Association of SIRT1 gene polymorphism and its expression for the risk of alcoholic fatty liver disease in the Han population

Hou, Yeting; Bing-zhong, SU; Chen, Ping; Niu, Haijing; Zhao, Sheng; Wang, Ruijun; Shen, Wei

doi:10.1007/s12072-017-9836-8

Cited by 11 publications

(6 citation statements)

References 33 publications

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“…It also confirmed SIRT1’s role in APE-mediated hepatic steatosis regulation and was consistent with the interactions of stilbenoid piceatannol, epigallocatechin-3-gallate, and alkaloid polyphenol berberine with SIRT1. Furthermore, individuals with SIRT1 single-nucleotide polymorphisms (SNPs) may be more sensitive to HFD and may develop more serious hepatic steatosis, which explains why people with SIRT1 mutations have a higher morbidity of hepatic steatosis . According to the current study, those individuals may also be more sensitive to a dietary polyphenol treatment.…”

Section: Discussionmentioning

confidence: 78%

The Ameliorating Effects of Apple Polyphenol Extract on High-Fat-Diet-Induced Hepatic Steatosis Are SIRT1-Dependent: Evidence from Hepatic-Specific SIRT1 Heterozygous Mutant C57BL/6 Mice

Yin

Liu

et al. 2022

J. Agric. Food Chem.

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Apple polyphenol extract (APE) has been reported to possess protective effects against hepatic steatosis. To explore whether APE-induced alleviation of hepatic steatosis is SIRT1-dependent, the present study was carried out using wild-type and hepatic SIRT1 heterozygous mutant (Sirt1+/–) C57BL/6 mice. On consideration of the sex disparity related to hepatic steatosis morbidity, both male and female mice were included in the study. Six to eight week old mice were fed a high-fat diet (HFD) and randomly assigned to one of the following groups: (1) wild-type mice (wt+HFD), (2) Sirt1+/– mice (Sirt1+/–+HFD), and (3) Sirt1+/– mice with 500 mg/(kg·bw·d) APE intragastric administration (Sirt1+/–+HAP). HFD-induced weight gain and triglyceride accumulation was more prominent in Sirt1+/– mice in comparison to wild-type mice. Following APE treatment, these effects were significantly reduced along with the alleviation of hepatic steatosis via upregulated expression of SIRT1 at the protein and mRNA levels in both male and female mice. However, APE differentially regulated the genes related to lipid metabolism (Lkb1, Ampk, Hsl, Srebp-1c, Abcg1, and Cd36) in a sex-specific manner. Moreover, APE treatment altered gut microbiota composition, with an increased relative abundance of Akkermansia and a decreased Firmicutes/Bacterodetes ratio. Thus, our study provided new evidence supporting our hypothesis that APE-induced alleviation of hepatic steatosis is SIRT1-dependent.

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Section: Discussionmentioning

confidence: 78%

The Ameliorating Effects of Apple Polyphenol Extract on High-Fat-Diet-Induced Hepatic Steatosis Are SIRT1-Dependent: Evidence from Hepatic-Specific SIRT1 Heterozygous Mutant C57BL/6 Mice

Yin

Liu

et al. 2022

J. Agric. Food Chem.

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“…60–62 Interestingly, serum SIRT1 was downregulated in AFLD patients compared with healthy controls. 63 Moreover, the mRNA level of Sirt1 was also lower in an AFLD group compared to a control group. 63 Our study shows that C3d, CYP2E1 and Gly-tRF are upregulated, but that Sirt1 is downregulated, in AFLD patients compared to healty controls.…”

Section: Discussionmentioning

confidence: 94%

“…63 Moreover, the mRNA level of Sirt1 was also lower in an AFLD group compared to a control group. 63 Our study shows that C3d, CYP2E1 and Gly-tRF are upregulated, but that Sirt1 is downregulated, in AFLD patients compared to healty controls. These results are consistent with previous preclinical studies, indicating a potential therapeutic strategy for AFLD.…”

