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Female mice lacking active NADPH‐oxidase enzymes are protected against “Western Diet”‐‐induced obesity and metabolic syndrome
Author(s) -
Ronis Martin J,
Sharma Neha,
Badeuax Jamie,
Ferguson Mat,
Badger Thomas M
Publication year - 2012
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.26.1_supplement.252.1
Subject(s) - medicine , endocrinology , nadph oxidase , metabolic syndrome , adipocyte , biology , enzyme , obesity , oxidase test , triglyceride , cholesterol , adipose tissue , biochemistry , oxidative stress
NADPH oxidase (Nox) enzymes, have been implicated in regulation of adipocyte differentiation and inflammation in a variety of tissues. We examined the effects of feeding AIN‐93G or a “Western diet” (WD) (45% fat, 0.5% cholesterol) on development of obesity and “metabolic syndrome” in wild type (WT) mice or p47phox −/− mice in which Nox enzymes 1–3 are inactive. Diets were fed between ages 4 and 12 wk. In both male and female WT mice, weight gain, fat pad weight and % adiposity were greater in WD‐fed mice compared to AIN‐93G (P< 0.05). In p47phox −/− mice, while the males behaved similarly to WT, the females were completely protected against the development of obesity and mean adipocyte size was lower than in WT females fed either diet (P<0.05). WD feeding resulted in hyperglycemia and hepatic triglyceride accumulation in WT, but not knockout mice of either sex (P< 0.05). p47phox −/− had reduced hepatic SREBP‐1c and downstream targets: fatty acid synthase and acyl CoA carboxylase mRNAs (P<0.05). These data suggest that signaling through reactive oxygen species derived from Nox enzymes plays an important role in development of obesity and metabolic syndrome particularly in females. USDA, CRIS 6251‐51000‐007‐03S.