Dysfunctional adipose tissue may play role in vitamin D deficiency

By David Douglas

NEW YORK (Reuters Health) - Biological processes associated with vitamin D metabolism in obese men may help explain why vitamin D deficiency is widespread in this group, according to Italian researchers.

“Our study shows for the first time a pathophysiological role of adiposity in hypovitaminosis D,” Dr. Andrea Di Nisio of the University of Padua told Reuters Health by email. “This has wider clinical implications, particularly in the choice of vitamin D supplementation and weight loss interventions."

In a paper online February 10 in The Journal of Clinical Endocrinology & Metabolism, Dr. Di Nisio and colleagues note that release of vitamin D is impaired in dysfunctional adipose tissue.

To investigate, the team randomly assigned 54 normal-weight and 67 obese men to supplementation with 50 mcg per week of 25-hydroxyvitamin-D3 (25(OH)D) or 150 mcg per week of vitamin D3 (cholecalciferol).

If after six months vitamin D sufficiency, defined as serum 25(OH)D >50 nmol/L, was not reached, the dose was increased by 50%.

Ninety-seven participants completed the one-year study.

Normal-weight subjects had comparable responses to either treatment, the researchers found.

“Conversely,” they wrote, “the proportion of obese subjects achieving vitamin D sufficiency was significantly higher after six months of supplementation with 25-hydroxyvitamin-D3, suggesting a more rapid effect of this treatment."

To investigate underlying mechanisms, the team examined control and insulin resistant (IR) 3T3-L1 adipocytes and subcutaneous adipose tissue (AT) from lean and obese subjects.

"The reduced bioavailability of vitamin D in obese individuals probably involves active sequestration in AT, due to a reduced catecholamine induced release of both D3 and 25(OH)D, rather than an active uptake, and altered autocrine/paracrine actions due to altered activity of vitamin D-metabolizing enzymes," the authors write.

Further studies, they conclude, "are needed in order to elucidate the molecular mechanisms controlling the deposition and release of vitamin D from AT."

Commenting by email, Dr. Michael A. Levine of The Children's Hospital of Philadelphia told Reuters Health that this is "an interesting study that addresses the conundrum of vitamin D deficiency in obese and overweight subjects. Increased sequestration of vitamin D in adipose tissue has long been considered the primary defect in vitamin D homeostasis in obesity."

Dr. Levine, who is chief of the division of endocrinology and medical director of the Center for Bone Health, noted that the researchers "propose that impaired conversion of parent cholecalciferol to 25-hydroxyvitamin D, at least in adipose tissue, may contribute to the lower circulating levels of 25-hydroxyvitamin D in these patients. Accordingly, these authors show that weekly administration of a standard dose of 25-hydroxyvitamin D (calcidiol) is more effective than cholecalciferol at normalizing serum levels of 25-hydroxyvitamin D, even when cholecalciferol is used at higher than conventional doses."

Dr. Levine concluded, "Although these observations provide a rationale for considering calcidiol therapy in obese patients who do not respond to cholecalciferol, it is important to consider that cholecalciferol may serve additional roles beyond that of a substrate for 25-hydroxylase in some tissues."

SOURCE: bit.ly/2mPrCaQ

J Clin Endocrinol Metab 2017.

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