scholarly journals Nonalcoholic liver disease: review with a focus on risks of progression

2021 ◽  
pp. 167-174
Author(s):  
D. A. Teplyuk ◽  
M. Ch. Semenistaya ◽  
S. M. Sorokoletov ◽  
L. B. Lazebnik ◽  
Ch. S. Pavlov
Keyword(s):  
Liver Disease ◽  
Fatty Liver Disease ◽  
Lipid Droplets ◽  
Nonalcoholic Fatty Liver ◽  
Current Review ◽  
Real World Setting ◽  
Diffi Cult ◽  
Risk Of Progression ◽  
Nonalcoholic Liver Disease ◽  
Prognosis Evaluation

Nonalcoholic fatty liver disease (NAFLD) is a disease which etiology is related to various metabolic, ethnic, genetic and even ecologic factors. Complexity of etiology and multiply pathogenesis ways, leading eventually to the lipid droplets appearance in hepatocytes, infl ammation process and parenchyma fi brosis in liver, and also frequent cardiometabolic comorbidities, together make diffi cult risks stratifi cation and prognosis evaluation in NAFLD patients. Another matter is a question of NAFLD therapy, since unifi ed pharmacotherapy approaches are not yet adopted worldwide, and lifestyle modifi cation being accepted as an eff ective therapeutic approach, is not followed by patients in real world setting. Current review is dedicated to the consideration of NAFLD diagnostics, its risk of progression and existing therapeutical capabilities.

scholarly journals Sheng-Jiang Powder Ameliorates High Fat Diet Induced Nonalcoholic Fatty Liver Disease via Inhibiting Activation of Akt/mTOR/S6 Pathway in Rats

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Juan Li ◽  
Lv Zhu ◽  
Yu-mei Zhang ◽  
Huan Chen ◽  
Yi-fan Miao ◽  
...  
Keyword(s):  
Oleic Acid ◽  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
High Fat Diet ◽  
Fatty Liver Disease ◽  
Lipid Droplets ◽  
Cell Cancer ◽  
High Fat ◽  
Nonalcoholic Fatty Liver

Background and Aims. Nonalcoholic fatty liver disease (NAFLD) is an alarming public health problem that directly contributes to increased prevalence of liver cirrhosis and hepatic cell cancer, but without any specific pharmacological option. Sheng-jiang powder (SJP), an empirical Chinese medicine formula to treat NAFLD, showed great efficacy but the specific mechanisms have never been reported. Therefore, we performed this study to explore the effect of SJP on NAFLD and the potential mechanism.Methods. NAFLD was induced by high fat diet (HFD) feeding. Rats were treated with SJP/normal saline daily for 10 weeks and all rats were euthanized after 12 weeks’ feeding. Liver tissue samples were obtained for biochemistry test and pathological evaluation. Additionally, oleic acid induced LO2 cells were employed to simulate a cell model of NAFLD. Cells were subjected to western blotting for Akt, mTOR, S6, SREBP1-c, and FASN detection after coincubated with SJP, LY294002 (a selective PI3K inhibitor), or the combination for 24h.Results. HFD significantly induced hepatic steatosis. Plenty of lipid droplets were observed under transmission electron microscope. The ultrastructure of liver cells showed distinct changes with obvious endoplasmic reticulum expansion, mitochondrial contraction, and cell matrix solidification. Although no difference was detected in serum hepatic enzymes and tissue proinflammatory cytokines, the tissue level of SOD and GSH-px was much lower and the pathologic injuries were much severe in HFD feeding rats. However, SJP treatment significantly attenuated the ultrastructure changes and protected rat liver against inflammatory injury. Abundant of lipid droplets and high expression of pAkt, pmTOR, pS6, and FASN were observed in oleic acid treated LO2 cells, while these changes were restored by SJP treatment.Conclusions. SJP is efficient in attenuating HFD induced NAFLD in rats and this effect might be partly related to the inhibition of Akt/mTOR/S6 pathway.

Nonalcoholic steatohepatitis

2010 ◽  
pp. 2480-2482
Author(s):  
Stephen F. Stewart ◽  
Chris P. Day
Keyword(s):  
Insulin Resistance ◽  
Metabolic Syndrome ◽  
Liver Disease ◽  
Nonalcoholic Steatohepatitis ◽  
Fatty Liver Disease ◽  
Liver Disorder ◽  
Nonalcoholic Fatty Liver ◽  
The Metabolic Syndrome ◽  
Developed World ◽  
Nonalcoholic Liver Disease

Nonalcoholic fatty liver disease (NAFLD) is the most common liver disorder in the developed world, affecting 20 to 30% of Western adults. Nonalcoholic liver disease occurs with a range of severity from simple steatosis through nonalcoholic steatohepatitis (NASH) to fatty fibrosis—and, ultimately, cirrhosis. The condition is a manifestation of the metabolic syndrome, strongly associated with obesity, insulin resistance, and dyslipidaemia; dietary and genetic factors appear to determine susceptibility to the disease and its progression....

scholarly journals Nonalcoholic Fatty Liver Disease (NAFLD). Mitochondria as Players and Targets of Therapies?

