Letter to the Editor: Consider More Factors When Studying Risk of Cirrhosis and Hepatocellular Cancer in Patients With Nonalcoholic Fatty Liver Disease

Yang, Naibin; Li, Guoxiang; Chu, Jinguo; Wang, Yun-Jing

doi:10.1002/hep.31075

Cited by 2 publications

(2 citation statements)

References 5 publications

(5 reference statements)

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“…Grade‐based recommendations for surveillance in patients with NASH did not justify a systematic surveillance in NAFLD patients without cirrhosis, as a result of low currently observed incidence of HCC in this setting 103 . Older age, diabetes, advanced fibrosis and obesity are the main risk factors associated with HCC development in NAFLD patients, with or without cirrhosis 104‐106 . In a US multicentre retrospective study, 107 the authors showed that there was significantly more non‐cirrhotic HCC in women than in men.…”

Section: Nash and Hccmentioning

confidence: 99%

“…103 Older age, diabetes, advanced fibrosis and obesity are the main risk factors associated with HCC development in NAFLD patients, with or without cirrhosis. [104][105][106] In a US multicentre retrospective study, 107 the authors showed that there was significantly more non-cirrhotic HCC in women than in men. This may reflect the large number of NAFLD-related HCC in women in the cohort.…”

Section: Na S H and H CCmentioning

confidence: 99%

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Clinical impact of sexual dimorphism in non‐alcoholic fatty liver disease (NAFLD) and non‐alcoholic steatohepatitis (NASH)

Burra

Bizzaro

Gonta

et al. 2021

Liver International

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NAFLD/NASH is a sex‐dimorphic disease, with a general higher prevalence in men. Women are at reduced risk of NAFLD compared to men in fertile age, whereas after menopause women have a comparable prevalence of NAFLD as men. Indeed, sexual category, sex hormones and gender habits interact with numerous NAFLD factors including cytokines, stress and environmental factors and alter the risk profiles and phenotypes of NAFLD. In the present review, we summarized the last findings about the influence of sex on epidemiology, pathogenesis, progression in cirrhosis, indication for liver transplantation and alternative therapies, including lifestyle modification and pharmacological strategies. We are confident that an appropriate consideration of sex, age, hormonal status and sociocultural gender differences will lead to a better understanding of sex differences in NAFLD risk, therapeutic targets and treatment responses and will aid in achieving sex‐specific personalized therapies.

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Section: Nash and Hccmentioning

confidence: 99%

Section: Na S H and H CCmentioning

confidence: 99%

Clinical impact of sexual dimorphism in non‐alcoholic fatty liver disease (NAFLD) and non‐alcoholic steatohepatitis (NASH)

Burra

Bizzaro

Gonta

et al. 2021

Liver International

View full text Add to dashboard Cite

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MCAD activation by empagliflozin promotes fatty acid oxidation and reduces lipid deposition in NASH

Wang

Shen

et al. 2022

Journal of Molecular Endocrinology

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Medium chain acyl-CoA dehydrogenase (MCAD) is one of the significant enzymes involved in β-oxidation of mitochondrial fatty acids. MCAD deficiency affects the β-oxidation of fatty acid and leads to lipid deposition in multiple organs, but little is known about its importance in nonalcoholic steatohepatitis (NASH). Empagliflozin is revealed to effectively improve NASH by increasing research, whereas the specific mechanism still has to explore. Human liver tissues of patients with or without NASH were obtained for proteomic analysis to screen proteins of interest. Db/db mice were given empagliflozin by gavage for 8 weeks. The expression of MCAD and signaling molecules involved in hepatic lipid metabolism were evaluated in human liver, mice and HL7702 cells. We found that the MCAD levels in the liver were significantly reduced in NASH patients compared to patients without NASH. Protein protein interaction (PPI) network analysis showed that MCAD was highly correlated with forkhead box A2 (FOXA2) and protein kinase AMP-activated catalytic subunit alpha (PRKAA). AMPK/FOXA2/MCAD signaling pathway was detected to be inhibited in the liver of NASH patients. Decreased expression of MCAD was also observed in the livers of db/db mice and hepatocyte treated with palmitic acid (PA) and glucose. Of note, empagliflozin could upregulate MCAD expression by activating AMPK/FOXA2 signaling pathway, reduce lipid deposition and improve NASH in vivo and in vitro. This research demonstrated that MCAD is a key player of hepatic lipid deposition and it’s targeting partially corrects NASH. MCAD thus may be a potential therapeutic target for the treatment of NASH.

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Letter to the Editor: Consider More Factors When Studying Risk of Cirrhosis and Hepatocellular Cancer in Patients With Nonalcoholic Fatty Liver Disease

Cited by 2 publications

References 5 publications

Clinical impact of sexual dimorphism in non‐alcoholic fatty liver disease (NAFLD) and non‐alcoholic steatohepatitis (NASH)

Clinical impact of sexual dimorphism in non‐alcoholic fatty liver disease (NAFLD) and non‐alcoholic steatohepatitis (NASH)

MCAD activation by empagliflozin promotes fatty acid oxidation and reduces lipid deposition in NASH

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