Table 1: Role of vitamin D deficiency in insulin resistance.

RoleReferences

Inherited gene polymorphisms[4468]
 (1) Including DBP, VDR, and CYP1alpha gene polymorphisms
 (2) Disturbance of vitamin D transport, action, and production
Immunoregulatory function[6983]
 (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[8490]
 (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[9095]
 (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.