2021 ◽  
Vol 22 (10) ◽  
pp. 5375
Author(s):  
Agostino Di Ciaula ◽  
Salvatore Passarella ◽  
Harshitha Shanmugam ◽  
Marica Noviello ◽  
Leonilde Bonfrate ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Fatty Liver Disease ◽  
Combined Treatment ◽  
Fat Accumulation ◽  
Nonalcoholic Fatty Liver ◽  
Hepatic Expression ◽  
Transport Chain ◽  
Risk Of Progression

Nonalcoholic fatty liver disease (NAFLD) is the most common chronic liver disease and represents the hepatic expression of several metabolic abnormalities of high epidemiologic relevance. Fat accumulation in the hepatocytes results in cellular fragility and risk of progression toward necroinflammation, i.e., nonalcoholic steatohepatitis (NASH), fibrosis, cirrhosis, and eventually hepatocellular carcinoma. Several pathways contribute to fat accumulation and damage in the liver and can also involve the mitochondria, whose functional integrity is essential to maintain liver bioenergetics. In NAFLD/NASH, both structural and functional mitochondrial abnormalities occur and can involve mitochondrial electron transport chain, decreased mitochondrial β-oxidation of free fatty acids, excessive generation of reactive oxygen species, and lipid peroxidation. NASH is a major target of therapy, but there is no established single or combined treatment so far. Notably, translational and clinical studies point to mitochondria as future therapeutic targets in NAFLD since the prevention of mitochondrial damage could improve liver bioenergetics.

scholarly journals The role and possible mechanism of the long noncoding RNA LINC01260 in nonalcoholic fatty liver disease

2022 ◽  
Vol 19 (1) ◽  
Author(s):  
Xiaoxiao Ge ◽  
Tao Sun ◽  
Yanmei Zhang ◽  
Yongqing Li ◽  
Peng Gao ◽  
...  
Keyword(s):  
Liver Disease ◽  
Fatty Liver ◽  
Nonalcoholic Fatty Liver Disease ◽  
Differential Expression ◽  
Fatty Liver Disease ◽  
Lipid Droplets ◽  
Expression Profiles ◽  
Nonalcoholic Fatty Liver ◽  
Oil Red O Staining ◽  
Oil Red O

Abstract Objective To investigate the differential expression profile of lncRNAs in the nonalcoholic fatty liver disease (NAFLD) model induced by oleic acid (OA) and to further explore the role of LINC01260 (ENST00000255183) in NAFLD, providing theoretical support for the clinical value of lncRNAs in NAFLD. Methods OA (50 μg/mL) was used to induce steatosis in normal human LO2 hepatocytes for 48 h and was verified by Oil red O staining. Differential expression profiles of lncRNAs were obtained by eukaryotic circular sequencing (RNA/lncRNA/circRNA-seq) techniques. A gain-of-function (GOF) strategy for LINC01260 was adopted, Oil red O staining and semiquantitative analysis were combined to explore whether the GOF of LINC01260 affects LO2 cell steatosis. CeRNA-based bioinformatics analysis of lncRNAs was performed, and the enriched mRNAs were further verified. RXRB siRNAs were applied and verify its role in LINC01260 regulated OA-induced hepatocytes steatosis. Results Lipid droplets of different sizes were observed in the cells of the OA group. Absorbance in the OA group was significantly increased after isopropanol decolorization (P < 0.05). Compared with those in the control group, there were 648 lncRNAs with differential expression greater than 1 time in the OA group, of which 351 were upregulated and 297 were downregulated. Fluorescence quantitative PCR showed that the expression of LINC01260 in the OA group was downregulated by 0.35 ± 0.07-fold (P < 0.05). The formation of lipid droplets in LO2 cells of the LINC01260 GOF group decreased significantly (P < 0.05). CeRNA analysis indicated that the mRNA levels of RXRB, RNPEPL1, CD82, MADD and KLC2 were changed to different degrees. Overexpression of LINC01260 significantly induced RXRB transcription (P < 0.05) and translation, and RXRB silence attenuated the lipids decrease induced by LINC01260 overexpression. Conclusion The OA-induced NAFLD cell model has a wide range of lncRNA differential expression profiles. LINC01260 participates in the regulation of the lipid droplet formation process of NAFLD, and its overexpression can significantly inhibit the steatosis process of LO2 cells. Mechanistically, LINC01260 may act as a ceRNA to regulate the expression of RXRB, thereby affecting the adipocytokine signaling pathway.

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