File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: High fat diet induced atherosclerosis is accompanied with low colonic bacterial diversity and altered abundances that correlates with plaque size, plasma A-FABP and cholesterol: a pilot study of high fat diet and its intervention with Lactobacillus rhamnosus GG (LGG) or telmisartan in ApoE-/- mice

TitleHigh fat diet induced atherosclerosis is accompanied with low colonic bacterial diversity and altered abundances that correlates with plaque size, plasma A-FABP and cholesterol: a pilot study of high fat diet and its intervention with Lactobacillus rhamnosus GG (LGG) or telmisartan in ApoE-/- mice
Authors
KeywordsAtherosclerosis
Gut microbitoa
LGG
Probiotics
Telmisartan
Issue Date8-Nov-2016
PublisherBioMed Central
Citation
BMC Microbiology, 2016, v. 16, n. 1, p. 1-13 How to Cite?
Abstract

Background

Atherosclerosis appears to have multifactorial causes – microbial component like lipopolysaccharides (LPS) and other pathogen associated molecular patterns may be plausible factors. The gut microbiota is an ample source of such stimulants, and its dependent metabolites and altered gut metagenome has been an established link to atherosclerosis. In this exploratory pilot study, we aimed to elucidate whether microbial intervention with probiotics L. rhamnosus GG (LGG) or pharmaceuticals telmisartan (TLM) could improve atherosclerosis in a gut microbiota associated manner.

Methods

Atherosclerotic phenotype was established by 12 weeks feeding of high fat (HF) diet as opposed to normal chow diet (ND) in apolipoprotein E knockout (ApoE−/−) mice. LGG or TLM supplementation to HF diet was studied.

Results

Both LGG and TLM significantly reduced atherosclerotic plaque size and improved various biomarkers including endotoxin to different extents. Colonial microbiota analysis revealed that TLM restored HF diet induced increase in Firmicutes/Bacteroidetes ratio and decrease in alpha diversity; and led to a more distinct microbial clustering closer to ND in PCoA plot. Eubacteria, Anaeroplasma, Roseburia, Oscillospira and Dehalobacteria appeared to be protective against atherosclerosis and showed significant negative correlation with atherosclerotic plaque size and plasma adipocyte – fatty acid binding protein (A-FABP) and cholesterol.

Conclusion

LGG and TLM improved atherosclerosis with TLM having a more distinct alteration in the colonic gut microbiota. Altered bacteria genera and reduced alpha diversity had significant correlations to atherosclerotic plaque size, plasma A-FABP and cholesterol. Future studies on such bacterial functional influence in lipid metabolism will be warranted.


Persistent Identifierhttp://hdl.handle.net/10722/337209
ISSN
2023 Impact Factor: 4.0
2023 SCImago Journal Rankings: 0.999
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorChan, Yee Kwan-
dc.contributor.authorBrar, Manreetpal Singh-
dc.contributor.authorKirjavainen, Pirkka V-
dc.contributor.authorChen, Yan-
dc.contributor.authorPeng, Jiao-
dc.contributor.authorLi, Daxu-
dc.contributor.authorLeung, Frederick Chi-Ching-
dc.contributor.authorEl-Nezami, Hani-
dc.date.accessioned2024-03-11T10:18:55Z-
dc.date.available2024-03-11T10:18:55Z-
dc.date.issued2016-11-08-
dc.identifier.citationBMC Microbiology, 2016, v. 16, n. 1, p. 1-13-
dc.identifier.issn1471-2180-
dc.identifier.urihttp://hdl.handle.net/10722/337209-
dc.description.abstract<h3>Background</h3><p>Atherosclerosis appears to have multifactorial causes – microbial component like lipopolysaccharides (LPS) and other pathogen associated molecular patterns may be plausible factors. The gut microbiota is an ample source of such stimulants, and its dependent metabolites and altered gut metagenome has been an established link to atherosclerosis. In this exploratory pilot study, we aimed to elucidate whether microbial intervention with probiotics <em>L. rhamnosus</em> GG (LGG) or pharmaceuticals telmisartan (TLM) could improve atherosclerosis in a gut microbiota associated manner.</p><h3>Methods</h3><p>Atherosclerotic phenotype was established by 12 weeks feeding of high fat (HF) diet as opposed to normal chow diet (ND) in apolipoprotein E knockout (ApoE<sup>−/−</sup>) mice. LGG or TLM supplementation to HF diet was studied.</p><h3>Results</h3><p>Both LGG and TLM significantly reduced atherosclerotic plaque size and improved various biomarkers including endotoxin to different extents. Colonial microbiota analysis revealed that TLM restored HF diet induced increase in Firmicutes/Bacteroidetes ratio and decrease in alpha diversity; and led to a more distinct microbial clustering closer to ND in PCoA plot. Eubacteria, Anaeroplasma, Roseburia, Oscillospira and Dehalobacteria appeared to be protective against atherosclerosis and showed significant negative correlation with atherosclerotic plaque size and plasma adipocyte – fatty acid binding protein (A-FABP) and cholesterol.</p><h3>Conclusion</h3><p>LGG and TLM improved atherosclerosis with TLM having a more distinct alteration in the colonic gut microbiota. Altered bacteria genera and reduced alpha diversity had significant correlations to atherosclerotic plaque size, plasma A-FABP and cholesterol. Future studies on such bacterial functional influence in lipid metabolism will be warranted.</p>-
dc.languageeng-
dc.publisherBioMed Central-
dc.relation.ispartofBMC Microbiology-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectAtherosclerosis-
dc.subjectGut microbitoa-
dc.subjectLGG-
dc.subjectProbiotics-
dc.subjectTelmisartan-
dc.titleHigh fat diet induced atherosclerosis is accompanied with low colonic bacterial diversity and altered abundances that correlates with plaque size, plasma A-FABP and cholesterol: a pilot study of high fat diet and its intervention with Lactobacillus rhamnosus GG (LGG) or telmisartan in ApoE-/- mice-
dc.typeArticle-
dc.identifier.doi10.1186/s12866-016-0883-4-
dc.identifier.scopuseid_2-s2.0-84994246744-
dc.identifier.volume16-
dc.identifier.issue1-
dc.identifier.spage1-
dc.identifier.epage13-
dc.identifier.eissn1471-2180-
dc.identifier.isiWOS:000387083300004-
dc.identifier.issnl1471-2180-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats