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논문 기본 정보

자료유형
학술저널
저자정보
Kouichi Miura (Akita University Graduate School of Medicine) Mitsuaki Ishioka (Akita University Graduate School of Medicine) Katsunori Iijima (Akita University Graduate School of Medicine)
저널정보
대한비만학회 Journal of Obesity & Metabolic Syndrome Journal of Obesity & Metabolic Syndrome Vol.26 No.2
발행연도
2017.1
수록면
86 - 96 (11page)

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Obesity is characterized by low-grade chronic inflammation and is closely associated with the cardiovascular diseases, diabetes, and nonalcoholic fatty liver disease. Emerging data demonstrate that the gut microbiota contributes to the development of obesity by regulating the innate immune system, including the Toll-like receptors (TLRs): an altered gut microbiota composition and elevated TLR ligands are observed in obese mice and humans. The changes in the gut microbiota include an increased abundance of Firmicutes phylum and a decreased abundance of Bacteroidetes phylum. The population of beneficial bacteria that function as probiotics is decreased whereas harmful bacteria that can produce lipopolysaccharide, a TLR4 ligand, are increased in the obese state. In addition, the gut permeability is increased in obesity, which allows the delivery of larger amounts of bacterial components to the liver through the portal vein. Immune cells recognize these bacterial components through TLRs and produce diverse cytokines that kill invading pathogens. However, the sustained activation of TLR signaling induces host damage due to chronic exposure to harmful cytokines, which are produced from TLR expressing cells, including monocytes/macrophages. In the obese state, the expression of TLR is increased in several organs, including the adipose tissue and the liver. At the cell level, negative regulators of TLR signaling are suppressed, leading to activation of TLR signaling. These alterations promote inflammation in many organs. Thus, the gut microbiota and TLR signaling are therapeutic targets in patients with obesity and its related diseases.

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