Mice fed with a high fat diet show a decrease in the expression of "toll like receptor (TLR)2 and TLR6 mRNAs in

G Betanzos-Cabrera1, D Estrada-Luna, H Belefant-Miller

  • 1Área Académica de Nutrición, Instituto de Ciencias de Salud, Universidad Autónoma del Estado de Hidalgo, Pachuca, Mexico.

Nutricion Hospitalaria
|November 21, 2012
PubMed
Abstract

Insights

Obesity-induced inflammation in fat tissue involves pattern-recognition receptors (PRRs). High-fat diets decreased Toll-like Receptor (TLR) 2, 6, and 7 expression, suggesting a regulatory role in diet-induced inflammation.

Area of Science:

  • Immunology
  • Metabolic Diseases
  • Cell Biology

Background:

  • Pattern-recognition receptors (PRRs), including Toll-like Receptors (TLRs), are key innate immunity molecules recognizing microbial and tissue ligands.
  • Adipocytes (fat cells) utilize TLRs for immune response regulation, with TLR4 activation by lipids triggering inflammation and altering insulin sensitivity during obesity.

Purpose of the Study:

  • Investigate the role of additional PRR family members in adipose tissue inflammation in obese mice.
  • Determine how high-fat diet (HFD) affects PRR expression in adipose and hepatic tissues.

Main Methods:

  • Quantitative reverse transcription PCR (RT-PCR) was used to analyze mRNA expression.
  • Examined TLRs, NLRP3-inflammasome components (NLRP3, ASC, caspase-1, IL-1β), IL-6, and TNFα.
  • Studied hepatic and adipose tissues from mice fed a HFD.

Main Results:

  • High-fat diet (HFD) consumption led to decreased expression of TLR2, TLR6, and TLR7 in adipose tissue, mirroring hepatic tissue patterns.
  • Interleukin-6 (IL-6) and Tumor Necrosis Factor-alpha (TNFα) expression were also reduced in adipose tissue of HFD mice.
  • NLRP3-inflammasome expression remained unchanged in adipose tissue from HFD mice.

Conclusions:

  • Reduced expression of TLR2 and TLR6 in adipose tissue of HFD mice may play a regulatory role in diet-induced inflammation.
  • These findings highlight specific TLRs' involvement in the inflammatory response to high-fat diets in adipose tissue.

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