding Author:
- Simone van de Sande-Lee
Universidade Federal de Santa Catarina, Hospital Universitário
Departamento de Clínica Médica, Campus Universitário–Trindade
88040-970, Florianópolis, SC, Brazil
Tel: +55 48 37219014
Fax: +55 48 37219149
E-mail: [email protected]
Received date: December 30, 2014; Accepted date: March 20, 2014; Published date: March 24, 2014
Citation: van de Sande-Lee S, Velloso LA (2014) Hypothalamic Alterations in Obesity. J Mol Genet Med S1:026. doi: 10.4172/1747-0862.S1-026
Copyright: © 2014 van de Sande-Lee S and Velloso LA. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Obesity is a major public health problem. Excess adiposity reflects an imbalance between food intake and energy expenditure, resulting from complex interactions between genetic and environmental factors. In animals and humans, the control of energy homeostasis is performed by the Central Nervous System (CNS) through neuroendocrine connections, in which circulating peripheral hormones such as leptin and insulin provide a signal to specialized neurons of the hypothalamus reflecting body fat stores, and inducing appropriate responses to maintain the stability of these stores. Obesity is commonly associated with central resistance to both leptin and insulin actions. In experimental animals, high-fat diets can induce an inflammatory process in the hypothalamus, which impairs leptin and insulin intracellular signaling pathways and results in hyperphagia, decreased energy expenditure and ultimately obesity. Recent evidence, obtained from neuroimaging studies and analysis of inflammatory markers in the cerebrospinal fluid of obese subjects, suggest that similar alterations may be also found in humans. In this review, we briefly present the mechanisms involved with deterioration of homeostatic control of energy balance in animal models of obesity and the current evidence of hypothalamic dysfunction in obese humans.