J Biomed Biotechnol. 2012;2012:634195. Epub 2012 Sep 3.
Sung CC, Liao MT, Lu KC, Wu CC.
Division of Nephrology, Department of Medicine, Tri-Service General Hospital, National Defense Medical Center, Taipei 114, Taiwan.
Vitamin D is characterized as a regulator of homeostasis of bone and mineral metabolism, but it can also provide nonskeletal actions because vitamin D receptors have been found in various tissues including the brain, prostate, breast, colon, pancreas, and immune cells.
Bone metabolism, modulation of the immune response, and regulation of cell proliferation and differentiation are all biological functions of vitamin D.
Vitamin D may play an important role in modifying the risk of cardiometabolic outcomes, including diabetes mellitus (DM), hypertension, and cardiovascular disease.
The incidence of type 2 DM is increasing worldwide and results from a lack of insulin or inadequate insulin secretion following increases in insulin resistance.
Therefore, it has been proposed that vitamin D deficiency plays an important role in insulin resistance resulting in diabetes.
The potential role of vitamin D deficiency in insulin resistance has been proposed to be associated with inherited gene polymorphisms including vitamin D-binding protein, vitamin D receptor, and vitamin D 1alpha-hydroxylase gene.
Other roles have been proposed to involve immunoregulatory function by
- activating innate and adaptive immunity and cytokine release,
- activating inflammation by upregulation of nuclear factor ?B and inducing tumor necrosis factor ?, and
- other molecular actions to maintain glucose homeostasis and mediate insulin sensitivity
by a low calcium status, obesity, or
by elevating serum levels of parathyroid hormone.
These effects of vitamin D deficiency, either acting in concert or alone, all serve to increase insulin resistance.
Although there is evidence to support a relationship between vitamin D status and insulin resistance, the underlying mechanism requires further exploration.
The purpose of this paper was to review the current information available concerning the role of vitamin D in insulin resistance.
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(1) Including DBP, VDR, and CYPlalpha gene polymorphisms
(2) Disturbance of vitamin D transport, action, and production
(1) Activating innate and adaptive immunity
(2) Enhancing dendritic cell maturation and macrophage differentiation, and cytokine release
(3) Enhancing T-cell proliferation
(4) Releases of IL-12, IL-2, INF-y, and TNFa (destruction of the beta-cell)
(1) Upregulation of NF-kB and inducing TNFa proinflammatory actions
(2) Downregulates IxB-a by decreasing mRNA stability and increasing IxB-a phosphorylation.
(3) Enhancing the expression of TLR2 and TLR4 protein and mRNA in human monocytes, reducing the release of cytokines
(1) Low calcium status: hypocalcemia can lower glucose-stimulated insulin secretion in beta-cell
(2) PTH level: elevating PTH reduces glucose uptake by liver, muscle and adipose cell
(3) Obesity: vitamin D deficiency can increase adiposity, and increasing sequestration of vitamin D in adipose tissue
DBP: vitamin D binding protein; VDR: vitamin D receptor; CYP1alpha: vitamin D 1alpha-hydroxylase;
IL-12: interleukin-12; INF-y: interferon-y;TNF a: tumor necrosis factor a;NF-«B: nuclear factor kB;
IicB-a: the inhibitor of NF-kB; TLR: Toll-like receptors; PTH: parathyroid hormone.
PDF is attached at the bottom of this page
- Overview Cognition and vitamin D
- Overview Diabetes and vitamin D
- Scientific explanation of vitamin D relationship to insulin resistance– Dec 2012
- INTERVENTION Clinical Trials for Diabetes and Vitamin D 129 trials as of Nov 2012
- INTERVENTION Clinical Trials for Type 1 Diabetes and Vitamin D 51 trials as of Nov 2012