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Condition: Alcoholism

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Total 251 results found since Jan 2013.

miR-192-5p regulates lipid synthesis in non-alcoholic fatty liver disease through SCD-1.
CONCLUSION: This study demonstrates that miR-192-5p has a negative regulatory role in lipid synthesis, which is mediated through its direct regulation of SCD-1. PMID: 29290651 [PubMed - in process]
Source: World Journal of Gastroenterology : WJG - December 14, 2017 Category: Gastroenterology Authors: Liu XL, Cao HX, Wang BC, Xin FZ, Zhang RN, Zhou D, Yang RX, Zhao ZH, Pan Q, Fan JG Tags: World J Gastroenterol Source Type: research

Omega-3 polyunsaturated fatty acids protect human hepatoma cells from developing steatosis through FFA4 (GPR120)
Publication date: Available online 7 November 2017 Source:Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids Author(s): Saeromi Kang, Jin Huang, Bo-Kyung Lee, Young-Suk Jung, Eunok Im, Jung-Min Koh, Dong-Soon Im Protective effect of omega-3 polyunsaturated fatty acids (n-3 PUFA) on non-alcoholic fatty liver disease has been demonstrated. FFA4 (also known as GPR120; a G protein-coupled receptor) has been suggested to be a target of n-3 PUFA. FFA4 expression in hepatocytes has also been reported from liver biopsies in child fatty liver patients. In order to assess the functional role of FFA4 in hepat...
Source: Biochimica et Biophysica Acta (BBA) Molecular and Cell Biology of Lipids - November 8, 2017 Category: Lipidology Source Type: research

Omega-3 polyunsaturated fatty acids protect human hepatoma cells from developing steatosis through FFA4 (GPR120).
Abstract Protective effect of omega-3 polyunsaturated fatty acids (n-3 PUFA) on non-alcoholic fatty liver disease has been demonstrated. FFA4 (also known as GPR120; a G protein-coupled receptor) has been suggested to be a target of n-3 PUFA. FFA4 expression in hepatocytes has also been reported from liver biopsies in child fatty liver patients. In order to assess the functional role of FFA4 in hepatic steatosis, we used an in vitro model of liver X receptor (LXR)-mediated hepatocellular steatosis. FFA4 expression was confirmed in Hep3B and HepG2 human hepatoma cells. T0901317 (a specific LXR activator) induced lip...
Source: Biochimica et Biophysica Acta - November 7, 2017 Category: Biochemistry Authors: Kang S, Huang J, Lee BK, Jung YS, Im E, Koh JM, Im DS Tags: Biochim Biophys Acta Source Type: research

CREB Protein Mediates Alcohol ‐Induced Circadian Disruption and Intestinal Permeability
ConclusionsTaken together, these data suggest that strategies to reduce alcohol‐induced oxidative stress may alleviate alcohol‐mediated circadian disruption and intestinal leakiness, critical drivers of ALD. CREB Mediates Alcohol‐Induced Circadian Disruption and Intestinal Permeability (A) CLOCK and BMAL1 initiate the transcription of circadian clock genes like PER2. PER2 forms a heterodimer with CRY1 inhibiting clock gene expression. This process takes approximately 24 h. (B) We hypothesize that Cyp2e1‐mediated alcohol metabolism activates cAMP response element‐binding (CREB) protein to induce circadian gene e...
Source: Alcoholism: Clinical and Experimental Research - October 30, 2017 Category: Addiction Authors: Booker T Davis, Robin M. Voigt, Maliha Shaikh, Christopher B. Forsyth, Ali Keshavarzian Tags: Original Article Source Type: research

PKC δ Silencing Alleviates Saturated Fatty Acid-Induced ER Stress by Enhancing SERCA Activity.
Conclusion : To the best of our knowledge, this is the first report demonstrating that the inhibition of PKCδ alleviates ERS by enhancing SERCA activity and stabilizing calcium homeostasis. PMID: 29046367 [PubMed - as supplied by publisher]
Source: Bioscience Reports - October 18, 2017 Category: Biomedical Science Authors: Lai S, Li Y, Kuang Y, Cui H, Yang Y, Sun W, Liu K, Chen D, Yan Q, Wen L Tags: Biosci Rep Source Type: research

