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Conference Paper: Increased colonization of lactococcus lactis could prevent development of non-alcoholic fatty liver disease: evidence from a human microbiota-associated rodent model

TitleIncreased colonization of lactococcus lactis could prevent development of non-alcoholic fatty liver disease: evidence from a human microbiota-associated rodent model
Authors
Issue Date2020
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.hepatology.org/
Citation
The Annual Meeting of the American Association for the Study of Liver Diseases (AASLD): The Liver Meeting Digital Experience 2020, Boston, USA, 13-16 November 2020. In Hepatology, 2020, v. 72 n. S1, p. 371A-372A, abstract no. 615 How to Cite?
AbstractBackground: Gut microbiota dysbiosis is increasingly linked to the development of non-alcoholic fatty liver disease (NAFLD). Yet, its causal relationship has not been well established. We aimed to investigate gut microbiota species related to NAFLD development in human microbiota-associated rodents using fecal microbiota transplantation (FMT). Methods: We recruited Asian human FMT donors categorized as three groups (n=8 each): obese NAFLD donors; non-obese NAFLD; and non-obese, non-diabetic healthy controls, with hepatic steatosis quantified using controlled attenuation parameter measurements via transient elastography (Fibroscan, Echosens). After antibiotic administration, collected human fecal samples were transplanted individually into C57BL/6J mice, categorized as FMT-obese, FMT-lean and FMT-healthy. We collected liver, adipose tissue and blood from mice after a 12-week high-fat diet for assessment of histology, lipid metabolism, hepatic inflammation and intestinal barrier function. Shotgun metagenomics sequencing was used to profile gut microbiome. Results: Obese NAFLD donors had a significantly higher controlled attenuation parameter measurement and BMI than non-obese NAFLD and healthy controls. Non-obese NAFLD donors had a distinct gut microbiota compared with healthy controls (p=0.03) and obese NAFLD donors (p=0.0479). Compared to FMT-healthy mice, FMT-obese had significantly higher plasma triglyceride levels and intrahepatic triglyceride content (p<0.01); and increased hepatic lipid accumulation and adipocyte size (p<0.05); but lower expression of tight junction protein zonula occludens-1, an intestinal barrier marker (p=0.03). No difference was observed between FMT-healthy vs. FMT-lean mice. Gut microbiota composition of FMT-obese mice was significantly distinct from FMT-healthy (p=0.03) and FMT-lean (p=0.038). Biomarker analysis confirmed a lower abundance of Lactococcus lactis in FMT-obese mice than FMT-healthy mice (43.50% vs. 24.82%, FDR-p=0.04). As low levels of L. lactis were not well-detected in human fecal metagenomes, we confirmed their colonization by targeted qPCR, which indicated a consistent trend of decreased colonization in obese NAFLD donors. L. lactis correlated positively with tricarboxylic acid cycle pathway, a major energy-producing pathway involved in triglyceride breakdown (rho=0.59, p=0.002), but correlated negatively with plasma triglyceride levels (rho=-0.45, p=0.03). Conclusion: In this study, we proposed the potential causative role of L. lactis in preventing NAFLD development. Future animal and human interventional studies are warranted to determine its therapeutic potential in NAFLD.
DescriptionPoster presentation- no. 615
Persistent Identifierhttp://hdl.handle.net/10722/305711
ISSN
2020 Impact Factor: 17.425
2020 SCImago Journal Rankings: 5.488

 