Section: Discussionmentioning

confidence: 94%

Complement C3 activation regulates the production of tRNA-derived fragments Gly-tRFs and promotes alcohol-induced liver injury and steatosis

Zhong

Jiang

et al. 2019

Cell Res

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Complement is known to play a role in alcoholic fatty liver disease (AFLD), but the underlying mechanisms are poorly understood, thereby constraining the development of a rational approach for therapeutic intervention in the complement system. C3 deficiency has been shown to impart protective effects against ethanol-induced hepatic steatosis and inflammation. Here we demonstrate a protection effect in wild-type mice by treatment with CR2-Crry, a specific inhibitor of C3 activation. The expression of glycine transfer (t) RNA-derived fragments (Gly-tRFs) is upregulated in ethanol-fed mice and inhibition of Gly-tRFs in vivo decreases chronic ethanol feeding-induced hepatosteatosis without affecting inflammation. The expression of Gly-tRF was downregulated in C3-deficient or CR2-Crry-treated mice, but not in C5-deficient mice; Gly-tRF expression was restored by the C3 activation products C3a or Asp (C3a-des-Arg) via the regulation of CYP2E1. Transcriptome profiling of hepatic tissues showed that Gly-tRF inhibitors upregulate the expression of sirtuin1 (Sirt1) and subsequently affect downstream lipogenesis and β-oxidation pathways. Mechanistically, Gly-tRF interacts with AGO3 to downregulate Sirt1 expression via sequence complementarity in the 3′ UTR. Notably, the expression levels of C3d, CYP2E1 and Gly-tRF are upregulated, whereas Sirt1 is decreased in AFLD patients compared to healthy controls. Collectively, our findings suggest that C3 activation products contribute to hepatosteatosis by regulating the expression of Gly-tRF. Complement inhibition at the C3 activation step and treatment with Gly-tRF inhibitors may be potential and precise therapeutic approaches for AFLD.

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“…Recently, a large case-control multicenter study conducted in China showed that both the allele and genotype frequencies of rs738409 in the PNPLA3 gene were significantly associated with ALD ( P = 6.25 × 10 -14 and P = 9.05 × 10 -13 )[46]. In addition, a polymorphism in the silent mating type information regulation 2 homolog 1 ( SIRT1 ) gene was associated with alcoholic fatty liver disease (AFLD) in the Han population[47].…”

Section: Risk Factors For Ald In Chinamentioning

confidence: 99%

Growing burden of alcoholic liver disease in China: A review

Wang

Xiao

et al. 2019

WJG

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Explosive economic growth and increasing social openness in China over the last 30 years have significantly boosted alcohol consumption, and consequently, the incidence of alcoholic liver disease (ALD) in China has increased. Because the epidemiologic and clinical features of ALD in the Chinese population may differ from those of the Caucasian population, this review describes the epidemiology, pathogenesis, genetic polymorphisms, diagnosis, and treatment of ALD in the Chinese population. This updated knowledge of ALD in China provides information needed for a global understanding of ALD and may help in the development of useful strategies for reducing the global ALD burden.

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Association of SIRT1 gene polymorphism and its expression for the risk of alcoholic fatty liver disease in the Han population

Abstract: SIRT1 polymorphisms and their expression were associated with the presence of AFLD, and there was a close relationship among four SNPs and BMI in AFLD patients, but no SNP was related to its expression.

Cited by 11 publications

References 33 publications

The Ameliorating Effects of Apple Polyphenol Extract on High-Fat-Diet-Induced Hepatic Steatosis Are SIRT1-Dependent: Evidence from Hepatic-Specific SIRT1 Heterozygous Mutant C57BL/6 Mice

The Ameliorating Effects of Apple Polyphenol Extract on High-Fat-Diet-Induced Hepatic Steatosis Are SIRT1-Dependent: Evidence from Hepatic-Specific SIRT1 Heterozygous Mutant C57BL/6 Mice

Complement C3 activation regulates the production of tRNA-derived fragments Gly-tRFs and promotes alcohol-induced liver injury and steatosis

Growing burden of alcoholic liver disease in China: A review

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