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Article: Hyodeoxycholic acid alleviates non-alcoholic fatty liver disease through modulating the gut-liver axis

TitleHyodeoxycholic acid alleviates non-alcoholic fatty liver disease through modulating the gut-liver axis
Authors
Keywordsbile acid
CYP7B1
farnesoid X receptor
hyodeoxycholic acid
NAFLD
Parabacteroides distasonis
PPARα
Issue Date2023
Citation
Cell Metabolism, 2023, v. 35, n. 10, p. 1752-1766.e8 How to Cite?
AbstractNon-alcoholic fatty liver disease (NAFLD) is regarded as a pandemic that affects about a quarter of the global population. Recently, host-gut microbiota metabolic interactions have emerged as distinct mechanistic pathways implicated in the development of NAFLD. Here, we report that a group of gut microbiota-modified bile acids (BAs), hyodeoxycholic acid (HDCA) species, are negatively correlated with the presence and severity of NAFLD. HDCA treatment has been shown to alleviate NAFLD in multiple mouse models by inhibiting intestinal farnesoid X receptor (FXR) and upregulating hepatic CYP7B1. Additionally, HDCA significantly increased abundances of probiotic species such as Parabacteroides distasonis, which enhances lipid catabolism through fatty acid-hepatic peroxisome proliferator-activated receptor alpha (PPARα) signaling, which in turn upregulates hepatic FXR. These findings suggest that HDCA has therapeutic potential for treating NAFLD, with a unique mechanism of simultaneously activating hepatic CYP7B1 and PPARα.
Persistent Identifierhttp://hdl.handle.net/10722/342680
ISSN
2023 Impact Factor: 27.7
2023 SCImago Journal Rankings: 11.406
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorKuang, Junliang-
dc.contributor.authorWang, Jieyi-
dc.contributor.authorLi, Yitao-
dc.contributor.authorLi, Mengci-
dc.contributor.authorZhao, Mingliang-
dc.contributor.authorGe, Kun-
dc.contributor.authorZheng, Dan-
dc.contributor.authorCheung, Kenneth C.P.-
dc.contributor.authorLiao, Boya-
dc.contributor.authorWang, Shouli-
dc.contributor.authorChen, Tianlu-
dc.contributor.authorZhang, Yinan-
dc.contributor.authorWang, Congrong-
dc.contributor.authorJi, Guang-
dc.contributor.authorChen, Peng-
dc.contributor.authorZhou, Hongwei-
dc.contributor.authorXie, Cen-
dc.contributor.authorZhao, Aihua-
dc.contributor.authorJia, Weiping-
dc.contributor.authorZheng, Xiaojiao-
dc.contributor.authorJia, Wei-
dc.date.accessioned2024-04-17T07:05:29Z-
dc.date.available2024-04-17T07:05:29Z-
dc.date.issued2023-
dc.identifier.citationCell Metabolism, 2023, v. 35, n. 10, p. 1752-1766.e8-
dc.identifier.issn1550-4131-
dc.identifier.urihttp://hdl.handle.net/10722/342680-
dc.description.abstractNon-alcoholic fatty liver disease (NAFLD) is regarded as a pandemic that affects about a quarter of the global population. Recently, host-gut microbiota metabolic interactions have emerged as distinct mechanistic pathways implicated in the development of NAFLD. Here, we report that a group of gut microbiota-modified bile acids (BAs), hyodeoxycholic acid (HDCA) species, are negatively correlated with the presence and severity of NAFLD. HDCA treatment has been shown to alleviate NAFLD in multiple mouse models by inhibiting intestinal farnesoid X receptor (FXR) and upregulating hepatic CYP7B1. Additionally, HDCA significantly increased abundances of probiotic species such as Parabacteroides distasonis, which enhances lipid catabolism through fatty acid-hepatic peroxisome proliferator-activated receptor alpha (PPARα) signaling, which in turn upregulates hepatic FXR. These findings suggest that HDCA has therapeutic potential for treating NAFLD, with a unique mechanism of simultaneously activating hepatic CYP7B1 and PPARα.-
dc.languageeng-
dc.relation.ispartofCell Metabolism-
dc.subjectbile acid-
dc.subjectCYP7B1-
dc.subjectfarnesoid X receptor-
dc.subjecthyodeoxycholic acid-
dc.subjectNAFLD-
dc.subjectParabacteroides distasonis-
dc.subjectPPARα-
dc.titleHyodeoxycholic acid alleviates non-alcoholic fatty liver disease through modulating the gut-liver axis-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.cmet.2023.07.011-
dc.identifier.pmid37591244-
dc.identifier.scopuseid_2-s2.0-85169801386-
dc.identifier.volume35-
dc.identifier.issue10-
dc.identifier.spage1752-
dc.identifier.epage1766.e8-
dc.identifier.eissn1932-7420-
dc.identifier.isiWOS:001088994200001-

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