Document Detail

Running exercise increases tumor necrosis factor-alpha secreting from mesenteric fat in insulin-resistant rats.
MedLine Citation:
PMID:  10447208     Owner:  NLM     Status:  MEDLINE    
Tumor necrosis factor-alpha (TNF-alpha) is an important mediator of insulin resistance in obese subjects, through its overexpression in fat tissue. However, how exercise can modify the expression of TNF-alpha is controversial. We examined TNF-alpha in adipose tissue using an animal model of insulin resistance that was produced by feeding rats a diet high in sucrose. The rats were allocated to one of three groups: those receiving a starch-based diet (control group): those fed a high-sucrose diet (sucrose-fed group): and those fed a high-sucrose diet and given wheel exercise (exercised group). The animals were allowed to eat and drink ad lib for 4 or 12 weeks (4 wk: control n=7, sucrose-fed n=7, exercised n=10; 12 wk: control n=5, sucrose-fed n=5, exercised n=9). The voluntary wheel exercise was initiated with the feeding of the high-sucrose diet. The rats in the exercise groups ran 15 +/- 3 km/week. We showed that 12-week voluntary running exercise significantly (P<0.05) increased both TNF-alpha protein (5-fold) and mRNA (1.4 fold) in the mesenteric fat of insulin-resistant rats compared to non-exercised sucrose-fed mice. Accordingly, in exercised group, plasma glucose (124 +/- 9 mEq/L vs 141 +/- 11 mEq/L). and free fatty acid (0.98 +/- 0.07 mEq/L vs 1.4 +/- 0.05 mEq/L) concentrating in portal vein blood were reduced compared to sucrose-fed group. The amounts of fatty tissue both in mesenteric and subcutaneous tissues were significantly (P<0.05) decreased through running exercise. We consider that up-regulation of TNF-alpha in mesenteric fat may be a compensatory mechanism for the reduction of fatty acid in adipose tissues and this change could control metabolic homeostasis during exercise to modulate a hyperinsulinemic state.
M Nara; T Kanda; S Tsukui; T Inukai; Y Shimomura; S Inoue; I Kobayashi
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Life sciences     Volume:  65     ISSN:  0024-3205     ISO Abbreviation:  Life Sci.     Publication Date:  1999  
Date Detail:
Created Date:  1999-08-27     Completed Date:  1999-08-27     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  0375521     Medline TA:  Life Sci     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  237-44     Citation Subset:  IM    
Department of Laboratory Medicine, Gunma University School of Medicine, Maebashi, Japan.
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MeSH Terms
Adipose Tissue / metabolism*
Blood Glucose / metabolism
Body Weight
Dietary Sucrose / metabolism
Energy Intake
Glucose / metabolism
Insulin Resistance*
Mesentery / metabolism
Physical Exertion / physiology*
RNA, Messenger / metabolism
Rats, Wistar
Reverse Transcriptase Polymerase Chain Reaction
Tumor Necrosis Factor-alpha / metabolism*
Reg. No./Substance:
0/Blood Glucose; 0/Dietary Sucrose; 0/RNA, Messenger; 0/Tumor Necrosis Factor-alpha; 50-99-7/Glucose

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