title: Differential effect of weight loss with low-fat diet or high-fat diet restriction on inflammation in the liver and adipose tissue of mice with diet-induced obesity.
abstract: OBJECTIVE
  We studied the effects of weight loss induced by either a low-fat normal diet (ND) or restriction of high-fat diet (HFD) on hepatic steatosis, inflammation in the liver and adipose tissue (AT), and blood monocytes of obese mice.
  
  
  METHODS
  In mice with HFD-induced obesity, weight loss was achieved by switching from HFD to ND and maintaining on ND ad libitum or by restricting HFD intake to match body weight of mice with ND-induced weight loss. After diet interventions for 4 weeks, hepatic steatosis, hepatic and AT inflammation, and blood CD11c(+) monocytes were examined.
  
  
  RESULTS
  At 4 weeks after switching diets, body weight was reduced by 23% from baseline. To achieve the same reduced body weight required restricting calorie intake from HFD. Weight loss with either ND or HFD restriction decreased body fat mass and ameliorated liver steatosis; both effects were greater with ND-induced weight loss than HFD restriction-induced weight loss. Weight loss with ND but not HFD restriction normalized blood CD11c(+) monocytes and attenuated hepatic inflammation assessed by chemokine and CD11c expression. In contrast, weight loss with HFD restriction significantly reduced chemokine levels and CD11c(+) cells in AT compared to obese controls, and tended to reduce AT chemokines and CD11c(+) cells more than ND-induced weight loss.
  
  
  CONCLUSIONS
  In mice with diet-induced obesity, weight loss with ND was superior in alleviating hepatic inflammation and steatosis, whereas weight loss with HFD calorie restriction provided greater amelioration of AT inflammation.
authors.affiliation: Division of Atherosclerosis and Vascular Medicine, Section of Cardiovascular Research, Department of Medicine, Baylor College of Medicine, 6565 Fannin, M.S. A-601, Houston, TX 77030, USA. wangqun@sdu.edu.cn
authors.forename: Qun
authors.initials: Q
authors.lastname: Wang
authors.forename: Xiaoyuan Dai
authors.initials: XD
authors.lastname: Perrard
authors.forename: Jerry L
authors.initials: JL
authors.lastname: Perrard
authors.forename: Amir
authors.initials: A
authors.lastname: Mansoori
authors.forename: Joe L
authors.initials: JL
authors.lastname: Raya
authors.forename: Ron
authors.initials: R
authors.lastname: Hoogeveen
authors.forename: C Wayne
authors.initials: CW
authors.lastname: Smith
authors.forename: Christie M
authors.initials: CM
authors.lastname: Ballantyne
authors.forename: Huaizhu
authors.initials: H
authors.lastname: Wu
mesh_terms: D000273:Adipose Tissue / Q000187:drug effects / Q000473:pathology*; D000818:Animals; D039521:CD11c Antigen / Q000096:biosynthesis; D031204:Caloric Restriction; D018932:Chemokine CCL2 / Q000097:blood; D018752:Diet, Fat-Restricted; D059305:Diet, High-Fat; D005234:Fatty Liver / Q000209:etiology / Q000628:therapy; D007249:Inflammation / Q000209:etiology / Q000628:therapy; D008099:Liver / Q000187:drug effects / Q000473:pathology*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D009000:Monocytes / Q000502:physiology; D009765:Obesity / Q000378:metabolism*; D015431:Weight Loss / Q000502:physiology*
chemical_list: D039521:CD11c Antigen; C491768:Ccl2 protein, mouse; D018932:Chemokine CCL2