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Title: Vitamin D and energy homeostasis-of mice and men
Authors: Bouillon, Roger ×
Carmeliet, Geert
Lieben, Liesbet
Watanabe, Mitsuhiro
Perino, Alessia
Auwerx, Johan
Schoonjans, Kristina
Verstuyf, Annemieke #
Issue Date: Feb-2014
Publisher: Nature Publishing Group
Series Title: Nature Reviews. Endocrinology vol:10 issue:2 pages:79-87
Article number: 10.1038/nrendo.2013.226
Abstract: The vitamin D endocrine system has many extraskeletal targets, including adipose tissue. 1,25-Dihydroxyvitamin D3, the active form of vitamin D, not only increases adipogenesis and the expression of typical adipocyte genes but also decreases the expression of uncoupling proteins. Mice with disrupted vitamin D action-owing to gene deletion of the nuclear receptor vitamin D receptor (Vdr) or the gene encoding 1α-hydroxylase (Cyp27b1)-lose fat mass over time owing to an increase in energy expenditure, whereas mice with increased Vdr-mediated signalling in adipose tissue become obese. The resistance to diet-induced obesity in mice with disrupted Vdr signalling is caused at least partially by increased expression of uncoupling proteins in white adipose tissue. However, the bile acid pool is also increased in these animals, and bile acids are known to be potent inducers of energy expenditure through activation of several nuclear receptors, including Vdr, and G-protein-coupled receptors, such as GPBAR1 (also known as TGR5). By contrast, in humans, obesity is strongly associated with poor vitamin D status. A causal link has not been firmly proven, but most intervention studies have failed to demonstrate a beneficial effect of vitamin D supplementation on body weight. The reasons for the major discrepancy between mouse and human data are unclear, but understanding the link between vitamin D status and energy homeostasis could potentially be very important for the human epidemic of obesity and the metabolic syndrome.
URI: 
ISSN: 1759-5029
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Clinical and Experimental Endocrinology
× corresponding author
# (joint) last author

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