scholarly journals The Effects of Butyrate on Induced Metabolic-Associated Fatty Liver Disease in Precision-Cut Liver Slices

Nutrients ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 4203
Author(s):  
Grietje H. Prins ◽  
Melany Rios-Morales ◽  
Albert Gerding ◽  
Dirk-Jan Reijngoud ◽  
Peter Olinga ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Type I Collagen ◽  
Smooth Muscle Actin ◽  
Liver Steatosis ◽  
Acid Oxidation ◽  
Type I ◽  
Triglyceride Accumulation ◽  
Liver Slices

Metabolic-associated fatty liver disease (MAFLD) starts with hepatic triglyceride accumulation (steatosis) and can progress to more severe stages such as non-alcoholic steatohepatitis (NASH) and even cirrhosis. Butyrate, and butyrate-producing bacteria, have been suggested to reduce liver steatosis directly and systemically by increasing liver β-oxidation. This study aimed to examine the influence of butyrate directly on the liver in an ex vivo induced MAFLD model. To maintain essential intercellular interactions, precision-cut liver slices (PCLSs) were used. These PCLSs were prepared from male C57BL/6J mice and cultured in varying concentrations of fructose, insulin, palmitic acid and oleic acid, to mimic metabolic syndrome. Dose-dependent triglyceride accumulation was measured after 24 and 48 h of incubation with the different medium compositions. PCLSs viability, as indicated by ATP content, was not affected by medium composition or the butyrate concentration used. Under induced steatotic conditions, butyrate did not prevent triglyceride accumulation. Moreover, it lowered the expression of genes encoding for fatty acid oxidation and only increased C4 related carnitines, which indicate butyrate oxidation. Nevertheless, butyrate lowered the fibrotic response of PCLSs, as shown by reduced gene expression of fibronectin, alpha-smooth muscle actin and osteopontin, and protein levels of type I collagen. These results suggest that in the liver, butyrate alone does not increase lipid β-oxidation directly but might aid in the prevention of MAFLD progression to NASH and cirrhosis.

scholarly journals Expression of genes encoding mitochondrial proteins can distinguish nonalcoholic steatosis from steatohepatitis.

2007 ◽  
Vol 54 (2) ◽  
pp. 341-348 ◽  
Author(s):  
Piotr Bragoszewski ◽  
Andrzej Habior ◽  
Bozena Walewska-Zielecka ◽  
Jerzy Ostrowski
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Expression Profiles ◽  
Liver Steatosis ◽  
Mitochondrial Proteins ◽  
Morphological Examination ◽  
Nonalcoholic Fatty Liver ◽  
Triglyceride Accumulation ◽  
Genes Encoding

In patients without substantial alcohol use, triglyceride accumulation in the liver can lead to nonalcoholic fatty liver disease (NAFLD) that may progress to nonalcoholic steatohepatitis (NASH). The differential diagnosis between NAFLD and NASH can be accomplished only by morphological examination. Although the relationship between mitochondrial dysfunction and the progression of liver pathologic changes has been described, the exact mechanisms initiating primary liver steatosis and its progression to NASH are unknown. We selected 16 genes encoding mitochondrial proteins which expression was compared by quantitative RT-PCR in liver tissue samples taken from patients with NAFLD and NASH. We found that 6 of the 16 examined genes were differentially expressed in NAFLD versus NASH patients. The expression of hepatic HK1, UCP2, ME2, and ME3 appeared to be higher in NASH than in NAFLD patients, whereas HMGCS2 and hnRNPK expression was lower in NASH patients. Although the severity of liver morphological injury in the spectrum of NAFLD-NASH may be defined at the molecular level, expression of these selected 6 genes cannot be used as a molecular marker aiding histological examination. Moreover, it is still unclear whether these differences in hepatic gene expression profiles truly reflect the progression of morphological abnormalities or rather indicate various metabolic and hormonal states in patients with different degrees of fatty liver disease.

Natural Aldose Reductase Inhibitor: A Potential Therapeutic Agent for Non-alcoholic Fatty Liver Disease

2020 ◽  
Vol 21 (6) ◽  
pp. 599-609 ◽  
Author(s):  
Longxin Qiu ◽  
Chang Guo
Keyword(s):  
Oxidative Stress ◽  
Liver Disease ◽  
Fatty Liver ◽  
Aldose Reductase ◽  
Fatty Liver Disease ◽  
Acid Oxidation ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Alcoholic Fatty Liver ◽  
Nonalcoholic Fatty Liver

Aldose reductase (AR) has been reported to be involved in the development of nonalcoholic fatty liver disease (NAFLD). Hepatic AR is induced under hyperglycemia condition and converts excess glucose to lipogenic fructose, which contributes in part to the accumulation of fat in the liver cells of diabetes rodents. In addition, the hyperglycemia-induced AR or nutrition-induced AR causes suppression of the transcriptional activity of peroxisome proliferator-activated receptor (PPAR) α and reduced lipolysis in the liver, which also contribute to the development of NAFLD. Moreover, AR induction in non-alcoholic steatohepatitis (NASH) may aggravate oxidative stress and the expression of inflammatory cytokines in the liver. Here, we summarize the knowledge on AR inhibitors of plant origin and review the effect of some plant-derived AR inhibitors on NAFLD/NASH in rodents. Natural AR inhibitors may improve NAFLD at least in part through attenuating oxidative stress and inflammatory cytokine expression. Some of the natural AR inhibitors have been reported to attenuate hepatic steatosis through the regulation of PPARα-mediated fatty acid oxidation. In this review, we propose that the natural AR inhibitors are potential therapeutic agents for NAFLD.

