Diet induced obesity is independent of metabolic endotoxemia and TLR4 signalling, but markedly increases hypothalamic expression of the acute phase protein, SerpinA3N
Hypothalamic inflammation is thought to contribute to obesity. One potential mechanism is via gut microbiota derived bacterial lipopolysaccharide (LPS) entering into the circulation and activation of Toll-like receptor-4. This is called metabolic endotoxemia. Another potential mechanism is systemic...
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Published in | Scientific reports Vol. 8; no. 1; pp. 15648 - 15 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
London
Nature Publishing Group UK
23.10.2018
Nature Publishing Group |
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Abstract | Hypothalamic inflammation is thought to contribute to obesity. One potential mechanism is via gut microbiota derived bacterial lipopolysaccharide (LPS) entering into the circulation and activation of Toll-like receptor-4. This is called metabolic endotoxemia. Another potential mechanism is systemic inflammation arising from sustained exposure to high-fat diet (HFD) over more than 12 weeks. In this study we show that mice fed HFD over 8 weeks become obese and show elevated plasma LPS binding protein, yet body weight gain and adiposity is not attenuated in mice lacking
Tlr4
or its co-receptor
Cd14
. In addition, caecal microbiota composition remained unchanged by diet. Exposure of mice to HFD over a more prolonged period (20 weeks) to drive systemic inflammation also caused obesity. RNAseq used to assess hypothalamic inflammation in these mice showed increased hypothalamic expression of
Serpina3n
and
Socs3
in response to HFD, with few other genes altered.
In situ
hybridisation confirmed increased
Serpina3n
and
Socs3
expression in the ARC and DMH at 20-weeks, but also at 8-weeks and increased SerpinA3N protein could be detected as early as 1 week on HFD. Overall these data show lack of hypothalamic inflammation in response to HFD and that metabolic endotoxemia does not link HFD to obesity. |
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AbstractList | Hypothalamic inflammation is thought to contribute to obesity. One potential mechanism is via gut microbiota derived bacterial lipopolysaccharide (LPS) entering into the circulation and activation of Toll-like receptor-4. This is called metabolic endotoxemia. Another potential mechanism is systemic inflammation arising from sustained exposure to high-fat diet (HFD) over more than 12 weeks. In this study we show that mice fed HFD over 8 weeks become obese and show elevated plasma LPS binding protein, yet body weight gain and adiposity is not attenuated in mice lacking
Tlr4
or its co-receptor
Cd14
. In addition, caecal microbiota composition remained unchanged by diet. Exposure of mice to HFD over a more prolonged period (20 weeks) to drive systemic inflammation also caused obesity. RNAseq used to assess hypothalamic inflammation in these mice showed increased hypothalamic expression of
Serpina3n
and
Socs3
in response to HFD, with few other genes altered.
In situ
hybridisation confirmed increased
Serpina3n
and
Socs3
expression in the ARC and DMH at 20-weeks, but also at 8-weeks and increased SerpinA3N protein could be detected as early as 1 week on HFD. Overall these data show lack of hypothalamic inflammation in response to HFD and that metabolic endotoxemia does not link HFD to obesity. Hypothalamic inflammation is thought to contribute to obesity. One potential mechanism is via gut microbiota derived bacterial lipopolysaccharide (LPS) entering into the circulation and activation of Toll-like receptor-4. This is called metabolic endotoxemia. Another potential mechanism is systemic inflammation arising from sustained exposure to high-fat diet (HFD) over more than 12 weeks. In this study we show that mice fed HFD over 8 weeks become obese and show elevated plasma LPS binding protein, yet body weight gain and adiposity is not attenuated in mice lacking Tlr4 or its co-receptor Cd14. In addition, caecal microbiota composition remained unchanged by diet. Exposure of mice to HFD over a more prolonged period (20 weeks) to drive systemic inflammation also caused obesity. RNAseq used to assess hypothalamic inflammation in these mice showed increased hypothalamic expression of Serpina3n and Socs3 in response to HFD, with few other genes altered. In situ hybridisation confirmed increased Serpina3n and Socs3 expression in the ARC and DMH at 20-weeks, but also at 8-weeks and increased SerpinA3N protein could be detected as early as 1 week on HFD. Overall these data show lack of hypothalamic inflammation in response to HFD and that metabolic endotoxemia does not link HFD to obesity. |
ArticleNumber | 15648 |
Author | Morgan, Peter J. Barrett, Perry Ross, Alexander W. Walker, Alan W. Dalby, Matthew J. Aviello, Gabriella |
Author_xml | – sequence: 1 givenname: Matthew J. orcidid: 0000-0002-1137-4337 surname: Dalby fullname: Dalby, Matthew J. organization: Rowett Institute, University of Aberdeen, Foresterhill – sequence: 2 givenname: Gabriella surname: Aviello fullname: Aviello, Gabriella organization: Rowett Institute, University of Aberdeen, Foresterhill – sequence: 3 givenname: Alexander W. surname: Ross fullname: Ross, Alexander W. organization: Rowett Institute, University of Aberdeen, Foresterhill – sequence: 4 givenname: Alan W. orcidid: 0000-0001-5099-8495 surname: Walker fullname: Walker, Alan W. organization: Rowett Institute, University of Aberdeen, Foresterhill – sequence: 5 givenname: Perry surname: Barrett fullname: Barrett, Perry organization: Rowett Institute, University of Aberdeen, Foresterhill – sequence: 6 givenname: Peter J. orcidid: 0000-0002-5071-6512 surname: Morgan fullname: Morgan, Peter J. email: p.morgan@abdn.ac.uk organization: Rowett Institute, University of Aberdeen, Foresterhill |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/30353127$$D View this record in MEDLINE/PubMed |
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Keywords | Metabolic Endotoxemia Caecal Microbiota Hypothalamic Inflammation Microbiota Composition Arcuate Nucleus |
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Snippet | Hypothalamic inflammation is thought to contribute to obesity. One potential mechanism is via gut microbiota derived bacterial lipopolysaccharide (LPS)... |
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Title | Diet induced obesity is independent of metabolic endotoxemia and TLR4 signalling, but markedly increases hypothalamic expression of the acute phase protein, SerpinA3N |
URI | https://link.springer.com/article/10.1038/s41598-018-33928-4 https://www.ncbi.nlm.nih.gov/pubmed/30353127 https://www.proquest.com/docview/2124454504 https://search.proquest.com/docview/2125310891 https://pubmed.ncbi.nlm.nih.gov/PMC6199263 |
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