Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease and is characterized by excessive hepatic lipid accumulation. Many studies have suggested that lipid overload is the key initial factor that contributes to hepatic steatosis. Our previous study indicated that diosgenin (DSG) has a beneficial effect on energy metabolism, but the underlying mechanism remains unclear. Human normal hepatocytes (LO2 cells) were incubated with palmitic acid to establish the cell model of nonalcoholic fatty liver. The effects of DSG on lipid metabolism, glucose uptake and mitochondrial function were evaluated. Furthermore, the mechanism of DSG on oxidative stress, lipid consumption and lipid synthesis in LO2 cells was investigated. The results indicated that palmitic acid induced obvious lipid accumulation in LO2 cells and that DSG treatment significantly reduced the intracellular lipid content. DSG treatment upregulated expression of lipolysis proteins, including phospho-AMP activated protein kinase (p-AMPK), phospho-acetyl-coA carboxylase (p-ACC) and carnitine acyl transferase 1A (CPT-1A), and inhibited expression of lipid synthesis-related proteins, including sterol regulatory element-binding protein 1c (SREBP-1c) and fatty acid synthase (FAS). Additionally, DSG-treated cells displayed a marked improvement in mitochondrial function, with less production of reactive oxygen species and a higher mitochondrial membrane potential compared with the model group. This study suggests that DSG can reduce intracellular lipid accumulation in LO2 cells and that the underlying mechanism may be related to the improving oxidative stress, increasing fatty acid β-oxidation and decreasing lipid synthesis. The above changes might be mediated by the activation of the AMPK/ACC/CPT-1A pathway and inhibition of the SREBP-1c/FAS pathway.

/pdf/diosgenin-ameliorates-palmitic-acid-induced-lipid-2619m5yj1b.pdf

Diosgenin ameliorates palmitic acid-induced lipid accumulation via AMPK/ACC/CPT-1A and SREBP-1c/FAS signaling pathways in LO2 cells

Spirulina platensis polysaccharides attenuate lipid and carbohydrate metabolism disorder in high-sucrose and high-fat diet-fed rats in association with intestinal microbiota.

The RNA-binding protein Apobec1 complementation factor (A1CF) regulates posttranscriptional ApoB mRNA editing, but the range of RNA targets and the long-term effect of altered A1CF expression on liver function are unknown. Here we studied hepatocyte-specific A1cf-transgenic (A1cf+/Tg), A1cf+/Tg Apobec1-/-, and A1cf-/- mice fed chow or high-fat/high-fructose diets using RNA-Seq, RNA CLIP-Seq, and tissue microarrays from human hepatocellular cancer (HCC). A1cf+/Tg mice exhibited increased hepatic proliferation and steatosis, with increased lipogenic gene expression (Mogat1, Mogat2, Cidea, Cd36) associated with shifts in polysomal RNA distribution. Aged A1cf+/Tg mice developed spontaneous fibrosis, dysplasia, and HCC, and this development was accelerated on a high-fat/high-fructose diet and was independent of Apobec1. RNA-Seq revealed increased expression of mRNAs involved in oxidative stress (Gstm3, Gpx3, Cbr3), inflammatory response (Il19, Cxcl14, Tnfα, Ly6c), extracellular matrix organization (Mmp2, Col1a1, Col4a1), and proliferation (Kif20a, Mcm2, Mcm4, Mcm6), and a subset of mRNAs (including Sox4, Sox9, Cdh1) were identified in RNA CLIP-Seq. Increased A1CF expression in human HCC correlated with advanced fibrosis and with reduced survival in a subset with nonalcoholic fatty liver disease. In conclusion, we show that hepatic A1CF overexpression selectively alters polysomal distribution and mRNA expression, promoting lipogenic, proliferative, and inflammatory pathways leading to HCC.

/pdf/apobec1-complementation-factor-overexpression-promotes-ocebijxbss.pdf

Apobec1 complementation factor overexpression promotes hepatic steatosis, fibrosis, and hepatocellular cancer

Mortality and re-admission rates for decompensated acute heart failure (AHF) is increasing overall and risk stratification might be challenging. We sought to evaluate the prognostic role of systemic venous ultrasonography in patients hospitalized for AHF. We prospectively recruited 74 AHF patients with a NT-proBNP level above 500 pg/mL. Then, multi-organ ultrasound assessments (lung, inferior vena cava (IVC), pulsed-wave Doppler (PW-Doppler) of hepatic, portal, intra-renal and femoral veins) were performed at admission, discharge, and follow-up (for 90 days). We also calculated the Venous Excess Ultrasound System (VExUS), a new score of systemic congestion based on IVC dilatation and pulsed-wave Doppler morphology of hepatic, portal and intra-renal veins. An intra-renal monophasic pattern (area under the curve (AUC) 0.923, sensitivity (Sn) 90%, specificity (Sp) 81%, positive predictive value (PPV) 43%, and negative predictive value (NPV) 98%), a portal pulsatility > 50% (AUC 0.749, Sn 80%, Sp 69%, PPV 30%, NPV 96%) and a VExUS score of 3 corresponding to severe congestion (AUC 0.885, Sn 80%, Sp 75%, PPV 33%, and NPV 96%) predicted death during hospitalization. An IVC above 2 cm (AUC 0.758, Sn 93.l% and Sp 58.3) and the presence of an intra-renal monophasic pattern (AUC 0. 834, sensitivity 0.917, specificity 67.4%) in the follow-up visit predicted AHF-related re-admission. Additional scans during hospitalization or the calculation of a VExUS score probably adds unnecessary complexity to the assessment of AHF patients. In conclusion, VExUS score does not contribute to the guidance of therapy or the prediction of complications, compared with the presence of an IVC greater than 2 cm, a venous monophasic intra-renal pattern or a pulsatility > 50% of the portal vein in AHF patients. Early and multidisciplinary follow-up visits remain necessary for the improvement of the prognosis of this highly prevalent disease.

