Regulatory effect of hydrogen sulfide on β oxidation in fatty liver in rats

2014 ◽  
Vol 22 (25) ◽  
pp. 3791
Author(s):  
Xin-Guo Wang
2020 ◽  
Author(s):  
Han Zhang ◽  
Qinghui Niu ◽  
Kun Liang ◽  
Xuesen Li ◽  
Jing Jiang ◽  
...  

Abstract Background: Non-alcoholic fatty liver (NAFLD) is the hepatic manifestation of metabolic syndromes, insulin resistance (IR) is related to the occurrence of NAFLD. The purpose of this study was to evaluate the expression of miR-129-5p in NAFLD patients and its clinical value, and explore its regulatory effect on IR.Methods: 117 NAFLD patients and 110 healthy controls were included. The levels of miR-129-5p were detected by qRT-PCR. To assess the diagnostic value of miR-129-5p for NAFLD, the receiver operating characteristic curve (ROC) was established. C57Bl/6 mice were supplied with high-fat diet to establish NAFLD model. Intraperitoneal insulin tolerance test (IPITT) was carried out to evaluate the effect of miR-129-5p on IR in NAFLD animal model.Results: miR-129-5p was highly expressed in the serum of NAFLD patients, and patients with HOMA-IR ≥ 2.5 had higher level of miR-129-5p than those with HOMA-IR < 2.5. miR-129-5p had the ability to differentiate NAFLD patients from healthy individuals, and might be associated with the development of IR. Serum miR-129-5p was positively correlated with the levels of HOMA-IR, BMI, total cholesterol (TC) and triglyceride (TG) in NAFLD patients. Downregulation of miR-129-5p regulates lipid metabolism and insulin sensitivity in NAFLD mice model.Conclusions: MiR-129-5p was up-regulated in NAFLD patients, and might be a potential diagnostic biomarker. The regulatory effect of miR-129-5p on NAFLD may function by regulating lipid accumulation and insulin sensitivity.


Author(s):  
Yuan Wang ◽  
Yujia Feng ◽  
Hong Li ◽  
Han Zhang ◽  
Qinghui Niu ◽  
...  

AbstractThis study was to evaluate the expression of miR-129–5p in non-alcoholic fatty liver (NAFLD) patients and its clinical value and explore its regulatory effect on insulin resistance (IR). A total of 117 NAFLD patients and 110 healthy controls were included. The levels of miR-129-5p were detected by qRT-PCR. To assess the diagnostic value of miR-129-5p for NAFLD, the receiver operating characteristic curve (ROC) was established. C57Bl/6 mice were supplied with high-fat diet to establish NAFLD model. Intraperitoneal insulin tolerance test (IPITT) was carried out to evaluate the effect of miR-129-5p on IR in NAFLD animal model. miR-129-5p was highly expressed in the serum of NAFLD patients, and patients with HOMA-IR ≥2.5 had higher level of miR-129-5p than those with HOMA-IR <2.5. miR-129-5p had the ability to differentiate NAFLD patients from healthy individuals and might be associated with the development of IR. Serum miR-129-5p was positively correlated with the levels of HOMA-IR, BMI, total cholesterol (TC), and triglyceride (TG) in NAFLD patients. Downregulation of miR-129-5p regulates lipid metabolism and insulin sensitivity in NAFLD mice model. MiR-129-5p was upregulated in NAFLD patients and might be a potential diagnostic biomarker. The regulatory effect of miR-129-5p on NAFLD may function by regulating lipid accumulation and insulin sensitivity.


2019 ◽  
Vol 128 (03) ◽  
pp. 137-143 ◽  
Author(s):  
Ya-Di Wang ◽  
Jiao-Yang Li ◽  
Yu Qin ◽  
Qiong Liu ◽  
Zhe-Zhen Liao ◽  
...  

AbstractFatty acids induced hepatic inflammation plays an important role in nonalcoholic fatty liver disease (NAFLD) pathogenesis. Hydrogen sulfide (H2S), an endogenous gasotransmitter, has been established to possess potent anti-inflammation in various human organs. However, the anti-inflammation property of H2S in the fatty liver is still needed to further elucidate. Hence, this study aimed to investigate whether exogenous H2S can protect hepatocytes against inflammation induced by palmitic acid (PA). HepG2 hepatocytes were exposed to PA for 24 h to induce free fatty acids-induced inflammation. The cells were pretreated with NaHS (a donor of H2S) before exposure to PA. Cell viability, inflammatory cytokines (TNF-α, IL-6 and IL-1β), NLRP3 inflammasome and NF-κB were measured by a combination of MTT assay, ELISA, Western blot and Immunofluorescence. Here, we found that exogenous H2S dose-dependently inhibited the expression of pro-inflammatory cytokines, NLRP3 inflammasome and activation of NF-κB signaling in PA-induced HepG2 cells. Thus, H2S might be a candidate therapeutic agent against NAFLD.


2008 ◽  
Vol 31 (8) ◽  
pp. 1619-1630 ◽  
Author(s):  
Xia ZHAO ◽  
Li-Ke ZHANG ◽  
Chun-Yu ZHANG ◽  
Xiang-Jun ZENG ◽  
Hui YAN ◽  
...  

2013 ◽  
Vol 91 (11) ◽  
pp. 913-919 ◽  
Author(s):  
Sun-Young Hwang ◽  
Lindsei K. Sarna ◽  
Yaw L. Siow ◽  
Karmin O

Cystathionine-β-synthase (CBS) and cystathionine-γ-lyase (CSE) catalyze homocysteine (Hcy) metabolism via the trans-sulfuration pathway. They are also responsible for hydrogen sulfide (H2S) production via desulfuration reactions. The liver contributes significantly to the regulation of Hcy and H2S homeostasis, which might participate in many physiological and pathological processes. The aim of this study was to investigate the effect of a high-fat diet (HFD) on hepatic CBS and CSE expression and its impact on Hcy and H2S metabolism. Mice (C57BL/6) fed a HFD (60% kcal fat) for 5 weeks developed fatty liver. The mRNA and protein levels of CBS and CSE in the liver were significantly elevated in mice fed a HFD. Subsequently the metabolism of Hcy by CBS and CSE was increased in the liver, and its level decreased in the circulation. Increased CBS and CSE expression also caused a significant elevation in H2S production in the liver. The level of lipid peroxides was elevated, indicating oxidative stress, while the level of total glutathione remained unchanged in the liver of HFD-fed mice. Upregulation of the trans-sulfuration pathway might play an adaptive role against oxidative stress by maintaining total glutathione levels in the liver.


2015 ◽  
Vol 5 (1) ◽  
pp. 1 ◽  
Author(s):  
Dongdong Wu ◽  
Nairui Zheng ◽  
Kunqing Qi ◽  
Huijun Cheng ◽  
Ziqiang Sun ◽  
...  

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