A possible link between BDNF and mTOR in control of food intake

Abstract

Food intake is intricately regulated by glucose, amino acids, hormones, neuropeptides, and trophic factors through a neural circuit in the hypothalamus. Brain-derived neurotrophic factor (BDNF), the most prominent neurotrophic factor in the brain, regulates differentiation, maturation, and synaptic plasticity throughout life. Among its many roles, BDNF exerts an anorexigenic function in the brain. However, the intracellular signaling induced by BDNF to control food intake is not fully understood. One candidate for the molecule involved in transducing the anorexigenic activity of BDNF is the mammalian target of rapamycin (mTOR). mTOR senses extracellular amino acids, glucose, growth factors, and neurotransmitters, and regulates anabolic reactions response to these signals. Activated mTOR increases protein and lipid synthesis and inhibits protein degradation. In the hypothalamus, mTOR activation is thought to reduce food intake. Here we summarize recent findings regarding BDNF- and mTOR-mediated feeding control, and propose a link between these molecules in eating behavior.

Pituitary Adenylate Cyclase-Activating Peptide in the Central Amygdala Causes Anorexia and Body Weight Loss via the Melanocortin and the TrkB Systems

“…Considerable evidence has shown that BDNF is involved in feeding and energy homeostasis via its TrkB receptor. Central infusion of BDNF suppresses appetite and reduces body weight in rodents; manipulations of the BDNF gene in animals as well as the study of BDNF gene mutations in humans have confirmed a pivotal role of the BDNF-TrkB system in feeding and weight control (Takei et al, 2014). However, while the majority of the reports have identified the hypothalamus as the main brain site responsible for the effects of BDNF on food intake, work investigating the function of the BDNF/TrkB system in the amygdala has only focused on anxiety and fear.…”

Weight‐sparing effect of insulin detemir: a consequence of central nervous system‐mediated reduced energy intake?

“…Food intake is regulated by glucose, amino acids, hormones, neuropeptides and trophic factors in the hypothalamus, and insulin is now well established as an adiposity signal acting within the brain and CNS to influence energy homeostasis through food intake and body weight [47,48]. Although it is difficult to assess the effects of insulin on the human CNS it has been suggested that insulin acts through the cerebral cortex [49] and studies have demonstrated reduced cerebrocortical response to hyperinsulinaemia in non-diabetic, obese subjects [49].…”

Effect of Rhodopseudomonas sphaeroides–Treated Wastewater on Yield, Digestive Enzymes, Antioxidants, Nonspecific Immunity, and Intestinal Microbiota of Common Carp

“…), widely exists in eukaryotes (Takei et al. ) and is important for food intake and dealing with environmental stresses (Abuhagr et al. ; Li et al.…”

“…As a signal transduction pathway, the mTOR signaling pathway, which plays a vital role in nutrition regulation and has complex impact on cell growth (Cota et al 2008), widely exists in eukaryotes (Takei et al 2014) and is important for food intake and dealing with environmental stresses (Abuhagr et al 2014;Li et al 2019). The mTOR pathway is a key regulator of the balance between protein synthesis and degradation in response to nutrition quality and quantity (Wullschleger et al 2006;Wu et al 2019e), and protein synthesis is essential for cell growth, proliferation, apoptosis, and autophagy (Rohde et al 2001).…”