Metabolic and Genetic Association of Vitamin D with Calcium Signaling and Insulin Resistance

Abstract

Various evidences have unveiled the significance of Vitamin D in diverse processes which include its action in prevention of immune dysfunction, cancer and cardiometabolic disorders. Studies have confirmed the function of VD in controlling the expression of approximately nine hundred genes including gene expression of insulin. VD insufficiency may be linked with the pathogenesis of diseases that are associated with insulin resistance (IR) including diabetes as well as obesity. Thus, VD lowers IR-related disorders such as inflammation and oxidative stress. This review provides an insight regarding the molecular mechanism manifesting, how insufficiency of VD may be connected with the IR and diabetes. It also discusses the effect of VD in maintaining the Ca²⁺ levels in beta cells of the pancreas and in the tissues that are responsive to insulin.

Keywords: Calcium; Diabetes; Insulin resistance (IR); Insulin sensitivity; Vitamin D; Vitamin D deficiency.

Fig. 1

Illustrates the attenuation of insulin signaling in insulin resistance state. Various kinases i.e., PKC-θ PKCζ/λ, JNK, IKK-β have a role in phosphorylating IRS that attenuates the signalling network in insulin pathway. This state is seen in insulin resistance (Dashed line) attenuation

Fig. 2

Illustrates the effect of Vitamin D and improvement in Glucose uptake

Fig. 3

Illustrates the effect of vitamin D on skeletal muscle

Fig. 4

Illustrates the mechanism of Vitamin D in liver cells

Fig. 5

Illustrates the role of vitamin D in inhibition of Inflammation. Pro-inflammatory genes such as TNF-α, IL-1β and, IL-6 are being activated by IL-6R and, TLR via NF-κB or P38MAPK dependent transcription. Vitamin D inhibits inflammation by suppressing phosphorylation of IκBα followed by translocation of NK-κB and P38MAPK into the nucleus resulting in the down expression of proinflammatory genes