Role of eating disorders-related polymorphisms in obesity pathophysiology.

Rev Endocr Metab Disord

Department of Health Sciences, Ribeirão Preto Medical School - FMRP/USP - Laboratory of Nutrigenomic Studies, University of São Paulo, Av Bandeirantes, 3900, Monte Alegre, Ribeirão Preto, SP, CEP: 14049-900, Brazil.

Published: March 2019

AI Article Synopsis

  • The human biological system controls food intake through a complex network of neuroendocrine signals that modulate appetite and satiety, involving various tissues, hormones, and neural circuits.
  • Dysregulation of these signaling pathways can lead to eating disorders and obesity, emphasizing the importance of these mechanisms for maintaining energy balance.
  • Genetic factors, particularly Single Nucleotide Polymorphisms (SNPs) in genes associated with appetite regulation and brain reward systems, play a significant role in the development of eating disorders like Binge Eating Disorder and Bulimia Nervosa.

Article Abstract

Human biological system provides innumerable neuroendocrine inputs for food intake control, with effects on appetite's modulation and the satiety signs. Its regulation is very complex, engaging several molecular interactions with many tissues, hormones, and neural circuits. Thus, signaling molecules that control food intake are critical for normal energy homeostasis and a deregulation of these pathways can lead to eating disorders and obesity. In line of this, genetic factors have a significantly influence of the regulation of neural circuits controlling the appetite and satiety pathways, as well as the regulation of brain reward systems. Single Nucleotide Polymorphisms (SNPs) in genes related to hypothalamic appetite and satiety mechanisms, further in multiple neurotransmitter systems may contribute to the development of major Eating Disorders (EDs) related to obesity, among them Binge Eating Disorder (BED) and Bulimia Nervosa (BN), which are discussed in this review.

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Source
http://dx.doi.org/10.1007/s11154-019-09489-wDOI Listing

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