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Effects of pregnancy vitamin D status on adipose tissue development and inflammation in lean, male adult mice offspring (1037.4)
Author(s) -
Belenchia Anthony,
Jones Karen,
Beversdorf David,
Will Matthew,
VieiraPotter Victoria,
Scroggins Rebecca,
Peterson Catherine
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.1037.4
Subject(s) - offspring , medicine , endocrinology , adipose tissue , biology , adipocyte , adipogenesis , vitamin d and neurology , resistin , pregnancy , inflammation , vitamin , obesity , insulin resistance , adiponectin , genetics
The bioactive form of vitamin D, 1,25‐dihydroxyvitamin D, and its receptor have been identified for a role in preadipocyte differentiation to adipocytes through the modulation of adipogenic transcript factor genes. We sought to determine if maternal vitamin D status influences adipose tissue development or inflammation in adult offspring. Female C57BL/6J mice were randomized to either a vitamin D deficient diet or a control diet (AIN‐93G) for 21 days prior to mating and maintained on this diet throughout pregnancy until postnatal (PN) day 7, at which point both dietary groups were switched to the control diet. At PN day 75, perigonadal (PGAT) and subcutaneous (SQAT) adipose tissue were collected from adult male offspring for general histology and mRNA expression of adipogenic genes. Serum was also collected. There were no differences between groups in whole body weight, fat pad weights, or adipocyte size or number. Mice born to vitamin D deficient dams had elevated serum concentrations of the pro‐inflammatory markers interleukin‐2 and resistin. Maternal vitamin D status during pregnancy does not appear to influence the development of adipose in lean male offspring maintained on a standard diet; however, increases in circulating resistin, an adipose‐derived protein, suggests an adipocyte response. Grant Funding Source : Supported by: UM Research Investment Fund and SIRC Research Grant