Molecular and neural bases underlying roles of BDNF in the control of body weight

Filip Vanevski,Baoji Xu

doi:10.3389/fnins.2013.00037

Abstract

Brain-derived neurotrophic factor (BDNF) is a potent regulator of neuronal development and synaptic plasticity that is fundamental to neural circuit formation and cognition. It is also involved in the control of appetite and body weight, with mutations in the genes for BDNF and its receptor, TrkB, resulting in remarkable hyperphagia and severe obesity in humans and mice. Recent studies have made significant progress in elucidating the source, action sites, and regulatory pathways of BDNF with regard to its role in the control of energy homeostasis, and have shed light on the relationships between BDNF and other molecules involved in the control of body weight. Here we provide a comprehensive review of evidence from pharmacological, genetic, and mechanistic studies, linking BDNF to the control of body weight. This review also aims to organize the main findings on this subject into a more refined framework and to discuss the future research directions necessary to advance the field.

Highlights

Brain-derived neurotrophic factor (BDNF) is a member of the neurotrophin family of secreted signaling molecules that includes nerve growth factor (NGF), neurotrophin-3 (NT3), and neurotrophin-4/5 (NT4/5)
The tropomyosin receptor kinase (Trk) receptors have different neurotrophins as their preferred ligands, with NGF binding to TrkA, BDNF and NT4/5 binding to TrkB and NT3 binding to TrkC, while all of the neurotrophins can bind to p75 neurotrophin receptor (p75NTR) (Barbacid, 1994; Bibel and Barde, 2000; Reichardt, 2006)
It is likely that BDNF acts downstream of many anorexigenic factors to control body weight

Summary

Introduction

Brain-derived neurotrophic factor (BDNF) is a member of the neurotrophin family of secreted signaling molecules that includes nerve growth factor (NGF), neurotrophin-3 (NT3), and neurotrophin-4/5 (NT4/5). The Trk receptors have different neurotrophins as their preferred ligands, with NGF binding to TrkA, BDNF and NT4/5 binding to TrkB and NT3 binding to TrkC, while all of the neurotrophins can bind to p75NTR (Barbacid, 1994; Bibel and Barde, 2000; Reichardt, 2006). Neurotrophins are expressed both during development and throughout adulthood (Hofer et al, 1990; Yan et al, 1997b). Recent genetic data has linked deficiencies in TrkB signaling to obesity (Rios et al, 2001; Xu et al, 2003; Yeo et al, 2004)

Objectives

Conclusion