Exercise-produced irisin effects on brain-related pathological conditions.

Abstract

Exercise increases peroxisome proliferator-activated receptor-gamma coactivator 1-alpha (PGC-1α) expression, which in turn causes the fibronectin type III domain containing 5 (FNDC5) protein to be produced. This protein is then cleaved, primarily in skeletal muscle fibers, to produce irisin. When the mature FNDC5 is cleaved by proteases, Irisin - which is the fibronectin III domain without the signal sequence - is released. Resistance, aerobic, and high-intensity interval training (HIIT) are recognized as forms of physical exercise that raise irisin levels, and insulin receptor phosphorylation in tyrosine residues, favoring an increase in the activity of the insulin-dependent pathway (PI3K pathway) and assisting in the fight against insulin resistance, inflammation, and cognitive decline. Irisin may represent a promising option for the therapeutic targeting in several brain-related pathological conditions, like Alzheimer's disease (AD), Parkinson's disease (PD), epilepsy, type 2 diabetes, and obesity. Exercise protocols are healthy and inexpensive interventions that can help find cellular and molecular changes in several brain-related pathological conditions. Here, it was reviewed what is known about exercise-produced irisin studies involving AD, PD, epilepsy, type 2 diabetes, and obesity.