DC FieldValueLanguage
dc.contributor.authorTun, HM-
dc.contributor.authorZhang, S-
dc.contributor.authorLee, CHP-
dc.contributor.authorChau, HT-
dc.contributor.authorZhang, D-
dc.contributor.authorLiang, S-
dc.contributor.authorHuang, FY-
dc.contributor.authorWong, DKH-
dc.contributor.authorLam, KSL-
dc.contributor.authorYuen, RMF-
dc.contributor.authorSeto, WKW-
dc.date.accessioned2021-10-20T10:13:14Z-
dc.date.available2021-10-20T10:13:14Z-
dc.date.issued2020-
dc.identifier.citationThe Annual Meeting of the American Association for the Study of Liver Diseases (AASLD): The Liver Meeting Digital Experience 2020, Boston, USA, 13-16 November 2020. In Hepatology, 2020, v. 72 n. S1, p. 371A-372A, abstract no. 615-
dc.identifier.issn0270-9139-
dc.identifier.urihttp://hdl.handle.net/10722/305711-
dc.descriptionPoster presentation- no. 615-
dc.description.abstractBackground: Gut microbiota dysbiosis is increasingly linked to the development of non-alcoholic fatty liver disease (NAFLD). Yet, its causal relationship has not been well established. We aimed to investigate gut microbiota species related to NAFLD development in human microbiota-associated rodents using fecal microbiota transplantation (FMT). Methods: We recruited Asian human FMT donors categorized as three groups (n=8 each): obese NAFLD donors; non-obese NAFLD; and non-obese, non-diabetic healthy controls, with hepatic steatosis quantified using controlled attenuation parameter measurements via transient elastography (Fibroscan, Echosens). After antibiotic administration, collected human fecal samples were transplanted individually into C57BL/6J mice, categorized as FMT-obese, FMT-lean and FMT-healthy. We collected liver, adipose tissue and blood from mice after a 12-week high-fat diet for assessment of histology, lipid metabolism, hepatic inflammation and intestinal barrier function. Shotgun metagenomics sequencing was used to profile gut microbiome. Results: Obese NAFLD donors had a significantly higher controlled attenuation parameter measurement and BMI than non-obese NAFLD and healthy controls. Non-obese NAFLD donors had a distinct gut microbiota compared with healthy controls (p=0.03) and obese NAFLD donors (p=0.0479). Compared to FMT-healthy mice, FMT-obese had significantly higher plasma triglyceride levels and intrahepatic triglyceride content (p<0.01); and increased hepatic lipid accumulation and adipocyte size (p<0.05); but lower expression of tight junction protein zonula occludens-1, an intestinal barrier marker (p=0.03). No difference was observed between FMT-healthy vs. FMT-lean mice. Gut microbiota composition of FMT-obese mice was significantly distinct from FMT-healthy (p=0.03) and FMT-lean (p=0.038). Biomarker analysis confirmed a lower abundance of Lactococcus lactis in FMT-obese mice than FMT-healthy mice (43.50% vs. 24.82%, FDR-p=0.04). As low levels of L. lactis were not well-detected in human fecal metagenomes, we confirmed their colonization by targeted qPCR, which indicated a consistent trend of decreased colonization in obese NAFLD donors. L. lactis correlated positively with tricarboxylic acid cycle pathway, a major energy-producing pathway involved in triglyceride breakdown (rho=0.59, p=0.002), but correlated negatively with plasma triglyceride levels (rho=-0.45, p=0.03). Conclusion: In this study, we proposed the potential causative role of L. lactis in preventing NAFLD development. Future animal and human interventional studies are warranted to determine its therapeutic potential in NAFLD.-
dc.languageeng-
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.hepatology.org/-
dc.relation.ispartofHepatology-
dc.relation.ispartofThe Annual Meeting of the American Association for the Study of Liver Diseases (AASLD): The Liver Meeting Digital Experience 2020-
dc.titleIncreased colonization of lactococcus lactis could prevent development of non-alcoholic fatty liver disease: evidence from a human microbiota-associated rodent model-
dc.typeConference_Paper-
dc.identifier.emailTun, HM: heinmtun@hku.hk-
dc.identifier.emailLee, CHP: pchlee@hku.hk-
dc.identifier.emailHuang, FY: fungyu@hkucc.hku.hk-
dc.identifier.emailWong, DKH: danywong@hku.hk-
dc.identifier.emailLam, KSL: ksllam@hku.hk-
dc.identifier.emailYuen, RMF: mfyuen@hku.hk-
dc.identifier.emailSeto, WKW: wkseto@hku.hk-
dc.identifier.authorityTun, HM=rp02389-
dc.identifier.authorityLee, CHP=rp02043-
dc.identifier.authorityWong, DKH=rp00492-
dc.identifier.authorityLam, KSL=rp00343-
dc.identifier.authorityYuen, RMF=rp00479-
dc.identifier.authoritySeto, WKW=rp01659-
dc.description.natureabstract-
dc.identifier.hkuros326969-
dc.identifier.volume72-
dc.identifier.issueS1-
dc.identifier.spage371A-
dc.identifier.epage372A-
dc.publisher.placeUnited States-
dc.identifier.partofdoi10.1002/hep.31579-

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