title: Effects of exercise and low-fat diet on adipose tissue inflammation and metabolic complications in obese mice.
abstract: Adipose tissue inflammation causes metabolic disturbances, including insulin resistance and hepatic steatosis. Exercise training (EX) may decrease adipose tissue inflammation, thereby ameliorating such disturbances, even in the absence of fat loss. The purpose of this study was to 1) compare the effects of low-fat diet (LFD), EX, and their combination on inflammation, insulin resistance, and hepatic steatosis in high-fat diet-induced obese mice and 2) determine the effect of intervention duration (i.e., 6 vs. 12 wk). C57BL/6 mice (n = 109) fed a 45% fat diet (HFD) for 6 wk were randomly assigned to an EX (treadmill: 5 days/wk, 6 or 12 wk, 40 min/day, 65-70% Vo(2max)) or sedentary (SED) group. Mice remained on HFD or were placed on a 10% fat diet (LFD) for 6 or 12 wk. Following interventions, fat pads were weighed and expressed relative to body weight; hepatic steatosis was assessed by total liver triglyceride and insulin resistance by HOMA-IR and glucose AUC. RT-PCR was used to determine adipose gene expression of MCP-1, F4/80, TNF-alpha, and leptin. By 12 wk, MCP-1, F4/80, and TNF-alpha mRNA were reduced by EX and LFD. Exercise (P = 0.02), adiposity (P = 0.03), and adipose F4/80 (P = 0.02) predicted reductions in HOMA-IR (r(2) = 0.75, P < 0.001); only adiposity (P = 0.04) predicted improvements in hepatic steatosis (r(2) = 0.51, P < 0.001). Compared with LFD, EX attenuated increases in adiposity, hepatic steatosis, and adipose MCP-1 expression from 6 to 12 wk. There are unique metabolic consequences of a sedentary lifestyle and HFD that are most evident long term, highlighting the importance of both EX and LFD in preventing obesity-related metabolic disturbances.
authors.affiliation: University of Illinois at Urbana-Champaign, Urbana, IL 61801, USA.
authors.forename: Victoria J
authors.initials: VJ
authors.lastname: Vieira
authors.forename: Rudy J
authors.initials: RJ
authors.lastname: Valentine
authors.forename: Kenneth R
authors.initials: KR
authors.lastname: Wilund
authors.forename: Nirav
authors.initials: N
authors.lastname: Antao
authors.forename: Tracy
authors.initials: T
authors.lastname: Baynard
authors.forename: Jeffrey A
authors.initials: JA
authors.lastname: Woods
mesh_terms: D054392:Adipokines / Q000096:biosynthesis / Q000235:genetics; D052242:Adiponectin / Q000378:metabolism; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001835:Body Weight / Q000502:physiology; D004041:Dietary Fats / Q000008:administration & dosage* / Q000378:metabolism; D005234:Fatty Liver / Q000378:metabolism* / Q000473:pathology; D007249:Inflammation / Q000378:metabolism / Q000473:pathology; D007333:Insulin Resistance; D050152:Intra-Abdominal Fat / Q000378:metabolism* / Q000473:pathology; D051379:Mice; D008810:Mice, Inbred C57BL; D009765:Obesity / Q000378:metabolism* / Q000473:pathology / Q000628:therapy; D010805:Physical Conditioning, Animal / Q000502:physiology*; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D011897:Random Allocation; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014280:Triglycerides / Q000378:metabolism
chemical_list: D054392:Adipokines; D052242:Adiponectin; D001786:Blood Glucose; D004041:Dietary Fats; D012333:RNA, Messenger; D014280:Triglycerides