作者: Paul Lips , Marelise Eekhoff , Natasja van Schoor , Mirjam Oosterwerff , Renate de Jongh
DOI: 10.1016/J.JSBMB.2016.11.021
关键词: Endocrinology 、 Vitamin D and neurology 、 Type 2 diabetes 、 Impaired fasting glucose 、 Insulin resistance 、 vitamin D deficiency 、 Medicine 、 Insulin 、 Prediabetes 、 Internal medicine 、 Impaired glucose tolerance
摘要: Vitamin D deficiency is associated with a decreased insulin release, resistance and type 2 diabetes in experimental epidemiological studies. Animal studies show that 1α,25-dihydroxyvitamin D3 (1,25(OH)2D3) stimulates the pancreatic β-cell to secrete insulin. The relationship between vitamin could develop through inflammation, as increased inflammatory markers. In addition, genetic polymorphisms of -related genes may predispose impaired glycemic control diabetes. Epidemiologic showed an association low serum 25-hydroxyvitamin (25(OH)D3) concentration risk for metabolic syndrome This be partly explained by fat mass. A possible causal should proven randomized clinical trials showing either can prevented or release sensitivity improved supplements. results on effect versus placebo, sometimes combined calcium, patients glucose tolerance ("prediabetes") are inconsistent. Some slight decrease fasting plasma improvement resistance, but often only posthoc analyses. These effects mainly visible at baseline. Meta-analyses general did not significant supplementation control. Currently, several large scale doses 1600-4000IU/d ongoing incidence mellitus outcome. needs cured, until these published, high-dose cannot recommended prevention amelioration