scholarly journals Leptin administration restores the altered adipose and hepatic expression of aquaglyceroporins improving the non-alcoholic fatty liver of ob/ob mice

2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Amaia Rodríguez ◽  
Natalia R. Moreno ◽  
Inmaculada Balaguer ◽  
Leire Méndez-Giménez ◽  
Sara Becerril ◽  
...  
Keyword(s):  
Fatty Liver ◽  
Alcoholic Fatty Liver ◽  
Hepatic Expression

HEPATIC EXPRESSION OF CYCLOOXYGENASE-2 IN NON-ALCOHOLIC FATTY LIVER DISEASE

2008 ◽  
Vol 19 ◽  
pp. S42
Author(s):  
L. Giannitrapani ◽  
S. Ingrao ◽  
M. Soresi ◽  
S. Petta ◽  
A.M. Florena ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Cyclooxygenase 2 ◽  
Alcoholic Fatty Liver ◽  
Hepatic Expression ◽  
Alcoholic Fatty Liver Disease

scholarly journals Metabolic Syndrome and Nonalcoholic Fatty Liver Disease

2019 ◽  
Vol 16 (1) ◽  
pp. 51-58
Author(s):  
Oana Irina Gavril ◽  
Lidia Iuliana Arhire ◽  
Ovidiu Mitu ◽  
Radu Sebastian Gavril ◽  
Alexandra Mastaleru ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Normal Liver ◽  
Liver Fat ◽  
Equal Distribution ◽  
Alcoholic Fatty Liver ◽  
Hepatic Expression ◽  
The Metabolic Syndrome

AbstractIntroduction. Non-alcoholic fatty liver disease (NAFLD) is regarded as the hepatic expression of the metabolic syndrome, both conditions presenting similar clinical features.Aim. The aim of this study was to evaluate, among diabetic subjects, the relationship between fatty liver load and the presence of metabolic syndrome criteria.Methods. An observational study was conducted on 92 subjects with type 2 diabetes. We followed anthropometric measurments, lipid profile, blood pressure and the degree of hepatic steatosis using ultrasonography.Results. The average age of the study group was 60,38 ± 10,37 years, with an approximately equal distribution by gender (48% male and 52% female). More than half of the subjects presented hypercholesterolemia, hypertriglyceridemia, and low HDL cholesterol level. Most of the patients included in the study had varying degrees of liver fat load (only 9,89% of cases of apparently normal liver on ultrasound), and met the criteria for metabolic syndrome (81,31%). It was found that the frequency of the cases with fatty liver impairment was significantly higher in subjects with metabolic syndrome (32,43% compared to 5,88% for those without metabolic syndrome, p = 0,01) and the frequency of the cases with normal liver were significantly higher in subjects without metabolic syndrome (23,53% to 6,76%, p=0,02).Conclusion. We can say that NAFLD is a risk factor for the presence of metabolic syndrome and it can be considered the hepatic expression of this syndrome.

scholarly journals Obesity-linked suppression of membrane-bound O-acyltransferase 7 (MBOAT7) drives non-alcoholic fatty liver disease

eLife ◽  
2019 ◽  
Vol 8 ◽  
Author(s):  
Robert N Helsley ◽  
Venkateshwari Varadharajan ◽  
Amanda L Brown ◽  
Anthony D Gromovsky ◽  
Rebecca C Schugar ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Dependent Manner ◽  
Loss Of Function ◽  
Alcoholic Fatty Liver ◽  
Hepatic Expression ◽  
Increased Risk ◽  
Membrane Bound ◽  
Alcoholic Fatty Liver Disease

Recent studies have identified a genetic variant rs641738 near two genes encoding membrane bound O-acyltransferase domain-containing 7 (MBOAT7) and transmembrane channel-like 4 (TMC4) that associate with increased risk of non-alcoholic fatty liver disease (NAFLD), non-alcoholic steatohepatitis (NASH), alcohol-related cirrhosis, and liver fibrosis in those infected with viral hepatitis (Buch et al., 2015; Mancina et al., 2016; Luukkonen et al., 2016; Thabet et al., 2016; Viitasalo et al., 2016; Krawczyk et al., 2017; Thabet et al., 2017). Based on hepatic expression quantitative trait loci analysis, it has been suggested that MBOAT7 loss of function promotes liver disease progression (Buch et al., 2015; Mancina et al., 2016; Luukkonen et al., 2016; Thabet et al., 2016; Viitasalo et al., 2016; Krawczyk et al., 2017; Thabet et al., 2017), but this has never been formally tested. Here we show that Mboat7 loss, but not Tmc4, in mice is sufficient to promote the progression of NAFLD in the setting of high fat diet. Mboat7 loss of function is associated with accumulation of its substrate lysophosphatidylinositol (LPI) lipids, and direct administration of LPI promotes hepatic inflammatory and fibrotic transcriptional changes in an Mboat7-dependent manner. These studies reveal a novel role for MBOAT7-driven acylation of LPI lipids in suppressing the progression of NAFLD.

