59 Hepatic expression of PPARα, PPARγ and SREBP-1 in patients with non-alcoholic fatty liver disease

2005 ◽  
Vol 42 ◽  
pp. 25
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Alcoholic Fatty Liver ◽  
Hepatic Expression ◽  
Alcoholic Fatty Liver Disease

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 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 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.

Abstract 464: Non-alcoholic Fatty Liver Disease Produced by Mas Deficiency in ApoE-KO Mice

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Analina R Silva ◽  
Edenil C Aguilar ◽  
Jacqueline I Alvarez-Leite ◽  
Séio H Santos ◽  
Rosa M Arantes ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Fatty Liver Disease ◽  
Oral Glucose ◽  
Alcoholic Fatty Liver ◽  
Hepatic Expression ◽  
Apoe Ko Mice ◽  
Alcoholic Fatty Liver Disease ◽  
Apoe Ko

The non-alcoholic fatty liver disease (NAFLD) is the hepatic manifestation of metabolic syndrome and recent studies have shown the involvement of the renin-angiotensin system in this pathology. We have previously shown that Mas deficiency in ApoE-KO mice results in a marked increase in hepatic triglyceride and total lipids. However, the role of the Ang-(1-7)/Mas in the NAFLD is still not fully understood. The aim of this study was to evaluate the role of Mas in liver steatosis using a double knockout Mas/ApoE (DKO) mice. C57Bl6, Mas-/- (Mas), ApoE-/- (ApoE), and DKO mice were killed at 20 weeks of age. Mas deficiency in ApoE leads to reduced insulin sensitivity and serum leptin (WT = 2.27 ± 0.73 ng/mL, n =5; Mas = 0.96 ± 0.25 ng/mL, n = 6; ApoE = 0.64 ± 0.05 ng/mL, n = 3; DKO = 0.27 ± 0.05, n = 4). Furthemore, the DKO mice presented decrease hepatic expression of the insulin receptor (WT = 0.739 ± 0.083 AU, n = 6; Mas = 0.567 ± 0.115 AU, n = 6; ApoE = 0.702 ± 0.073 AU, n = 6; DKO = 0.321 ± 0.053 AU, n = 6). The oral glucose tolerance test did not differ between groups, as well as serum insulin levels. The liver levels of lipid peroxidation were increased in DKO (WT = 0.58 ± 0.04 μM/g of protein, n = 6; Mas = 0.74 ± 0.09 μM/g of protein, n = 6; ApoE = 0.56 ± 0.01 μM/g of protein, n = 6; DKO = 0.78 ± 0.08 μM/g of protein, n = 6). Consistent with this alteration, histological analysis showed degenerative changes of DKO hepatocytes associated with macro-and microvesicular steatosis, but with few inflammatory infiltrates. The mechanism involved in the development of hepatic steatosis was assessed by Western blotting using primary antibodies to PPAR-α, LXR, FoxO1 S256, glycogen phosphorylase (GP) and glucose 6-phosphatase (G6Pase). The DKO group showed lower levels of hepatic expression of PPAR-α and phosphorylated FoxO1. In addition, the Mas deficiency in ApoE animals significantly increased the expression of LXR. However, no changes were observed in the hepatic expression of GP and G6Pase. In conclusion, our data show that the Mas modulates the activity of key transcriptional factors in hepatic lipid homeostasis.

Sign in / Sign up

Export Citation Format

Share Document