title: Steroidogenic Acute Regulatory Protein (StAR) Overexpression Reduces Inflammation and Insulin Resistance in Obese Mice.
abstract: Steroidogenic acute regulatory protein (StAR), a mitochondrial cholesterol delivery protein, plays a beneficial role in hyperlipidemia, NAFLD, and endothelial inflammation. Elevated circulating fatty acids and low grade inflammation are known as key risk factors of insulin resistance and type 2 diabetes. In the present study, C57BL/6J mice were fed with HFD and infected with recombinant adenovirus expressing StAR by tail-vein injection. Intraperitoneal glucose/insulin tolerance test was performed to assess the insulin sensitivity. Morphological analysis and intramuscular lipid determination were used to illustrate the adipose hypertrophy and ectopic fat accumulation in skeletal muscle. The levels of inflammatory factor and nitric oxide were determined by ELISA and classic Griess reagent methods, respectively. The fatty acids composition was analysis using gas chromatography-mass spectrometry (GC-MS). The expression of genes associated with inflammation and insulin resistance were determined by Western blotting and qPCR to elucidate the underlying mechanism. We demonstrated that StAR overexpression ameliorated insulin resistance and systemic inflammatory response with the reduction of adipose hypertrophy and intramuscular lipid in HFD-fed mice. In addition, StAR overexpression increased serum unsaturated fatty acids (UFAs) and PPARγ expression in muscle and adipose tissue of obese mice. In conclusion, StAR may activate PPARγ by increasing UFAs, which leads to a protective role in systemic inflammation and insulin resistance in obese mice. J. Cell. Biochem. 118: 3932-3942, 2017. © 2017 Wiley Periodicals, Inc.
authors.affiliation: Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai, China.
authors.forename: Yanyan
authors.initials: Y
authors.lastname: Qiu
authors.affiliation: Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai, China.
authors.forename: Xianxian
authors.initials: X
authors.lastname: Sui
authors.affiliation: Laboratory of Medical Molecular Biology, Experimental Teaching Center, School of Basic Medical Sciences, Fudan University, Shanghai, China.
authors.forename: Shengxuan
authors.initials: S
authors.lastname: Cao
authors.affiliation: Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai, China.
authors.forename: Xiaobo
authors.initials: X
authors.lastname: Li
authors.affiliation: Department of Internal Medicine, School of Medicine, Virginia Commonwealth University, Richmond, Virginia.
authors.forename: Yanxia
authors.initials: Y
authors.lastname: Ning
authors.affiliation: Laboratory of Medical Molecular Biology, Experimental Teaching Center, School of Basic Medical Sciences, Fudan University, Shanghai, China.
authors.forename: Songmei
authors.initials: S
authors.lastname: Wang
authors.affiliation: Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Fudan University, Shanghai, China.|Laboratory of Medical Molecular Biology, Experimental Teaching Center, School of Basic Medical Sciences, Fudan University, Shanghai, China.
authors.forename: Lianhua
authors.initials: L
authors.lastname: Yin
authors.affiliation: Laboratory of Medical Molecular Biology, Experimental Teaching Center, School of Basic Medical Sciences, Fudan University, Shanghai, China.
authors.forename: Xiuling
authors.identifier: 0000-0002-8248-4090
authors.initials: X
authors.lastname: Zhi
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism / Q000473:pathology; D000818:Animals; D004041:Dietary Fats / Q000009:adverse effects* / Q000494:pharmacology; D005231:Fatty Acids, Unsaturated / Q000097:blood; D007249:Inflammation; D007333:Insulin Resistance; D008297:Male; D051379:Mice; D018482:Muscle, Skeletal / Q000378:metabolism / Q000473:pathology; D017942:Nitric Acid / Q000097:blood; D009765:Obesity / Q000139:chemically induced / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D047495:PPAR gamma / Q000235:genetics / Q000378:metabolism; D010750:Phosphoproteins / Q000096:biosynthesis* / Q000235:genetics; D000098682:Steroidogenic Acute Regulatory Protein
chemical_list: D004041:Dietary Fats; D005231:Fatty Acids, Unsaturated; D047495:PPAR gamma; D010750:Phosphoproteins; D000098682:Steroidogenic Acute Regulatory Protein; D017942:Nitric Acid
keywords: FATTY ACID; INFLAMMATION; INSULIN RESISTANCE; PPARγ; STEROIDOGENIC ACUTE REGULATORY PROTEIN