scholarly journals The Role of Fatty Acids in Non-Alcoholic Fatty Liver Disease Progression: An Update

2021 ◽  
Vol 22 (13) ◽  
pp. 6900
Author(s):  
Aleksandra Hliwa ◽  
Bruno Ramos-Molina ◽  
Dariusz Laski ◽  
Adriana Mika ◽  
Tomasz Sledzinski
Keyword(s):  
Fatty Acids ◽  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Public Health Problem ◽  
Major Public Health Problem ◽  
Alcoholic Fatty Liver ◽  
Hepatic Expression ◽  
Depth Analysis ◽  
Alcoholic Fatty Liver Disease

Non-alcoholic fatty liver disease (NAFLD) is a major public health problem worldwide. NAFLD (both simple steatosis and steatohepatitis) is characterized by alterations in hepatic lipid metabolism, which may lead to the development of severe liver complications including cirrhosis and hepatocellular carcinoma. Thus, an exhaustive examination of lipid disorders in the liver of NAFLD patients is much needed. Mass spectrometry-based lipidomics platforms allow for in-depth analysis of lipid alterations in a number of human diseases, including NAFLD. This review summarizes the current research on lipid alterations associated with NAFLD and related complications, with special emphasis on the changes in long-chain and short-chain fatty acids levels in both serum and liver tissue, as well as in the hepatic expression of genes encoding the enzymes catalyzing lipid interconversions.

scholarly journals Coffee Restores Expression of lncRNAs Involved in Steatosis and Fibrosis in a Mouse Model of NAFLD

Nutrients ◽  
2021 ◽  
Vol 13 (9) ◽  
pp. 2952
Author(s):  
Stefania Di Mauro ◽  
Federico Salomone ◽  
Alessandra Scamporrino ◽  
Agnese Filippello ◽  
Filomena Morisco ◽  
...  
Keyword(s):  
Fatty Liver ◽  
Coenzyme A ◽  
Coffee Consumption ◽  
De Novo Lipogenesis ◽  
Standard Diet ◽  
Coffee Intake ◽  
Alcoholic Fatty Liver ◽  
Hepatic Expression ◽  
Mrna Targets ◽  
Decaffeinated Coffee

Background and aim: Coffee intake exerts protective effects against non-alcoholic fatty liver disease (NAFLD), although without fully cleared mechanisms. In this study we aimed to assess whether coffee consumption may influence the expression of long non-coding RNAs (lncRNAs) in the liver. Methods: C57BL/6J mice were fed a 12-week standard diet (SD), high-fat diet (HFD) or HFD plus decaffeinated coffee solution (HFD + coffee). Expression of specific lncRNAs involved in NAFLD was analyzed by real-time PCR. For the most differentially expressed lncRNAs, the analysis was also extended to their mRNA targets. Results: Decaffeinated coffee intake reduced body weight gain, prevented NAFLD, lowered hyperglycemia and hypercholesterolemia. NAFLD was associated with lower hepatic expression of Gm16551, a lncRNA inhibiting de novo lipogenesis, and higher expression of H19, a lncRNA promoting fibrogenesis. Coffee intake restored Gm16551 to levels observed in lean mice and downregulated gene expression of its targets acetyl coenzyme A carboxylase 1 and stearoyl coenzyme A desaturase 1. Furthermore, coffee consumption markedly decreased hepatic expression of H19 and of its target gene collagen alpha-1(I) chain; consistently, in mice fed HFD + coffee liver expression of αSMA protein returned to levels of mice fed SD. Expression of lncRNA involved in circadian clock such as fatty liver-related lncRNA 1 (FLRL1) and fatty liver-related lncRNA 2 (FLRL2) were upregulated by HFD and were also modulated by coffee intake. Conclusion. Hepatoprotective effects of coffee may be depending on the modulation of lncRNAs involved in key pathways of NAFLD onset and progression.

