title: Increased oxidative stress and the apoptosis of regulatory T cells in obese mice but not resistant mice in response to a high-fat diet.
abstract: High fat feeding induces a variety of obese and lean phenotypes in inbred rodents. Obesity is a pro-inflammatory state, and regulatory T cells (Tregs) are essential negative regulators of inflammation. We aimed to determine the involvement of Tregs in the mice susceptible or resistant to high-fat diet (HFD). In the study, diet-induced obese (DIO) mice experienced significant increases in weight gain, energy intake, fat masses, plasma lipid and proinflammatory cytokines in comparison with control and diet-resistant (DR) mice. Also, Tregs production decreased in DIO mice. HFD diminished mitochondrial transmembrane potential (MTP) in the spleen Tregs of DIO mice and reinforced apoptosis compared with that in DR mice. Moreover, HFD significantly decreased antioxidant enzymes expressions and increased reactive oxygen species (ROS) productions in the Tregs of DIO mice, but not in those of DR mice, which should provide valuable evidence for unraveling the pathogenesis of inflammation found in this obese mice model.
authors.affiliation: State Key Laboratory of Food Science and Technology, School of Food Science and Technology, Jiangnan University, 1800 Lihu Avenue, Wuxi 214122, Jiangsu, China. Electronic address: yantaibingo@gmail.com.
authors.forename: Bin
authors.initials: B
authors.lastname: Wang
authors.affiliation: State Key Laboratory of Food Science and Technology, School of Food Science and Technology, Jiangnan University, 1800 Lihu Avenue, Wuxi 214122, Jiangsu, China.
authors.forename: Jin
authors.initials: J
authors.lastname: Sun
authors.affiliation: State Key Laboratory of Food Science and Technology, School of Food Science and Technology, Jiangnan University, 1800 Lihu Avenue, Wuxi 214122, Jiangsu, China.
authors.forename: Yuhua
authors.initials: Y
authors.lastname: Ma
authors.affiliation: State Key Laboratory of Food Science and Technology, School of Food Science and Technology, Jiangnan University, 1800 Lihu Avenue, Wuxi 214122, Jiangsu, China.
authors.forename: Guirong
authors.initials: G
authors.lastname: Wu
authors.affiliation: State Key Laboratory of Food Science and Technology, School of Food Science and Technology, Jiangnan University, 1800 Lihu Avenue, Wuxi 214122, Jiangsu, China.
authors.forename: Yonghui
authors.initials: Y
authors.lastname: Shi
authors.affiliation: State Key Laboratory of Food Science and Technology, School of Food Science and Technology, Jiangnan University, 1800 Lihu Avenue, Wuxi 214122, Jiangsu, China. Electronic address: lgw@jiangnan.edu.cn.
authors.forename: Guowei
authors.initials: G
authors.lastname: Le
mesh_terms: D000818:Animals; D017209:Apoptosis; D001835:Body Weight; D053148:Caspase 3 / Q000235:genetics / Q000378:metabolism; D016207:Cytokines / Q000235:genetics / Q000276:immunology; D018752:Diet, Fat-Restricted; D059305:Diet, High-Fat; D015870:Gene Expression; D007249:Inflammation / Q000235:genetics / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D008055:Lipids / Q000097:blood; D008297:Male; D053078:Membrane Potential, Mitochondrial / Q000276:immunology; D051379:Mice; D008810:Mice, Inbred C57BL; D008820:Mice, Obese; D008928:Mitochondria / Q000276:immunology / Q000473:pathology; D009765:Obesity / Q000235:genetics / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D018384:Oxidative Stress / Q000276:immunology*; D017382:Reactive Oxygen Species / Q000378:metabolism; D013154:Spleen / Q000276:immunology / Q000473:pathology; D050378:T-Lymphocytes, Regulatory / Q000276:immunology* / Q000473:pathology; D050998:bcl-2 Homologous Antagonist-Killer Protein / Q000235:genetics / Q000378:metabolism; D051028:bcl-2-Associated X Protein / Q000235:genetics / Q000378:metabolism
chemical_list: D016207:Cytokines; D008055:Lipids; D017382:Reactive Oxygen Species; D050998:bcl-2 Homologous Antagonist-Killer Protein; D051028:bcl-2-Associated X Protein; C505409:Casp3 protein, mouse; D053148:Caspase 3
keywords: Apoptosis; Diet resistance; Diet-induced obesity; High-fat diet; Oxidative stress; Regulatory T cells