Please use this identifier to cite or link to this item: http://repositorio.unicamp.br/jspui/handle/REPOSIP/200196
Type: Artigo de periódico
Title: [hypothalamic Dysfunction In Obesity].
Author: van de Sande-Lee, Simone
Velloso, Licio A
Abstract: Obesity, defined as abnormal or excessive fat accumulation that may impair life quality, is one of the major public health problems worldwide. It results from an imbalance between food intake and energy expenditure. The control of energy balance in animals and humans is performed by the central nervous system (CNS) by means of neuroendocrine connections, in which circulating peripheral hormones, such as leptin and insulin, provide signals to specialized neurons of the hypothalamus reflecting body fat stores, and induce appropriate responses to maintain the stability of these stores. The majority of obesity cases are 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 assessment of inflammatory markers in the cerebrospinal fluid of obese subjects suggests that similar alterations may be also present in humans. In this review, we briefly present the mechanisms involved with the loss of homeostatic control of energy balance in animal models of obesity, and the current evidence of hypothalamic dysfunction in obese humans.
Subject: Adipose Tissue
Animals
Eating
Energy Metabolism
Homeostasis
Humans
Hypothalamic Diseases
Hypothalamus
Insulin
Insulin Resistance
Leptin
Obesity
Rights: aberto
Identifier DOI: 
Address: http://www.ncbi.nlm.nih.gov/pubmed/22990637
Date Issue: 2012
Appears in Collections:Unicamp - Artigos e Outros Documentos

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