Female Mice Lacking p47phox Have Altered Adipose Tissue Gene Expression and are Protected against High Fat-Induced Obesity and Metabolic Syndrome
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ABSTRACT: Oxidative stress in adipose tissue and liver has been linked to the development of obesity. NADPH oxidases (NOX) enzymes are a major source of reactive oxygen species (ROS). The current study was designed to determine if NOX2-generated ROS play a role in development of obesity and metabolic syndrome after high fat feeding. Wild type (WT) mice and mice lacking the cytosolic NOX2 activated protein p47phox (P47KO) were fed AIN-93G diets or high fat diets (HFD) containing 45% fat and 0.5% cholesterol for 13 weeks from weaning. Affymetrix array analysis revealed dramatically less expression of mRNA of genes linked to energy metabolism, adipocyte differentiation (PPARM-NM-3, Runx2) and fatty acid uptake (CD36, lipoprotein lipase) in fat pads from female HFD-P47KO mice compared to HFD-WT females. These data suggest that NOX2 is an important regulator of metabolic homeostasis and that NOX2-associated ROS plays an important role in development of diet-induced obesity particularly in the female fat pads from p47phox and wild type fed a high fat or control diet
ORGANISM(S): Mus musculus
SUBMITTER: Horacio Gomez-Acevedo
PROVIDER: E-GEOD-41932 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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