The Molecular Mechanisms by Which Vitamin D Prevents Insulin Resistance and Associated Disorders

Numerous studies have shown that vitamin D deficiency is very common in modern societies and is perceived as an important risk factor in the development of insulin resistance and related diseases such as obesity and type 2 diabetes (T2DM). While it is generally accepted that vitamin D is a regulator...

Full description

Saved in:
Bibliographic Details
Published inInternational journal of molecular sciences Vol. 21; no. 18; p. 6644
Main Authors Szymczak-Pajor, Izabela, Drzewoski, Józef, Śliwińska, Agnieszka
Format Journal Article
LanguageEnglish
Published Switzerland MDPI AG 11.09.2020
MDPI
Subjects
Online AccessGet full text
ISSN1422-0067
1661-6596
1422-0067
DOI10.3390/ijms21186644

Cover

More Information
Summary:Numerous studies have shown that vitamin D deficiency is very common in modern societies and is perceived as an important risk factor in the development of insulin resistance and related diseases such as obesity and type 2 diabetes (T2DM). While it is generally accepted that vitamin D is a regulator of bone homeostasis, its ability to counteract insulin resistance is subject to debate. The goal of this communication is to review the molecular mechanism by which vitamin D reduces insulin resistance and related complications. The university library, PUBMED, and Google Scholar were searched to find relevant studies to be summarized in this review article. Insulin resistance is accompanied by chronic hyperglycaemia and inflammation. Recent studies have shown that vitamin D exhibits indirect antioxidative properties and participates in the maintenance of normal resting ROS level. Appealingly, vitamin D reduces inflammation and regulates Ca2+ level in many cell types. Therefore, the beneficial actions of vitamin D include diminished insulin resistance which is observed as an improvement of glucose and lipid metabolism in insulin-sensitive tissues.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 14
ObjectType-Review-3
content type line 23
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms21186644