Diabetes Research and Clinical Practice, Год журнала: 2024, Номер 212, С. 111688 - 111688
Опубликована: Май 1, 2024
Язык: Английский
Diabetes Research and Clinical Practice, Год журнала: 2024, Номер 212, С. 111688 - 111688
Опубликована: Май 1, 2024
Язык: Английский
International Journal of Molecular Sciences, Год журнала: 2023, Номер 24(15), С. 12232 - 12232
Опубликована: Июль 31, 2023
Non-alcoholic fatty liver disease (NAFLD) affects about 20-40% of the adult population in high-income countries and is now a leading indication for transplantation can lead to hepatocellular carcinoma. The link between gut microbiota dysbiosis NAFLD clearly established. Through analyses with shotgun metagenomics, we observe that compared healthy controls, Adlercreutzia equolifaciens depleted patients diseases such as NAFLD. Its abundance also decreases progresses eventually disappears last stages indicating strong association severity. Moreover, show A. possesses anti-inflammatory properties, both vitro vivo humanized mouse model Therefore, our results demonstrate severity presence its actions. Counterbalancing this bacterium may be promising live biotherapeutic strategy diseases.
Язык: Английский
Процитировано
29Diabetes Research and Clinical Practice, Год журнала: 2023, Номер 201, С. 110733 - 110733
Опубликована: Май 26, 2023
Язык: Английский
Процитировано
23Journal of Hepatology, Год журнала: 2024, Номер 81(4), С. 600 - 608
Опубликована: Май 16, 2024
Язык: Английский
Процитировано
14Signal Transduction and Targeted Therapy, Год журнала: 2024, Номер 9(1)
Опубликована: Янв. 24, 2024
Abstract A lasting imbalance between fatty acid synthesis and consumption leads to non-alcoholic liver disease (NAFLD), coupled with hepatitis insulin resistance. Yet the details of underlying mechanisms are not fully understood. Here, we unraveled that expression transcription factor Zbtb18 is markedly decreased in livers both patients murine models NAFLD. Hepatic knockout promoted NAFLD features like impaired energy expenditure oxidation (FAO), induced Conversely, hepatic overexpression alleviated hepato-steatosis, resistance, hyperglycemia mice fed on a high-fat diet (HFD) or diabetic mice. Notably, vitro vivo mechanistic studies revealed transcriptional activation Farnesoid X receptor ( FXR ) mediated FAO Clathrin Heavy Chain CLTC protein hinders NLRP3 inflammasome activity. This key mechanism by which hepatocyte’s alleviates consequent fibrosis was further verified FXR’ s deletion forced cultured mouse primary hepatocytes (MPHs). Moreover, significantly abrogated overexpression-driven inhibition activity macrophages. Altogether, transcriptionally activates -mediated expression, inhibits inflammasome’s alleviating inflammatory stress representing an attractive remedy for steatosis fibrosis.
Язык: Английский
Процитировано
10Diabetes Research and Clinical Practice, Год журнала: 2024, Номер 212, С. 111688 - 111688
Опубликована: Май 1, 2024
Язык: Английский
Процитировано
10