Exercise-induced signalling in alleviating neuronal insulin resistance.

Abstract

Exercise contributes to a multitude of positive changes within the body and brain with regard to glucose homeostasis, insulin sensitivity, synaptic plasticity, neuroprotection and neurogenesis, among other effects. It provides a non-pharmaceutical alternative for addressing metabolic disorders in individuals with type 2 diabetes, who also face an increased risk of developing Alzheimer's disease. A number of molecules are evoked upon exercise and circulate through the bloodstream, transmitting the wide-reaching advantages of exercise. The ensuing cross-talk has been shown to improve conditions associated with Alzheimer's disease. The vast signalling network mediated by exercise is currently being studied extensively and its implications in improving neuronal insulin resistance, especially as a bypass mechanism, are of major interest. Taking into account sirtuin 1/peroxisome proliferator-activated receptor γ co-activator 1-α, AMP-activated protein kinase, phosphoinositide 3-kinase/AKT, phospholipase C-γ and brain-derived neurotrophic factor/tropomyosin receptor kinase B among many pathways and cross-interactions involved, researching the molecular characteristics of brain exercise signalling and the mechanisms by which it compensates for hampered signalling is crucial for future research.