/pdf/usefulness-of-systemic-venous-ultrasound-protocols-in-the-18fduokr.pdf

Usefulness of Systemic Venous Ultrasound Protocols in the Prognosis of Heart Failure Patients: Results from a Prospective Multicentric Study

For many adult human organs, tissue regeneration during chronic disease remains a controversial subject. Regenerative processes are easily observed in animal models, and their underlying mechanisms are becoming well characterized 

Acquisition of epithelial plasticity in human chronic liver disease.

Objectives The aim of this study was to develop and validate a novel risk score to predict in-hospital mortality in patients with acute myocardial infarction (AMI) using the Heart Failure after Acute Myocardial Infarction with Optimal Treatment (HAMIOT) cohort in China. Methods The HAMIOT cohort was a multicenter, prospective, observational cohort of consecutive patients with AMI in China. All participants were enrolled between December 2017 and December 2019. The cohort was randomly assigned (at a proportion of 7:3) to the training and validation cohorts. Logistic regression model was used to develop and validate a predictive model of in-hospital mortality. The performance of discrimination and calibration was evaluated using the Harrell’s c-statistic and the Hosmer-Lemeshow goodness-of-fit test, respectively. The new simplified risk score was validated in an external cohort that included independent patients with AMI between October 2019 and March 2021. Results A total of 12,179 patients with AMI participated in the HAMIOT cohort, and 136 patients were excluded. In-hospital mortality was 166 (1.38%). Ten predictors were found to be independently associated with in-hospital mortality: age, sex, history of percutaneous coronary intervention (PCI), history of stroke, presentation with ST-segment elevation, heart rate, systolic blood pressure, initial serum creatinine level, initial N-terminal pro-B-type natriuretic peptide level, and PCI treatment. The c-statistic of the novel simplified HAMIOT risk score was 0.88, with good calibration (Hosmer–Lemeshow test: P = 0.35). Compared with the Global Registry of Acute Coronary Events risk score, the HAMIOT score had better discrimination ability in the training (0.88 vs. 0.81) and validation (0.82 vs. 0.72) cohorts. The total simplified HAMIOT risk score ranged from 0 to 121. The observed mortality in the HAMIOT cohort increased across different risk groups, with 0.35% in the low risk group (score ≤ 50), 3.09% in the intermediate risk group (50 < score ≤ 74), and 14.29% in the high risk group (score > 74). Conclusion The novel HAMIOT risk score could predict in-hospital mortality and be a valid tool for prospective risk stratification of patients with AMI. Clinical Trial Registration [https://clinicaltrials.gov], Identifier: [NCT03297164].

A Novel Risk Score to Predict In-Hospital Mortality in Patients With Acute Myocardial Infarction: Results From a Prospective Observational Cohort

Erratum. SRY-Box Containing Gene 4 Promotes Liver Steatosis by Upregulation of SREBP-1c. Diabetes 2018;67:2227-2238.

Obesity is usually associated with an increased risk of nonalcoholic fatty liver disease that is characterized by accumulation of excessive triglyceride (TG) in hepatocytes. However, the factors involved in the obesity-induced hepatosteatosis are poorly defined. Here, we report that SRY-box containing gene 4 (Sox4), a transcription factor that regulates cell proliferation and differentiation, plays an important role in hepatic TG metabolism. Sox4 expression levels are markedly upregulated in livers of obese rodents and humans. Adenovirus-medicated overexpression of Sox4 in the livers of lean mice promotes liver steatosis, whereas liver-specific knockdown of Sox4 ameliorates TG accumulation and improves insulin resistance in obese mice. At the molecular level, we show that Sox4 could directly control the transcription of SREBP-1c gene through binding to its proximal promoter region. Thus, we have identified Sox4 as an important component of hepatic TG metabolism.

https://diabetes.diabetesjournals.org/content/diabetes/67/11/2227.full.pdf

SRY-Box Containing Gene 4 Promotes Liver Steatosis by Upregulation of SREBP-1c

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A Novel Risk Score to Predict In-Hospital Mortality in Patients With Acute Myocardial Infarction: Results From a Prospective Observational Cohort

Erratum. SRY-Box Containing Gene 4 Promotes Liver Steatosis by Upregulation of SREBP-1c. Diabetes 2018;67:2227-2238.

SRY-Box Containing Gene 4 Promotes Liver Steatosis by Upregulation of SREBP-1c