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Adipocyte‐specific deletion of HuR reduces diet‐induced obesity
Author(s) -
Anthony Sarah R,
Slone Samuel,
Hui David Y,
Owens Albert Phillip,
Tranter Michael
Publication year - 2017
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.31.1_supplement.1014.26
Subject(s) - adipocyte , obesity , type 2 diabetes , medicine , endocrinology , disease , lean body mass , knockout mouse , diabetes mellitus , adipose tissue , biology , body weight , receptor
Obesity is classified by the World Health Organization as one of eight principle causes of preventable chronic disease, and is directly associated with decreased life expectancy due to increased risk of type II diabetes, chronic respiratory disease, stroke, peripheral vascular disease, cancer, and cardiovascular disease. As a serious threat to human health, research into novel pharmaceutical targets and therapies to combat obesity is of growing interest to the scientific community. Although the RNA‐binding protein HuR (Human antigen R) is highly expressed in adipocytes, its role in adipocyte function and adipocity is largely unknown. To conclusively determine the mechanistic role of HuR in adipocyte function, our laboratory has developed an adipocyte‐specific HuR knockout mouse (Adipo‐HuR −⁄− ). These mice weigh less than wild‐type mice at baseline and have a reduced lean/fat body mass ratio. In addition, when placed on a chronic (22‐week) high fat diet (HFD, 60% kcal/fat), Adipo‐HuR −⁄− mice gain less weight compared to their wild‐type counterparts and display a decreased cold tolerance. Ongoing efforts to identify an underlying mechanism of action have shown no difference between wild‐type and Adipo‐HuR −⁄− mice following chronic HFD with regard to glucose tolerance or ratio of lean/fat body mass, but our data indicates a loss of UCP1 in the brown fat of Adipo‐HuR −⁄− mice. Support or Funding Information This work was partially funded by a University of Cincinnati Heart, Lung and Vascular Institute Near Horizons Collaborative Grant (MT, APO).