Lipid metabolism disorders are the primary causes for the occurrence and progression of various liver diseases, including non-alcoholic fatty liver disease (NAFLD) and alcoholic fatty liver disease (AFLD) caused by a high-fat diet and ethanol. AMPK signaling pathway plays an important role in ameliorating lipid metabolism disorders. Progressive research has clarified that AMPK signal axes are involved in the prevention and reduction of liver injury. Upregulation of AMK can alleviate FLD in mice induced by alcohol or insulin resistance, type 2 diabetes, and obesity, and most natural AMPK agonists can regulate lipid metabolism, inflammation, and oxidative stress in hepatocytes, consequently regulating FLD in mice. In NAFLD and AFLD, increasing the activity of AMPK can inhibit the synthesis of fatty acids and cholesterol by down-regulating the expression of adipogenesis gene (FAS, SREBP-1c, ACC and HMGCR); Simultaneously, by increasing the expression of fatty acid oxidation and lipid decomposition genes (CPT1, PGC1, and HSL, ATGL) involved in fatty acid oxidation and lipid decomposition, the body’s natural lipid balance can be maintained. At present, some AMPK activators are thought to be beneficial during therapeutic treatment. Therefore, activation of AMPK signaling pathway is a potential therapeutic target for disorders of the liver. We summarized the most recent research on the role of the AMPK pathway in FLD in this review. Simultaneously, we performed a detailed description of each signaling axis of the AMPK pathway, as well as a discussion of its mechanism of action and therapeutic significance.

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Diallyl disulfide (DADS) is one of the primary components of garlic and it exhibits a broad range of biological activities. In the present study, the effects of DADS on lipid metabolism and its potential role in the modulation of the gut microbiome were determined. Hematoxylin and eosin and oil-red O staining were used to assess the liver and intestinal tissues of mice treated with DADS. The expression of lipid metabolism-associated genes was measured using reverse transcription-quantitative PCR (RT-qPCR). The effects of DADS on the gut microbiome were measured using 16S recombinant (r)DNA gene analysis. The results revealed that the serum non-esterified free fatty acids, high density lipopro-tein-cholesterol, low density lipoprotein-cholesterol, serum total cholesterol, liver triglyceride and total cholesterol levels of the mice fed with a low-dose of DADS was significantly higher when compared with the control. Hematoxylin and eosin and oil-red O staining demonstrated that DADS induced fatty liver in mice. The results of the RT-qPCR revealed that the expression levels of a number of lipid metabolism-associated genes were altered in the livers of mice treated with DADS.The 16S rDNA gene analysis demonstrated that the mice fed on a normal diet treated with a low-dose of DADS had decreased levels of bacteria from the Bacteroidetes phyla and increased levels of bacteria from the Firmicutes phyla. The Kyoto Encyclopedia of Genes and Genomes pathway analysis revealed the top 20 pathways enriched in the low-dose DADS group of mice fed with a normal diet. In the present study, low-dose DADS induced fatty liver and altered the gut micro-biota, similar to the phenotype induced by a high fat diet, by regulating the expression of lipid metabolism associated genes.

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To date, the coronavirus disease 2019 (COVID‐19) has a worldwide distribution. Risk factors for mortality in critically ill patients, especially detailed self‐evaluation indicators and laboratory‐examination indicators, have not been well described. In this paper, a total of 192 critically ill patients (142 were discharged and 50 died in the hospital) with COVID‐19 were included. Self‐evaluation indicators including demographics, baseline characteristics and symptoms and detailed lab‐examination indicators were extracted. Data were first compared between survivors and non‐survivors. Multivariate pattern analysis (MVPA) was performed to identify possible risk factors for mortality of COVID‐19 patients. MVPA achieved a relatively high classification accuracy of 93% when using both self‐evaluation indicators and laboratory‐examination indicators. Several self‐evaluation factors related to COVID‐19 were highly associated with mortality, including age, duration (time from illness onset to admission), and the Barthel index score. When the duration, age and Barthel index increased by one day, one year and one point, the mortality increased by 3.6%, 2.4% and 0.9% respectively. Laboratory‐examination indicators including C‐reactive protein (CRP), white blood cell (WBC) count, platelet count, fibrin degradation products (FDP), oxygenation index (OI), lymphocyte count and D‐dimer were also risk factors. Among them, duration was the strongest predictor of all‐cause mortality. Several self‐evaluation indicators that can simply be obtained by questionnaires and without clinical examination were the risk factors of all‐cause mortality in critically ill COVID‐19 patients. The prediction model can be used by individuals to improve health awareness, and by clinicians to identify high‐risk individuals. This article is protected by copyright. All rights reserved.