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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
Title | Increased colonization of lactococcus lactis could prevent development of non-alcoholic fatty liver disease: evidence from a human microbiota-associated rodent model |
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Authors | |
Issue Date | 2020 |
Publisher | John 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? |
Abstract | Background: 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. |
Description | Poster presentation- no. 615 |
Persistent Identifier | http://hdl.handle.net/10722/305711 |
ISSN | 2023 Impact Factor: 12.9 2023 SCImago Journal Rankings: 5.011 |
DC Field | Value | Language |
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dc.contributor.author | Tun, HM | - |
dc.contributor.author | Zhang, S | - |
dc.contributor.author | Lee, CHP | - |
dc.contributor.author | Chau, HT | - |
dc.contributor.author | Zhang, D | - |
dc.contributor.author | Liang, S | - |
dc.contributor.author | Huang, FY | - |
dc.contributor.author | Wong, DKH | - |
dc.contributor.author | Lam, KSL | - |
dc.contributor.author | Yuen, RMF | - |
dc.contributor.author | Seto, WKW | - |
dc.date.accessioned | 2021-10-20T10:13:14Z | - |
dc.date.available | 2021-10-20T10:13:14Z | - |
dc.date.issued | 2020 | - |
dc.identifier.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 | - |
dc.identifier.issn | 0270-9139 | - |
dc.identifier.uri | http://hdl.handle.net/10722/305711 | - |
dc.description | Poster presentation- no. 615 | - |
dc.description.abstract | Background: 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.language | eng | - |
dc.publisher | John Wiley & Sons, Inc. The Journal's web site is located at http://www.hepatology.org/ | - |
dc.relation.ispartof | Hepatology | - |
dc.relation.ispartof | The Annual Meeting of the American Association for the Study of Liver Diseases (AASLD): The Liver Meeting Digital Experience 2020 | - |
dc.title | Increased colonization of lactococcus lactis could prevent development of non-alcoholic fatty liver disease: evidence from a human microbiota-associated rodent model | - |
dc.type | Conference_Paper | - |
dc.identifier.email | Tun, HM: heinmtun@hku.hk | - |
dc.identifier.email | Lee, CHP: pchlee@hku.hk | - |
dc.identifier.email | Huang, FY: fungyu@hkucc.hku.hk | - |
dc.identifier.email | Wong, DKH: danywong@hku.hk | - |
dc.identifier.email | Lam, KSL: ksllam@hku.hk | - |
dc.identifier.email | Yuen, RMF: mfyuen@hku.hk | - |
dc.identifier.email | Seto, WKW: wkseto@hku.hk | - |
dc.identifier.authority | Tun, HM=rp02389 | - |
dc.identifier.authority | Lee, CHP=rp02043 | - |
dc.identifier.authority | Wong, DKH=rp00492 | - |
dc.identifier.authority | Lam, KSL=rp00343 | - |
dc.identifier.authority | Yuen, RMF=rp00479 | - |
dc.identifier.authority | Seto, WKW=rp01659 | - |
dc.description.nature | abstract | - |
dc.identifier.hkuros | 326969 | - |
dc.identifier.volume | 72 | - |
dc.identifier.issue | S1 | - |
dc.identifier.spage | 371A | - |
dc.identifier.epage | 372A | - |
dc.publisher.place | United States | - |
dc.identifier.partofdoi | 10.1002/hep.31579 | - |