PMID- 24247221
OWN - NLM
STAT- MEDLINE
DCOM- 20140930
LR  - 20211021
IS  - 1759-5037 (Electronic)
IS  - 1759-5029 (Linking)
VI  - 10
IP  - 2
DP  - 2014 Feb
TI  - Vitamin D and energy homeostasis: of mice and men.
PG  - 79-87
LID - 10.1038/nrendo.2013.226 [doi]
AB  - The vitamin D endocrine system has many extraskeletal targets, including adipose 
      tissue. 1,25-Dihydroxyvitamin D(3), 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 1alpha-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.
FAU - Bouillon, Roger
AU  - Bouillon R
AD  - Clinical and Experimental Endocrinology, KU Leuven, O&NI Herestraat 49 - bus 902, 
      3000 Leuven, Belgium.
FAU - Carmeliet, Geert
AU  - Carmeliet G
AD  - Clinical and Experimental Endocrinology, KU Leuven, O&NI Herestraat 49 - bus 902, 
      3000 Leuven, Belgium.
FAU - Lieben, Liesbet
AU  - Lieben L
AD  - Clinical and Experimental Endocrinology, KU Leuven, O&NI Herestraat 49 - bus 902, 
      3000 Leuven, Belgium.
FAU - Watanabe, Mitsuhiro
AU  - Watanabe M
AD  - Health Science Laboratory, Graduate School of Media and Governance, Keio 
      University, 5322 Endo Fujisawa-shi, 252-0882 Kanagawa, Japan.
FAU - Perino, Alessia
AU  - Perino A
AD  - Institute of Bioengineering, Ecole Polytechnique Federale de Lausanne, Station 
      15, AI 1149, CH-1015 Lausanne, Switzerland.
FAU - Auwerx, Johan
AU  - Auwerx J
AD  - Institute of Bioengineering, Ecole Polytechnique Federale de Lausanne, Station 
      15, AI 1149, CH-1015 Lausanne, Switzerland.
FAU - Schoonjans, Kristina
AU  - Schoonjans K
AD  - Institute of Bioengineering, Ecole Polytechnique Federale de Lausanne, Station 
      15, AI 1149, CH-1015 Lausanne, Switzerland.
FAU - Verstuyf, Annemieke
AU  - Verstuyf A
AD  - Clinical and Experimental Endocrinology, KU Leuven, O&NI Herestraat 49 - bus 902, 
      3000 Leuven, Belgium.
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20131119
PL  - England
TA  - Nat Rev Endocrinol
JT  - Nature reviews. Endocrinology
JID - 101500078
RN  - 1406-16-2 (Vitamin D)
SB  - IM
MH  - Adipogenesis/physiology
MH  - Animals
MH  - Disease Models, Animal
MH  - Energy Metabolism/*physiology
MH  - Homeostasis/*physiology
MH  - Humans
MH  - Mice
MH  - Obesity/physiopathology
MH  - Vitamin D/*physiology
EDAT- 2013/11/20 06:00
MHDA- 2014/10/01 06:00
CRDT- 2013/11/20 06:00
PHST- 2013/11/20 06:00 [entrez]
PHST- 2013/11/20 06:00 [pubmed]
PHST- 2014/10/01 06:00 [medline]
AID - nrendo.2013.226 [pii]
AID - 10.1038/nrendo.2013.226 [doi]
PST - ppublish
SO  - Nat Rev Endocrinol. 2014 Feb;10(2):79-87. doi: 10.1038/nrendo.2013.226. Epub 2013 
      Nov 19.