Analysis of Association between Vitamin D Deficiency and Insulin Resistance

被引:207
作者
Szymczak-Pajor, Izabela [1 ]
Sliwinska, Agnieszka [1 ]
机构
[1] Med Univ Lodz, Dept Nucle Acid Biochem, 251 Pomorska, PL-92213 Lodz, Poland
关键词
insulin resistance; insulin-responsive tissues; vitamin D; pancreatic -cells dysfunction; sub-inflammation; oxidative stress; SERUM 25-HYDROXYVITAMIN D; PANCREATIC BETA-CELL; PROLIFERATOR-ACTIVATED RECEPTOR; ADIPOSE-TISSUE FUNCTION; KINASE-C-THETA; 1,25-DIHYDROXYVITAMIN D-3; D SUPPLEMENTATION; OXIDATIVE STRESS; PROTEIN-KINASE; PARATHYROID-HORMONE;
D O I
10.3390/nu11040794
中图分类号
R15 [营养卫生、食品卫生]; TS201 [基础科学];
学科分类号
100403 ;
摘要
Recent evidence revealed extra skeleton activity of vitamin D, including prevention from cardiometabolic diseases and cancer development as well as anti-inflammatory properties. It is worth noting that vitamin D deficiency is very common and may be associated with the pathogenesis of insulin-resistance-related diseases, including obesity and diabetes. This review aims to provide molecular mechanisms showing how vitamin D deficiency may be involved in the insulin resistance formation. The PUBMED database and published reference lists were searched to find studies published between 1980 and 2019. It was identified that molecular action of vitamin D is involved in maintaining the normal resting levels of ROS and Ca2+, not only in pancreatic -cells, but also in insulin responsive tissues. Both genomic and non-genomic action of vitamin D is directed towards insulin signaling. Thereby, vitamin D reduces the extent of pathologies associated with insulin resistance such as oxidative stress and inflammation. More recently, it was also shown that vitamin D prevents epigenetic alterations associated with insulin resistance and diabetes. In conclusion, vitamin D deficiency is one of the factors accelerating insulin resistance formation. The results of basic and clinical research support beneficial action of vitamin D in the reduction of insulin resistance and related pathologies.
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页数:28
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