Abstract
Type 2 diabetes mellitus is an epidemic worldwide and a proved risk factor for cardiovascular complications. In 89% of the cases, it deals, in fact, with metabolic syndrome of multifactorial etiopathogenesis. This paradigm has been generalized by the neurotrophic theory emphasizing the role of hyponeurotrophinemia of key factor. Both type 2 diabetes mellitus and metabolic syndrome are characterized by insulin resistance and pancreatic β-cell damage. Cyclic keeping the fast enhances plasma neurotrophin levels. Fasting induces prenatal-development gene expression in adult pancreas and promotes neurogenin (Ngn)-3 gene expression to generate insulin producing β-cells. Probably, the increased plasma and tissue levels of the nerve growth factor and brain-derived neurotrophic factor after fasting reprogramme Ngn-3 gene expression as this genotrophic action enhances Ngn-3 protein synthesis. This results in regeneration of damaged pancreatic β-cells and restores insulin secretion in type 1 and type 2 diabetes mellitus.
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