High Fat Diet-Induced Gut Microbiota Exacerbates Inflammation and Obesity in Mice via the TLR4 Signaling Pathway

We investigated the effect of endotoxin-induced inflammation via Toll-like receptor 4 signaling pathway at both systemic and intestinal levels in response to a high-fat diet

Kyung-Ah Kim; Wan Gu; In-Ah Lee; Eun-Ha Joh; Dong-Hyun Kim


Scholarcy highlights

  • Metabolic syndrome, a group of inter-related metabolic abnormalities that include hyperglycemia, insulin resistance, dyslipidemia, hypertension, and obesity, is exacerbated by environmental factors, such as a fat-enriched diet, a sedentary life style, and perhaps by aging
  • After 8 weeks on a LFD or high-fat diet, body weight and epididymal fat pad weight were increased in HFD mice as compared with LFD mice
  • Plasma levels of proinflammatory cytokines, such as TNFa, IL-1b, and IL-6 were higher in HFD mice than the LFD mice
  • When we measured the mRNA expression levels of F4/80 and CD68, specific markers of macrophages, and TNFa, IL-1b, and IL-6, in isolated epididymal fat, all mRNA levels were increased in HFD mice as compared with LFD mice
  • HFD-induced intestinal and systemic inflammation manifested by increases in TNFa, IL-1b, and IL-6 expression was attenuated in Toll-like receptor 4-deficient mice
  • Fresh mouse stools were cultured in HFD-contained or in LFD-contained general anaerobic media, which contain 0.5% glucose, or glucose-excluded GAM for 24 h and inoculated in BL and DHL agar plates
  • Since LPS from gramnegative bacteria triggered low-grade inflammation, it is conceivable that the changes in the gut microbiota by HFD may play a pivotal role in the induction of LPS-induced inflammatory status in the intestine and may contribute to the phenotype observed in HFD mice
  • high-fat diet induces inflammation by increasing endotoxin levels in the intestinal lumen as well as in the plasma by altering the gut microbiota composition and increasing its intestinal permeability through the induction of Toll-like receptor 4, thereby accelerating obesity

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