Abstract
Obesity and type 2 diabetes have both rapidly increased during the last decades and are continuing to increase at an alarming rate worldwide. Obesity and impaired glucose homeostasis are closely related, and during the last decades of investigation about vitamin D, several clinical and epidemiological studies documented an inverse correlation between circulating vitamin D levels, central adiposity and the development of insulin resistance and diabetes. The insufficient sun exposure and outdoor activities of obese individuals, the storage of vitamin D in adipose tissue, because of its lipophilic properties, and the vitamin D-mediated modulation of adipogenesis, insulin secretion, insulin sensitivity and the immune system, are the main reasons for the close relationship between obesity, glucose homeostasis and hypovitaminosis D. Then objective of this review is to explore the pathophysiological mechanism(s) by which vitamin D modulates glycemic control and insulin sensitivity in obese individuals.
Highlights
Type 2 diabetes (T2DM) and obesity are both rapidly increased during the last decades and are continuing to increase at an alarming rate worldwide
Vitamin D is essential in maintaining extracellular calcium concentrations and calcium influx into β-cells for insulin secretion; vitamin D receptor (VDR) signaling may play a direct role in glucose-induced insulin secretion
How vitamin D interacts with adiponectin is not well understood. They are linked because adiponectin and glucose metabolism are regulated by osteocalcin, an osteoblast-derived protein, which in turn is influenced by vitamin D, and because 1,25(OH)2 D modulates adipogenesis through a VDR-dependent mechanism [63,64], interacting with PPARγ [60,65,66]
Summary
Role of Hypovitaminosis D in the Pathogenesis of Obesity-Induced Insulin Resistance. Department of Experimental Medicine, Section of Physiopathology, Endocrinology and Food Science, University of Rome Sapienza, 00161 Rome, Italy.
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