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Protective effects of AdipoRon on the liver of Huoyan goose fed a high-fat diet
Adiponectin can participate in the regulation of glucose and lipid metabolism, energy regulation, immune response, resistance to inflammation, oxidative stress, and apoptosis. Studies in rodents demonstrated that the small molecule compound adiponectin receptor agonist AdipoRon could activate the ad...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8844248/ https://www.ncbi.nlm.nih.gov/pubmed/35150940 http://dx.doi.org/10.1016/j.psj.2022.101708 |
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author | Cao, Zhongzan Ma, Ben Cui, Chengyu Zhao, Jiahui Liu, Sidi Qiu, Yunqiao Zheng, Yan Gao, Ming Luan, Xinhong |
author_facet | Cao, Zhongzan Ma, Ben Cui, Chengyu Zhao, Jiahui Liu, Sidi Qiu, Yunqiao Zheng, Yan Gao, Ming Luan, Xinhong |
author_sort | Cao, Zhongzan |
collection | PubMed |
description | Adiponectin can participate in the regulation of glucose and lipid metabolism, energy regulation, immune response, resistance to inflammation, oxidative stress, and apoptosis. Studies in rodents demonstrated that the small molecule compound adiponectin receptor agonist AdipoRon could activate the adiponectin receptor and played the same biological role as adiponectin. To explore the influence and regulation of AdipoRon on lipid metabolism disorder in Huoyan goose liver, in this study, goslings were fed a high-fat diet and then administered different dosages of AdipoRon. Subsequently, goose body weight, liver index, liver histopathological changes, blood glucose, blood and liver lipid, biochemical indexes related to liver function and oxidative stress, and the expression levels of genes related to lipid metabolism, inflammation, apoptosis, and autophagy, adiponectin and its receptors, key molecules of adiponectin involved signal pathway, and transcription factors in the liver, were detected using H&E and Oil red O staining, ELISA, and qRT-PCR methods. The results indicated that AdipoRon could alter the expression of lipid metabolism-related genes, inflammatory factors, apoptosis and autophagy genes, and adiponectin and its receptor genes in liver tissues through signaling pathways such as AMPK and p38 MAPK, as well as the involvement of transcription factors such as PPARα, PPARγ, SIRT1, and FOXO1, reduce the lipid content in blood and liver tissues of geese fed high-fat diets, improve liver antioxidant capacity, regulate apoptosis and autophagy of hepatocytes, and reduce liver inflammatory injury. Our study suggests that AdipoRon has a protective effect on fatty liver injury in goslings fed a high-fat diet. |
format | Online Article Text |
id | pubmed-8844248 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Elsevier |
record_format | MEDLINE/PubMed |
spelling | pubmed-88442482022-02-22 Protective effects of AdipoRon on the liver of Huoyan goose fed a high-fat diet Cao, Zhongzan Ma, Ben Cui, Chengyu Zhao, Jiahui Liu, Sidi Qiu, Yunqiao Zheng, Yan Gao, Ming Luan, Xinhong Poult Sci IMMUNOLOGY, HEALTH AND DISEASE Adiponectin can participate in the regulation of glucose and lipid metabolism, energy regulation, immune response, resistance to inflammation, oxidative stress, and apoptosis. Studies in rodents demonstrated that the small molecule compound adiponectin receptor agonist AdipoRon could activate the adiponectin receptor and played the same biological role as adiponectin. To explore the influence and regulation of AdipoRon on lipid metabolism disorder in Huoyan goose liver, in this study, goslings were fed a high-fat diet and then administered different dosages of AdipoRon. Subsequently, goose body weight, liver index, liver histopathological changes, blood glucose, blood and liver lipid, biochemical indexes related to liver function and oxidative stress, and the expression levels of genes related to lipid metabolism, inflammation, apoptosis, and autophagy, adiponectin and its receptors, key molecules of adiponectin involved signal pathway, and transcription factors in the liver, were detected using H&E and Oil red O staining, ELISA, and qRT-PCR methods. The results indicated that AdipoRon could alter the expression of lipid metabolism-related genes, inflammatory factors, apoptosis and autophagy genes, and adiponectin and its receptor genes in liver tissues through signaling pathways such as AMPK and p38 MAPK, as well as the involvement of transcription factors such as PPARα, PPARγ, SIRT1, and FOXO1, reduce the lipid content in blood and liver tissues of geese fed high-fat diets, improve liver antioxidant capacity, regulate apoptosis and autophagy of hepatocytes, and reduce liver inflammatory injury. Our study suggests that AdipoRon has a protective effect on fatty liver injury in goslings fed a high-fat diet. Elsevier 2022-01-10 /pmc/articles/PMC8844248/ /pubmed/35150940 http://dx.doi.org/10.1016/j.psj.2022.101708 Text en © 2022 The Authors https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). |
spellingShingle | IMMUNOLOGY, HEALTH AND DISEASE Cao, Zhongzan Ma, Ben Cui, Chengyu Zhao, Jiahui Liu, Sidi Qiu, Yunqiao Zheng, Yan Gao, Ming Luan, Xinhong Protective effects of AdipoRon on the liver of Huoyan goose fed a high-fat diet |
title | Protective effects of AdipoRon on the liver of Huoyan goose fed a high-fat diet |
title_full | Protective effects of AdipoRon on the liver of Huoyan goose fed a high-fat diet |
title_fullStr | Protective effects of AdipoRon on the liver of Huoyan goose fed a high-fat diet |
title_full_unstemmed | Protective effects of AdipoRon on the liver of Huoyan goose fed a high-fat diet |
title_short | Protective effects of AdipoRon on the liver of Huoyan goose fed a high-fat diet |
title_sort | protective effects of adiporon on the liver of huoyan goose fed a high-fat diet |
topic | IMMUNOLOGY, HEALTH AND DISEASE |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8844248/ https://www.ncbi.nlm.nih.gov/pubmed/35150940 http://dx.doi.org/10.1016/j.psj.2022.101708 |
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