Mechanisms Linking Vitamin D Deficiency to Impaired Metabolism: An Overview

Abstract

Vitamin D deficiency is a common health problem worldwide. Despite its known skeletal effects, studies have begun to explore its extra-skeletal effects, that is, in preventing metabolic diseases such as obesity, hyperlipidemia, and diabetes mellitus. The mechanisms by which vitamin D deficiency led to these unfavorable metabolic consequences have been explored. Current evidence indicates that the deficiency of vitamin D could impair the pancreatic β-cell functions, thus compromising its insulin secretion. Besides, vitamin D deficiency could also exacerbate inflammation, oxidative stress, and apoptosis in the pancreas and many organs, which leads to insulin resistance. Together, these will contribute to impairment in glucose homeostasis. This review summarizes the reported metabolic effects of vitamin D, in order to identify its potential use to prevent and overcome metabolic diseases.

The Mutual Interplay between Bone, Glucose and Lipid Metabolism: The Role of Vitamin D and PTH

“…The pathophysiology of the multiple actions of vitamin D beyond those on bone and mineral metabolism focus on the expression by a number of systems and organs of vitamin D receptor (VDR), 1α-hydroxylase (the enzyme mediating the activation of the hormone) and the intra-nuclear response to vitamin D by many genes [15]. As such, vitamin D exerts its favorable effects on glucose metabolism by a fine regulation of insulin sensitivity involving different organs (liver, adipose tissue, skeletal muscle and kidneys) [2,18]. Actions of vitamin D include the stimulation of the expression of glucose transporters, hormones and signaling pathways enhancing insulin sensitivity, increased metabolism of fatty acids and the suppression of the renin-angiotensin-aldosterone system [18].…”

“…As such, vitamin D exerts its favorable effects on glucose metabolism by a fine regulation of insulin sensitivity involving different organs (liver, adipose tissue, skeletal muscle and kidneys) [2,18]. Actions of vitamin D include the stimulation of the expression of glucose transporters, hormones and signaling pathways enhancing insulin sensitivity, increased metabolism of fatty acids and the suppression of the renin-angiotensin-aldosterone system [18]. These mechanisms are amongst those considered as playing a central role in the complex and multifactorial link between vitamin D deficiency and metabolic syndrome [18,19].…”

“…Actions of vitamin D include the stimulation of the expression of glucose transporters, hormones and signaling pathways enhancing insulin sensitivity, increased metabolism of fatty acids and the suppression of the renin-angiotensin-aldosterone system [18]. These mechanisms are amongst those considered as playing a central role in the complex and multifactorial link between vitamin D deficiency and metabolic syndrome [18,19]. As far as lipid metabolism, vitamin D may exert direct (by inhibiting the sterol regulatory element-binding proteins with the consequent suppression of free fatty acid synthesis and uptake) and indirect positive effects (by ameliorating insulin sensitivity, enhancing intestinal calcium absorption that in turn reduces hepatic secretion of triglycerides) [4].…”

“…The suppression of serum PTH secretion by parathyroid glands is one of the most important indirect mechanisms through which vitamin D may regulate insulin, glucose and adipose tissue metabolism, with significant effect on serum lipids as well [4,18]. Similar to vitamin D, PTH may also exert a significant action on the adipose tissue.…”

Vitamin D Deficiency in Both Oral and Systemic Manifestations in SARS-CoV-2 Infection: Updated Review

“…Rabbits and mice with experimentally induced vitamin D deficiency show low insulin secretion, and following vitamin D supplementation, a normalization of insulin secretion is observed [ 28 , 35 , 36 , 37 ]. Mice with abnormalities in the specific receptor for vitamin D have been found to have reduced glucose tolerance compared to animals that have this functional receptor.…”