PMID- 10447208
OWN - NLM
STAT- MEDLINE
DCOM- 19990827
LR  - 20190701
IS  - 0024-3205 (Print)
IS  - 0024-3205 (Linking)
VI  - 65
IP  - 3
DP  - 1999
TI  - Running exercise increases tumor necrosis factor-alpha secreting from mesenteric 
      fat in insulin-resistant rats.
PG  - 237-44
AB  - 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.
FAU - Nara, M
AU  - Nara M
AD  - Department of Laboratory Medicine, Gunma University School of Medicine, Maebashi, 
      Japan.
FAU - Kanda, T
AU  - Kanda T
FAU - Tsukui, S
AU  - Tsukui S
FAU - Inukai, T
AU  - Inukai T
FAU - Shimomura, Y
AU  - Shimomura Y
FAU - Inoue, S
AU  - Inoue S
FAU - Kobayashi, I
AU  - Kobayashi I
LA  - eng
PT  - Journal Article
PL  - Netherlands
TA  - Life Sci
JT  - Life sciences
JID - 0375521
RN  - 0 (Blood Glucose)
RN  - 0 (Dietary Sucrose)
RN  - 0 (RNA, Messenger)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - IY9XDZ35W2 (Glucose)
SB  - IM
MH  - Adipose Tissue/*metabolism
MH  - Animals
MH  - Blood Glucose/metabolism
MH  - Body Weight
MH  - Dietary Sucrose/metabolism
MH  - Energy Intake
MH  - Glucose/metabolism
MH  - *Insulin Resistance
MH  - Male
MH  - Mesentery/metabolism
MH  - Mice
MH  - Physical Exertion/*physiology
MH  - RNA, Messenger/metabolism
MH  - Rats
MH  - Rats, Wistar
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Tumor Necrosis Factor-alpha/*metabolism
EDAT- 1999/08/14 00:00
MHDA- 1999/08/14 00:01
CRDT- 1999/08/14 00:00
PHST- 1999/08/14 00:00 [pubmed]
PHST- 1999/08/14 00:01 [medline]
PHST- 1999/08/14 00:00 [entrez]
AID - S0024320599002428 [pii]
AID - 10.1016/s0024-3205(99)00242-8 [doi]
PST - ppublish
SO  - Life Sci. 1999;65(3):237-44. doi: 10.1016/s0024-3205(99)00242-8.