scholarly journals Probiotic Bifidobacterium Lactis V9 attenuates hepatic steatosis and inflammation in rats with non-alcoholic fatty liver disease

2020 ◽  
Author(s):  
Yan Yan ◽  
Chunyan Liu ◽  
Shimin Zhao ◽  
Xinxu Wang ◽  
Jinling Wang ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Hepatic Steatosis ◽  
Fatty Liver Disease ◽  
Inflammatory Responses ◽  
Probiotic Properties ◽  
Bifidobacterium Lactis ◽  
Alcoholic Fatty Liver ◽  
Hepatic Expression ◽  
Alcoholic Fatty Liver Disease

Abstract Both steatosis and inflammation are key pathological events in the progression of non-alcoholic fatty liver disease (NAFLD). Probiotics are beneficial in the prevention and treatment of NAFLD. Bifidobacterium animalis subsp.lactis V9 (V9) is a newly isolated strain with favorable probiotic properties. The study aims to evaluate the effects and mechanisms of V9 on the hepatic steatosis and inflammatory responses in a rat model of NAFLD induced by high-fat diets (HFD). Our results showed that administration with V9 significantly attenuated HFD-induced increases in the levels of alanine transaminase (ALT) and aspartate aminotransferase (AST), accompanied by alleviated hepatic steatosis. V9 supplementation decreased the accumulation of hepatic triglyceride (TG) and free fatty acid (FFA), while increasing the levels of glycogen. The levels of serum glucose were also decreased in HFD rats administrated with V9. Meanwhile, the transcription of SREBP-1c and FAS was reduced and the hepatic expression of phosphorylated-AMPK and PPAR-α was restored by V9 administration. V9 suppressed the production of inflammatory cytokines (e.g. IL-6, IL-1β, and TNF-α) in HFD-fed rats. The anti-inflammatory effect of V9 was found to be associated with the inhibition of hepatic expression of TLR4, TLR9, NLRP3, and ASC mRNA. Furthermore, the activation of ERK, JNK, AKT and NF-κB was suppressed by V9 treatment. These results indicated that Bifidobacterium Lactis V9 improved NAFLD by regulating de novo lipid synthesis and suppressing inflammation through AMPK and TLR-NF-κB pathways, respectively.

Protective effect of rimonabant, a canabinoid receptor 1 antagonist, on nonalcoholic fatty liver disease in a rat model through modulation of the hepatic expression of activin A and follistatin

2017 ◽  
Vol 95 (12) ◽  
pp. 1433-1441 ◽  
Author(s):  
Noha I. Hussien ◽  
Hanan I. El-kerdasy ◽  
Mohammad El-tantawy Ibrahim
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Transforming Growth Factor ◽  
Histopathological Examination ◽  
Activin A ◽  
Control Group ◽  
Alcoholic Fatty Liver ◽  
Hepatic Expression ◽  
Tgf Β1

Non-alcoholic fatty liver disease (NAFLD) is a major cause of liver morbidity and mortality, and there is still no proven effective therapy. The endocannabinoid system plays an important role in various liver diseases. Activin A is a member of the transforming growth factor beta (TGF-β) superfamily and inhibits hepatocyte growth. Follistatin antagonizes the biological actions of activin A. This study was designed to investigate the effect of rimonabant (a potent cannabinoid receptor1 (CB1) antagonist) on NAFLD induced with a choline-deficient (CD) diet in rats, as well as to detect whether it can alter the hepatic expression of activin A and follistatin. Forty rats were distributed among 4 groups: the control group, the rimonabant treatment group (normal rats that received rimonabant); the CD diet group (NAFLD induced with a CD diet); and the CD diet + rimonabant group (NAFLD treated with rimonabant). It was found that the CD diet caused significant increase in liver index, serum levels of liver enzymes, malondialdehyde (MDA), TGF-β1, activin A, and CB1 expression in liver tissue, with a significant decrease in glutathione peroxidase (GSH-Px) and follistatin mRNA expression in liver tissues. The administration of rimonabant significantly improved all of the studied parameters compared with the group fed the CD diet alone. Histopathological examination supported these results. We concluded that rimonabant significantly counteracted NAFLD induced with the CD diet by decreasing oxidative stress and hepatic expression of TGF-β1, and modulating the hepatic expression of activin A and follistatin.

Sign in / Sign up

Export Citation Format

Share Document