title: Voluntary exercise prevents colonic inflammation in high-fat diet-induced obese mice by up-regulating PPAR-γ activity.
abstract: Obesity is associated with increased colonic inflammation, which elevates the risk of colon cancer. Although exercise exerts anti-inflammatory actions in multiple chronic diseases associated with inflammation, it is unknown whether this strategy prevents colonic inflammation in obesity. We hypothesized that voluntary exercise would suppress colonic inflammation in high-fat diet (HFD)-induced obesity by modulation of peroxisome proliferator-activated receptor (PPAR)-γ. Male C57Bl/6J mice fed either a control diet (6.5% fat, CON) or a high-fat diet (24% fat, HFD) were divided into sedentary, voluntary exercise or voluntary exercise with PPAR-γ antagonist GW9662 (10 mg/kg/day). All interventions took place for 12 weeks. Compared with CON-sedentary group, HFD-sedentary mice gained significantly more body weight and exhibited metabolic disorders. Molecular studies revealed that HFD-sedentary mice had increased expression of inflammatory mediators and activation of nuclear factor (NF)-κB in the colons, which were associated with decreased expression and activity of PPAR-γ. Voluntary exercise markedly attenuated body weight gain, improved metabolic disorders, and normalized the expression of inflammatory mediators and activation of NF-κB in the colons in HFD-mice while having no effects in CON-animals. Moreover, voluntary exercise significantly increased expression and activity of PPAR-γ in the colons in both HFD- and CON-animals. However, all of these beneficial effects induced by voluntary exercise were abolished by GW9662, which inhibited expression and activity of PPAR-γ. The results suggest that decreased PPAR-γ activity in the colon of HFD-induced obesity may facilitate the inflammatory response and colon carcinogenesis. Voluntary exercise prevents colonic inflammation in HFD-induced obesity by up-regulating PPAR-γ activity.
authors.affiliation: Department of Gastroenterology, First Affiliated Hospital of China Medical University, Shenyang 110001, Liaoning, China. Electronic address: weixinliu@yahoo.com.
authors.forename: Wei-Xin
authors.initials: WX
authors.lastname: Liu
authors.affiliation: Department of Gastroenterology, First Affiliated Hospital of China Medical University, Shenyang 110001, Liaoning, China.
authors.forename: Ting
authors.initials: T
authors.lastname: Wang
authors.affiliation: Department of Gastroenterology, First Affiliated Hospital of China Medical University, Shenyang 110001, Liaoning, China.
authors.forename: Feng
authors.initials: F
authors.lastname: Zhou
authors.affiliation: Department of Gastroenterology, First Affiliated Hospital of China Medical University, Shenyang 110001, Liaoning, China.
authors.forename: Ying
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Department of Gastroenterology, First Affiliated Hospital of China Medical University, Shenyang 110001, Liaoning, China.
authors.forename: Jun-Wei
authors.initials: JW
authors.lastname: Xing
authors.affiliation: Department of Gastroenterology, First Affiliated Hospital of China Medical University, Shenyang 110001, Liaoning, China.
authors.forename: Shen
authors.initials: S
authors.lastname: Zhang
authors.affiliation: Department of Anatomy, Seirei Christopher College, Hamamatsu 433-8558, Japan.
authors.forename: Shou-Zhi
authors.initials: SZ
authors.lastname: Gu
authors.affiliation: Department of Cadre Ward II, First Affiliated Hospital of China Medical University, Shenyang 110001, Liaoning, China.
authors.forename: Li-Xuan
authors.initials: LX
authors.lastname: Sang
authors.affiliation: Department of Gastroenterology, First Affiliated Hospital of China Medical University, Shenyang 110001, Liaoning, China.
authors.forename: Cong
authors.initials: C
authors.lastname: Dai
authors.affiliation: Guangdong Province Hospital for Occupational Disease Prevention and Treatment, Guangzhou 510300, Guangdong, China.
authors.forename: Hai-Lan
authors.initials: HL
authors.lastname: Wang
mesh_terms: D052242:Adiponectin / Q000097:blood; D000813:Anilides / Q000494:pharmacology; D000818:Animals; D001835:Body Weight; D003092:Colitis / Q000209:etiology / Q000378:metabolism* / Q000517:prevention & control*; D003106:Colon / Q000187:drug effects / Q000378:metabolism; D059305:Diet, High-Fat / Q000009:adverse effects; D004435:Eating; D005951:Glucose Tolerance Test; D018836:Inflammation Mediators / Q000378:metabolism; D007328:Insulin / Q000097:blood; D020738:Leptin / Q000097:blood; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D016328:NF-kappa B / Q000378:metabolism; D009765:Obesity / Q000150:complications / Q000378:metabolism / Q000473:pathology; D047495:PPAR gamma / Q000037:antagonists & inhibitors / Q000378:metabolism*; D005082:Physical Exertion; D015854:Up-Regulation
chemical_list: C457499:2-chloro-5-nitrobenzanilide; D052242:Adiponectin; C499919:Adipoq protein, mouse; D000813:Anilides; D018836:Inflammation Mediators; D007328:Insulin; D020738:Leptin; D016328:NF-kappa B; D047495:PPAR gamma
keywords: Colon; Inflammation; Obesity; PPAR-γ activity; Voluntary exercise