Role of Vitamin D in Insulin Resistance

Table 1

Role of vitamin D deficiency in insulin resistance.

Role	References
Inherited gene polymorphisms	[44–68]
(1) Including DBP, VDR, and CYP1alpha gene polymorphisms
(2) Disturbance of vitamin D transport, action, and production
Immunoregulatory function	[69–83]
(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-γ, and TNFα (destruction of the β-cell)
Inflammation	[84–90]
(1) Upregulation of NF-κB and inducing TNFα proinflammatory actions
(2) Downregulates IκB-α by decreasing mRNA stability and increasing IκB-α phosphorylation.
(3) Enhancing the expression of TLR2 and TLR4 protein and mRNA in human monocytes, reducing the release of cytokines
Other molecular actions of vitamin D to alter glucose homeostasis	[90–95]
(1) Low calcium status: hypocalcemia can lower glucose-stimulated insulin secretion in β-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-γ: interferon-γ; TNF α: tumor necrosis factor α; NF-κB: nuclear factor κB; IκB-α: the inhibitor of NF-κB; TLR: Toll-like receptors; PTH: parathyroid hormone.