Exhaustive exercise increases inflammatory response via Toll like receptor-4 and NF-κBp65 pathway in rat adipose tissue

J Cell Physiol. 2011 Jun;226(6):1604-7. doi: 10.1002/jcp.22490.

Abstract

Cytokines (IL-6, IL-10, and TNF-α) are increased after exhaustive exercise in the retroperitoneal adipose tissue (RPAT) and mesenteric adipose tissue (MEAT). An exhaustive acute exercise protocol induces inflammation in adipose tissue that lasts 6 h after the exercise has ended. It is well-established that this protocol increases circulating plasma levels of non-esterified fatty acids (NEFAs) and lipopolysaccharides (LPS), compounds that are important in stimulating signaling via toll like receptor-4 (TLR-4) in different type cells. In the present study, we investigated the regulation of TLR-4 and DNA-binding of nuclear factor-κBp65 (NF-κBp65) in different depots of adipose tissue in rats after exhaustive exercise. Rats were killed by decapitation immediately (E0 group, n=6), 2 (E2 group, n=6), and 6 h (E6 group, n=6) after the exhaustive exercise, which consisted of running on a treadmill (approximately 70% V(O2max) ) for 50 min and then running at an elevated rate that increased at 1 m/min, until exhaustion. The control group (C group, n=6) was not subjected to exercise. In RPAT, TLR-4, MYD-88, and IkBα increased in the E2 group after exercise. MYD-88 and TRAF6 remained increased in the E6 group in comparison with the control group. DNA-binding of NF-κBp65 was not altered. In MEAT, TLR-4, MYD-88, TRAF6, and DNA-binding of NF-κBp65 were increased only in the E6 group. In conclusion, we have shown that increases in pro-inflammatory cytokines in adipose tissue pads after exhaustive exercise may be mediated via TLR-4 signaling, leading to increases in NF-κBp65 binding to DNA in MEAT.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adipose Tissue / metabolism*
  • Adipose Tissue / pathology
  • Animals
  • DNA / metabolism
  • I-kappa B Proteins / metabolism
  • Inflammation / metabolism*
  • Inflammation / pathology*
  • Intra-Abdominal Fat / metabolism
  • Intra-Abdominal Fat / pathology
  • Male
  • Myeloid Differentiation Factor 88 / metabolism
  • NF-KappaB Inhibitor alpha
  • Physical Conditioning, Animal*
  • Protein Binding
  • Rats
  • Rats, Wistar
  • Signal Transduction*
  • TNF Receptor-Associated Factor 6 / metabolism
  • Toll-Like Receptor 4 / metabolism*
  • Transcription Factor RelA / metabolism*

Substances

  • I-kappa B Proteins
  • Myeloid Differentiation Factor 88
  • Nfkbia protein, rat
  • TNF Receptor-Associated Factor 6
  • Tlr4 protein, rat
  • Toll-Like Receptor 4
  • Transcription Factor RelA
  • NF-KappaB Inhibitor alpha
  • DNA