Division of Endocrinology, Medical Centre of Varna, Varna, Bulgaria.
Med Hypotheses. 2017 Sep;107:9-11. doi: 10.1016/j.mehy.2017.06.025. Epub 2017 Jun 29.
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.
2 型糖尿病是一种全球性的流行疾病,也是心血管并发症的已知危险因素。事实上,在 89%的病例中,它与多因素发病机制的代谢综合征有关。神经营养理论强调关键因素低神经营养素血症的作用,从而将这一范式推广。2 型糖尿病和代谢综合征的特征均为胰岛素抵抗和胰腺β细胞损伤。禁食可使血浆神经营养素水平保持周期性升高。禁食会诱导成年胰腺中产前发育基因的表达,并促进神经基因(Ngn)-3 基因的表达,从而产生产生胰岛素的β细胞。可能是由于禁食后神经生长因子和脑源性神经营养因子的血浆和组织水平升高,重新编程了 Ngn-3 基因的表达,因为这种营养作用增强了 Ngn-3 蛋白的合成。这导致受损的胰腺β细胞再生,并恢复 1 型和 2 型糖尿病的胰岛素分泌。