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Obesity and a low vitamin D (VD) status, as well as a positive association between them, are prevalent worldwide. Additionally, a low VD status has been positively correlated with metabolic dysfunction (although not so convincingly as for obesity). The VD receptor (VDR) mediates VD biological actions in adipose tissue (AT), where VD can be activated or inactivated/degraded through specific hydroxylation steps. Additionally, AT can also store and release VD when needed. A lower VD activation/VD inactivation ratio and an impaired VDR signaling in AT could contribute to metabolic dysfunction besides the aforementioned association between obesity and VD status. However, subcutaneous (SAT) and visceral AT (VAT) are not expected to be similarly accountable as these two fat depots play differential roles in metabolic regulation/dysfunction. To our knowledge, only three articles disclose the evaluation of the expression of VDR and/or VD hydroxylating enzymes in human SAT and VAT. A clear dependence on the subcutaneous and/or the visceral fat depot is missing for the relationships of a) obesity and/or metabolic dysfunction with VD status and b) adipose VDR signaling and adipose VD activation/VD inactivation ratio with VD status, obesity and/or metabolic dysfunction. Further studies are warranted to unravel the influence of adipose VD metabolism on VD status.

Vitamin D metabolism in human adipose tissue: could it explain low vitamin D status in obesity?