Gut microbiota-derived lipopolysaccharide uptake and trafficking to adipose tissue: implications for inflammation and obesity

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Gut microbiota-derived lipopolysaccharide uptake and trafficking to adipose tissue : implications for inflammation and obesity. / Hersoug, L-G.; Møller, Peter; Loft, Steffen.

In: Obesity Reviews, Vol. 17, No. 4, 04.2016, p. 297-312.

Research output: Contribution to journalReviewResearchpeer-review

Harvard

Hersoug, L-G, Møller, P & Loft, S 2016, 'Gut microbiota-derived lipopolysaccharide uptake and trafficking to adipose tissue: implications for inflammation and obesity', Obesity Reviews, vol. 17, no. 4, pp. 297-312. https://doi.org/10.1111/obr.12370

APA

Hersoug, L-G., Møller, P., & Loft, S. (2016). Gut microbiota-derived lipopolysaccharide uptake and trafficking to adipose tissue: implications for inflammation and obesity. Obesity Reviews, 17(4), 297-312. https://doi.org/10.1111/obr.12370

Vancouver

Hersoug L-G, Møller P, Loft S. Gut microbiota-derived lipopolysaccharide uptake and trafficking to adipose tissue: implications for inflammation and obesity. Obesity Reviews. 2016 Apr;17(4):297-312. https://doi.org/10.1111/obr.12370

Author

Hersoug, L-G. ; Møller, Peter ; Loft, Steffen. / Gut microbiota-derived lipopolysaccharide uptake and trafficking to adipose tissue : implications for inflammation and obesity. In: Obesity Reviews. 2016 ; Vol. 17, No. 4. pp. 297-312.

Bibtex

@article{28cbe8b70b28472e89ebc9b8533ab125,
title = "Gut microbiota-derived lipopolysaccharide uptake and trafficking to adipose tissue: implications for inflammation and obesity",
abstract = "The composition of the gut microbiota and excessive ingestion of high-fat diets (HFD) are considered to be important factors for development of obesity. In this review we describe a coherent mechanism of action for the development of obesity, which involves the composition of gut microbiota, HFD, low-grade inflammation, expression of fat translocase and scavenger receptor CD36, and the scavenger receptor class B type 1 (SR-BI). SR-BI binds to both lipids and lipopolysaccharide (LPS) from Gram-negative bacteria, which may promote incorporation of LPS in chylomicrons (CMs). These CMs are transported via lymph to the circulation, where LPS is transferred to other lipoproteins by translocases, preferentially to HDL. LPS increases the SR-BI binding, transcytosis of lipoproteins over the endothelial barrier,and endocytosis in adipocytes. Especially large size adipocytes with high metabolic activity absorb LPS-rich lipoproteins. In addition, macrophages in adipose tissue internalize LPS-lipoproteins. This may contribute to the polarization from M2 to M1 phenotype, which is a consequence of increased LPS delivery into the tissue during hypertrophy. In conclusion, evidence suggests that LPS is involved in the development of obesity as a direct targeting molecule for lipid delivery and storage in adipose tissue.",
author = "L-G. Hersoug and Peter M{\o}ller and Steffen Loft",
note = "{\circledC} 2015 World Obesity.",
year = "2016",
month = "4",
doi = "10.1111/obr.12370",
language = "English",
volume = "17",
pages = "297--312",
journal = "Obesity Reviews",
issn = "1467-7881",
publisher = "Wiley-Blackwell",
number = "4",

}

RIS

TY - JOUR

T1 - Gut microbiota-derived lipopolysaccharide uptake and trafficking to adipose tissue

T2 - implications for inflammation and obesity

AU - Hersoug, L-G.

AU - Møller, Peter

AU - Loft, Steffen

N1 - © 2015 World Obesity.

PY - 2016/4

Y1 - 2016/4

N2 - The composition of the gut microbiota and excessive ingestion of high-fat diets (HFD) are considered to be important factors for development of obesity. In this review we describe a coherent mechanism of action for the development of obesity, which involves the composition of gut microbiota, HFD, low-grade inflammation, expression of fat translocase and scavenger receptor CD36, and the scavenger receptor class B type 1 (SR-BI). SR-BI binds to both lipids and lipopolysaccharide (LPS) from Gram-negative bacteria, which may promote incorporation of LPS in chylomicrons (CMs). These CMs are transported via lymph to the circulation, where LPS is transferred to other lipoproteins by translocases, preferentially to HDL. LPS increases the SR-BI binding, transcytosis of lipoproteins over the endothelial barrier,and endocytosis in adipocytes. Especially large size adipocytes with high metabolic activity absorb LPS-rich lipoproteins. In addition, macrophages in adipose tissue internalize LPS-lipoproteins. This may contribute to the polarization from M2 to M1 phenotype, which is a consequence of increased LPS delivery into the tissue during hypertrophy. In conclusion, evidence suggests that LPS is involved in the development of obesity as a direct targeting molecule for lipid delivery and storage in adipose tissue.

AB - The composition of the gut microbiota and excessive ingestion of high-fat diets (HFD) are considered to be important factors for development of obesity. In this review we describe a coherent mechanism of action for the development of obesity, which involves the composition of gut microbiota, HFD, low-grade inflammation, expression of fat translocase and scavenger receptor CD36, and the scavenger receptor class B type 1 (SR-BI). SR-BI binds to both lipids and lipopolysaccharide (LPS) from Gram-negative bacteria, which may promote incorporation of LPS in chylomicrons (CMs). These CMs are transported via lymph to the circulation, where LPS is transferred to other lipoproteins by translocases, preferentially to HDL. LPS increases the SR-BI binding, transcytosis of lipoproteins over the endothelial barrier,and endocytosis in adipocytes. Especially large size adipocytes with high metabolic activity absorb LPS-rich lipoproteins. In addition, macrophages in adipose tissue internalize LPS-lipoproteins. This may contribute to the polarization from M2 to M1 phenotype, which is a consequence of increased LPS delivery into the tissue during hypertrophy. In conclusion, evidence suggests that LPS is involved in the development of obesity as a direct targeting molecule for lipid delivery and storage in adipose tissue.

U2 - 10.1111/obr.12370

DO - 10.1111/obr.12370

M3 - Review

VL - 17

SP - 297

EP - 312

JO - Obesity Reviews

JF - Obesity Reviews

SN - 1467-7881

IS - 4

ER -

ID: 161083151