Non-Invasive Approaches to Estimate Liver Steatosis and Stiffness in Children with Non-Alcoholic Fatty Liver Disease

2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Toshifumi Yodoshi ◽  
Sarah Orkin ◽  
Andrew T. Trout ◽  
Ana Catalina Arce-Clachar ◽  
Kristin Bramlage ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Liver Steatosis ◽  
Alcoholic Fatty Liver ◽  
Non Invasive ◽  
Alcoholic Fatty Liver Disease

Relationship of serum vaspin, nafld fibrosis score to ultrasonographic detection and quantification of steatosis in nonalcoholic fatty liver disease patients

QJM ◽  
2021 ◽  
Vol 114 (Supplement_1) ◽  
Author(s):  
Essam Mohamed Byoumy ◽  
Moataz Mohamed Sayed ◽  
Shereen Abo Baker Abd El-Rahman ◽  
Sara Abd Elkader Al-Nakib ◽  
Mohamed Magdy Salama ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Liver Steatosis ◽  
Control Group ◽  
P Value ◽  
Fibrosis Score ◽  
Alcoholic Fatty Liver ◽  
Nafld Fibrosis Score ◽  
Detection And Quantification

Abstract Background Ectopic hepatic lipid accumulation is closely related to the development of insulin resistance, which is regarded as one of the most significant risk factors of non-alcoholic fatty liver disease (NAFLD). The aim of the study was to evaluate and validate the diagnostic value of serum vaspin, NAFLD Fibrosis Score and sonograghic parameters in detection and quantification of liver steatosis and determining further need for liver biopsy or other means to establish NAFLD diagnosis. Methods This study was carried out on 60 patients having bright liver in ultrasonography and 30 healthy persons as controls. The subjects were divided into the following groups; group A: 30 age and sex matched healthy volunteers (control group), group B: 20 patients with fatty liver grade I, group C: 20 patients with fatty liver grade II and group D: 20 patients with fatty liver grade III. Results serum vaspine levels and NAFLD fibrosis score, were significantly higher in patients than in controls with p-value:<0.001. There was a significant positive correlation between NAFLD fibrosis score and serum vaspin and ultrasonographic findngs of NAFLD with p-value: <0.001. Conclusion Vaspin seem to be the most suitable non-invasive biomarker in predicting both intrahepatic lipid contents in NAFLD group.

scholarly journals Sex Dimorphism of Nonalcoholic Fatty Liver Disease (NAFLD) in Pparg-Null Mice

2021 ◽  
Vol 22 (18) ◽  
pp. 9969
Author(s):  
Mariano Schiffrin ◽  
Carine Winkler ◽  
Laure Quignodon ◽  
Aurélien Naldi ◽  
Martin Trötzmüller ◽  
...  
Keyword(s):  
Gene Expression ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Molecular Mechanisms ◽  
Liver Steatosis ◽  
Whole Body ◽  
Sex Dimorphism ◽  
Nonalcoholic Fatty Liver

Men with nonalcoholic fatty liver disease (NAFLD) are more exposed to nonalcoholic steatohepatitis (NASH) and liver fibrosis than women. However, the underlying molecular mechanisms of NALFD sex dimorphism are unclear. We combined gene expression, histological and lipidomic analyses to systematically compare male and female liver steatosis. We characterized hepatosteatosis in three independent mouse models of NAFLD, ob/ob and lipodystrophic fat-specific (PpargFΔ/Δ) and whole-body PPARγ-null (PpargΔ/Δ) mice. We identified a clear sex dimorphism occurring only in PpargΔ/Δ mice, with females showing macro- and microvesicular hepatosteatosis throughout their entire life, while males had fewer lipid droplets starting from 20 weeks. This sex dimorphism in hepatosteatosis was lost in gonadectomized PpargΔ/Δ mice. Lipidomics revealed hepatic accumulation of short and highly saturated TGs in females, while TGs were enriched in long and unsaturated hydrocarbon chains in males. Strikingly, sex-biased genes were particularly perturbed in both sexes, affecting lipid metabolism, drug metabolism, inflammatory and cellular stress response pathways. Most importantly, we found that the expression of key sex-biased genes was severely affected in all the NAFLD models we tested. Thus, hepatosteatosis strongly affects hepatic sex-biased gene expression. With NAFLD increasing in prevalence, this emphasizes the urgent need to specifically address the consequences of this deregulation in humans.

FRI-317-Progression of fatty liver disease to steatohepatitis and liver fibrosis is associated with altered Oncostatin M type I and type II receptor expression

2019 ◽  
Vol 70 (1) ◽  
pp. e536
Author(s):  
Philipp Lederer ◽  
Martin Roderfeld ◽  
Daniela Kroy ◽  
Elke Roeb ◽  
Andreas Geier ◽  
...  
Keyword(s):  
Liver Disease ◽  
Liver Fibrosis ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Receptor Expression ◽  
Oncostatin M ◽  
Type I ◽  
Type Ii
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