Abstract

In addition to their stimulatory action on neuronal differentiation and survival, the neurotrophins nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) improve glucose and lipid metabolism and control energy balance and feeding behavior. These latter activities are referred to here as the metabotrophic potential of neurotrophins. We recently reported that circulating NGF and BDNF levels are reduced in the metabolic syndrome and in acute coronary syndromes, and that the tissue content of NGF is reduced in atherosclerotic coronary arteries. Thus we hypothesize that a metabotrophic deficit due to reduction of neurotrophin availability may be implicated in the pathogenesis of obesity and related metabolic diseases, such as metabolic syndrome, type 2 diabetes, and atherosclerosis. The metabotrophic deficit hypothesis also considers metabolism-related beneficial effects exerted by other neurotrophic factors, particularly ciliary neurotrophic factor, leukemia inhibitory factor, and bone morphogenetic proteins.

Keywords: Glucose - metabolism, Nerve Growth Factors - metabolism, Obesity - metabolism