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Review
. 2024 Apr 13;25(8):4305.
doi: 10.3390/ijms25084305.

The Effect of Enteric-Derived Lipopolysaccharides on Obesity

Kai Wang  1   2 , Weiwen Lai  1   2 , Tianqi Min  1   2 , Jintao Wei  1   2 , Yan Bai  3 , Hua Cao  4 , Jiao Guo  2 , Zhengquan Su  1   2
Affiliations
Review

The Effect of Enteric-Derived Lipopolysaccharides on Obesity

Kai Wang et al. Int J Mol Sci. .

Abstract

Endotoxin is a general term for toxic substances in Gram-negative bacteria, whose damaging effects are mainly derived from the lipopolysaccharides (LPS) in the cell walls of Gram-negative bacteria, and is a strong pyrogen. Obesity is a chronic, low-grade inflammatory condition, and LPS are thought to trigger and exacerbate it. The gut flora is the largest source of LPS in the body, and it is increasingly believed that altered intestinal microorganisms can play an essential role in the pathology of different diseases. Today, the complex axis linking gut flora to inflammatory states and adiposity has not been well elucidated. This review summarises the evidence for an interconnection between LPS, obesity, and gut flora, further expanding our understanding of LPS as a mediator of low-grade inflammatory disease and contributing to lessening the effects of obesity and related metabolic disorders. As well as providing targets associated with LPS, obesity, and gut flora, it is hoped that interventions that combine targets with gut flora address the individual differences in gut flora treatment.

Keywords: endotoxin; intestinal flora; lipopolysaccharide; obesity; targeted therapy.

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Conflict of interest statement

The authors declare no conflicts of interest.

Figures

Figure 1
Figure 1
LPS structure. GlcN: glucosamine. P: phosphate group. Kdo: 3-deoxy-D-manno-octulosonic acid. Hep: glycero mannoheptose. Glc: glucose. Gal: galactose. Hex: hexose.
Figure 2
Figure 2
LPS inflammatory mechanisms. LPS: (lipopolysaccharide); LBP: (lipopolysaccharide binding protein); CD14: (cluster of differentiation 14); TLR4: (toll-like receptor 4); MyD88: (myeloid differentiation factor 88); IRAK: (IL-1 receptor-associated kinase); TRIF: (toll/interleukin-1 receptor); TRAM: (tRIF-related adaptor molecule); TLR: (toll-like receptor); TRAF: (tumour necrosis factor receptor-associated factor); IKK: (IκB kinase); TAK1: (transforming growth factor-β-activating kinase); ECSIT: (evolutionarily conserved signalling intermediate in toll pathway); IRF: (IFN regulatory factor); TAB: (TAK1 binding protein); IκB: (inhibitor of NF-κB); P50 and P65: (NF-κB family member factor); TBK1: (TANK-binding kinase); MAPK: (mitogen-activated protein kinase); p38: (p38 mitogen-activated protein kinase); JNK: (c-Jun amino-terminal kinase); AP-1: (transcription activator protein 1); NF-kB: (nuclear factor kappa-B); IL: (interleukin); TNF-α: (tumour necrosis factor-alpha).
Figure 3
Figure 3
The relationship between LPS, obesity, and intestinal flora. ECS: endocannabinoid system; GLP: glucagon-like peptide; Apelin–APJ: Apelin is a regulatory peptide and a ligand of the G protein-coupled receptor (APJ); GPR120: G protein-coupled receptor 120.
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