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Exogenous hydrogen sulfide mitigates the fatty liver in obese mice through improving lipid metabolism and antioxidant potential

BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease in the world. Hydrogen sulfide (H2S) plays an important role in physiology and pathophysiology of liver. However, whether exogenous H2S could mitigate the hepatic steatosis in mice remains unclear. The aim of this...

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Autores principales: Wu, Dongdong, Zheng, Nairui, Qi, Kunqing, Cheng, Huijun, Sun, Ziqiang, Gao, Biao, Zhang, Youjing, Pang, Wuyan, Huangfu, Chaoshen, Ji, Shaoping, Xue, Mengzhou, Ji, Ailing, Li, Yanzhang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4299593/
https://www.ncbi.nlm.nih.gov/pubmed/25606341
http://dx.doi.org/10.1186/s13618-014-0022-y
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author Wu, Dongdong
Zheng, Nairui
Qi, Kunqing
Cheng, Huijun
Sun, Ziqiang
Gao, Biao
Zhang, Youjing
Pang, Wuyan
Huangfu, Chaoshen
Ji, Shaoping
Xue, Mengzhou
Ji, Ailing
Li, Yanzhang
author_facet Wu, Dongdong
Zheng, Nairui
Qi, Kunqing
Cheng, Huijun
Sun, Ziqiang
Gao, Biao
Zhang, Youjing
Pang, Wuyan
Huangfu, Chaoshen
Ji, Shaoping
Xue, Mengzhou
Ji, Ailing
Li, Yanzhang
author_sort Wu, Dongdong
collection PubMed
description BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease in the world. Hydrogen sulfide (H2S) plays an important role in physiology and pathophysiology of liver. However, whether exogenous H2S could mitigate the hepatic steatosis in mice remains unclear. The aim of this study is to evaluate the effects of H2S on fatty liver. METHODS: C57BL/6 mice were fed with either a high-fat diet (HFD) or a normal fat diet (NFD) for 16 weeks. After 12 weeks of feeding, the HFD-fed mice were injected one time per day with NaHS or saline for the followed 4 weeks. RESULTS: Compared to NFD, HFD could induce an accumulation of lipids in liver and a damage of hepatic structure. Compared to saline treatment, in the liver of HFD fed mice H2S treatment could significantly (1) recover the structure; (2) decrease the accumulation of lipids including triglyceride (TG) and total cholesterol (TC); (3) decrease the expression of fatty acid synthase (FAS) and increase the expression of carnitine palmitoyltransferase-1 (CPT-1); (4) reduce malondialdehyde (MDA) levels; (5) increase the activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx). CONCLUSION: H2S could mitigate the fatty liver by improving lipid metabolism and antioxidant potential in HFD-induced obese mice.
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spelling pubmed-42995932015-01-21 Exogenous hydrogen sulfide mitigates the fatty liver in obese mice through improving lipid metabolism and antioxidant potential Wu, Dongdong Zheng, Nairui Qi, Kunqing Cheng, Huijun Sun, Ziqiang Gao, Biao Zhang, Youjing Pang, Wuyan Huangfu, Chaoshen Ji, Shaoping Xue, Mengzhou Ji, Ailing Li, Yanzhang Med Gas Res Research BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) is the most common liver disease in the world. Hydrogen sulfide (H2S) plays an important role in physiology and pathophysiology of liver. However, whether exogenous H2S could mitigate the hepatic steatosis in mice remains unclear. The aim of this study is to evaluate the effects of H2S on fatty liver. METHODS: C57BL/6 mice were fed with either a high-fat diet (HFD) or a normal fat diet (NFD) for 16 weeks. After 12 weeks of feeding, the HFD-fed mice were injected one time per day with NaHS or saline for the followed 4 weeks. RESULTS: Compared to NFD, HFD could induce an accumulation of lipids in liver and a damage of hepatic structure. Compared to saline treatment, in the liver of HFD fed mice H2S treatment could significantly (1) recover the structure; (2) decrease the accumulation of lipids including triglyceride (TG) and total cholesterol (TC); (3) decrease the expression of fatty acid synthase (FAS) and increase the expression of carnitine palmitoyltransferase-1 (CPT-1); (4) reduce malondialdehyde (MDA) levels; (5) increase the activities of superoxide dismutase (SOD) and glutathione peroxidase (GPx). CONCLUSION: H2S could mitigate the fatty liver by improving lipid metabolism and antioxidant potential in HFD-induced obese mice. BioMed Central 2015-01-10 /pmc/articles/PMC4299593/ /pubmed/25606341 http://dx.doi.org/10.1186/s13618-014-0022-y Text en © Wu et al.; licensee Springer. 2015 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research
Wu, Dongdong
Zheng, Nairui
Qi, Kunqing
Cheng, Huijun
Sun, Ziqiang
Gao, Biao
Zhang, Youjing
Pang, Wuyan
Huangfu, Chaoshen
Ji, Shaoping
Xue, Mengzhou
Ji, Ailing
Li, Yanzhang
Exogenous hydrogen sulfide mitigates the fatty liver in obese mice through improving lipid metabolism and antioxidant potential
title Exogenous hydrogen sulfide mitigates the fatty liver in obese mice through improving lipid metabolism and antioxidant potential
title_full Exogenous hydrogen sulfide mitigates the fatty liver in obese mice through improving lipid metabolism and antioxidant potential
title_fullStr Exogenous hydrogen sulfide mitigates the fatty liver in obese mice through improving lipid metabolism and antioxidant potential
title_full_unstemmed Exogenous hydrogen sulfide mitigates the fatty liver in obese mice through improving lipid metabolism and antioxidant potential
title_short Exogenous hydrogen sulfide mitigates the fatty liver in obese mice through improving lipid metabolism and antioxidant potential
title_sort exogenous hydrogen sulfide mitigates the fatty liver in obese mice through improving lipid metabolism and antioxidant potential
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4299593/
https://www.ncbi.nlm.nih.gov/pubmed/25606341
http://dx.doi.org/10.1186/s13618-014-0022-y
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