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Abstract
Adipose tissue has traditionally only been considered as an energy storage organ. Nevertheless, the importance of this tissue in systemic physiology and, especially, in systemic inflammation has been highlighted in recent years. Adipose tissue expresses proteins related to vitamin D (VD) metabolism, and it has been proposed that it can act as a VD storage tissue. The active form of VD, 1,25-dihydroxyvitamin D3 (1,25(OH)2D3), is able to modify adipocyte and adipose tissue physiology via the VD receptor (VDR), decreasing the expression of pro-inflammatory cytokines in adipose tissue. Moreover, VD deficiency and VDR has been reported to be associated with obesity and diabetes. However, the results of the different studies are not conclusive. Insulin growth binding proteins (IGFBPs) have been identified in adipose tissue, but their roles are poorly understood. Therefore, the objective of this study was to analyze the plasma levels of VD and the gene expression of VDR in the adipose tissue of subjects with morbid obesity (MO) and with different degrees of insulin resistance (IR), as well as the functionality of direct interaction between IGFBP-3 and VDR, which could explain its inhibitory role in adipogenesis. Our results show a novel role of the VD system in the regulation and activation of IGFBP-3 in visceral adipose tissue (VAT) of patients with MO, as a new and alternative mechanism proposed in the insulin signaling associated with obesity.
Highlights
Adipose tissue has long been identified as the main storage site for vitamin D (VD) [1]
Emerging studies suggest a role of VD deficiency in the etiology of type 2 diabetes [25], it has been argued that the influence of VD could be weak and that obesity may modify the association between 25-OH-VD and insulin sensitivity [26]
The data presented here demonstrate that subjects with obesity and a high degree of insulin resistance (IR) have a clear decline in serum 25-OH-VD
Summary
Adipose tissue has long been identified as the main storage site for vitamin D (VD) [1]. It has been shown that VD regulates adipogenic gene expression, and is active in adipocytes at all levels. VD reduces the release of cytokines and the inflammation of the visceral adipose tissue (VAT) through the inhibition of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling. Recent studies have shown that the vitamin D receptor (VDR) is expressed in adipocytes. VDR is a transcription factor which binds to specific VD response elements (VDREs) within the regulatory regions of its primary target genes [2]. The protein-DNA complex of a VDR-RXR heterodimer binding to a VDRE, can be considered as a molecular switch for primary 1,25(OH)2D3 responding genes [4]
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