CREB Mediates Alcohol-Induced Circadian Disruption and Intestinal Permeability.
CONCLUSIONS: Taken together, these data suggest that strategies to reduce alcohol-induced oxidative stress may alleviate alcohol mediated circadian disruption and intestinal leakiness, critical drivers of ALD. This article is protected by copyright. All rights reserved. PMID: 28960346 [PubMed - as supplied by publisher]
Source: Alcoholism, Clinical and Experimental Research - September 27, 2017 Category: Addiction Authors: Davis BT, Voigt RM, Shaikh M, Forsyth CB, Keshavarzian A Tags: Alcohol Clin Exp Res Source Type: research

MiR ‐21‐mediated suppression of Smad7 induces TGFβ1 and can be inhibited by activation of Nrf2 in alcohol‐treated lung fibroblasts
ConclusionsAlcohol treatment increases TGFβ1 in fibroblasts, at least in part, through augmentation of miR‐21, which then inhibits Smad7 expression. These effects can be attenuated by activation of Nrf2 with SFP.This article is protected by copyright. All rights reserved.
Source: Alcoholism: Clinical and Experimental Research - September 9, 2017 Category: Addiction Authors: Lucian T. Marts, David E. Green, Stephen T. Mills, Tamara Murphy, Viranuj Sueblinvong Tags: Original Research Article Source Type: research

MiR-21-mediated suppression of Smad7 induces TGF β1 and can be inhibited by activation of Nrf2 in alcohol-treated lung fibroblasts.
CONCLUSIONS: Alcohol treatment increases TGFβ1 in fibroblasts, at least in part, through augmentation of miR-21, which then inhibits Smad7 expression. These effects can be attenuated by activation of Nrf2 with SFP. This article is protected by copyright. All rights reserved. PMID: 28888052 [PubMed - as supplied by publisher]
Source: Alcoholism, Clinical and Experimental Research - September 9, 2017 Category: Addiction Authors: Marts LT, Green DE, Mills ST, Murphy T, Sueblinvong V Tags: Alcohol Clin Exp Res Source Type: research

CREB Mediates Alcohol ‐Induced Circadian Disruption and Intestinal Permeability
ConclusionsTaken together, these data suggest that strategies to reduce alcohol‐induced oxidative stress may alleviate alcohol mediated circadian disruption and intestinal leakiness, critical drivers of ALD.This article is protected by copyright. All rights reserved.
Source: Alcoholism: Clinical and Experimental Research - September 1, 2017 Category: Addiction Authors: Booker T Davis, Robin M. Voigt, Maliha Shaikh, Christopher B. Forsyth, Ali Keshavarzian Tags: Original Research Article Source Type: research

Apelin protects against liver X receptor-mediated steatosis through AMPK and PPAR α in human and mouse hepatocytes.
Apelin protects against liver X receptor-mediated steatosis through AMPK and PPARα in human and mouse hepatocytes. Cell Signal. 2017 Aug 15;39:84-94 Authors: Huang J, Kang S, Park SJ, Im DS Abstract Non-alcoholic fatty liver disease is the most commonly occurring chronic liver disease, and hepatic steatosis, a condition defined as extensive lipid accumulation in hepatocytes, is associated with liver dysfunction and metabolic diseases, such as, obesity and type II diabetes. Apelin is an adipokine that acts on a G protein-coupled receptor named APJ, and has been established to play pivotal roles in var...
Source: Cellular Signalling - August 15, 2017 Category: Cytology Authors: Huang J, Kang S, Park SJ, Im DS Tags: Cell Signal Source Type: research

Down-regulation of the expression of alcohol dehydrogenase 4 and CYP2E1 by the combination of α-endosulfan and dioxin in HepaRG human cells.
Abstract Pesticides and other persistent organic pollutants are considered as risk factors for liver diseases. We treated the human hepatic cell line HepaRG with both 2,3,7,8 tetrachlorodibenzo-p-dioxin (TCDD) and the organochlorine pesticide, α-endosulfan, to evaluate their combined impact on the expression of hepatic genes involved in alcohol metabolism. We show that the combination of the two pollutants (25nM TCDD and 10μM α-endosulfan) led to marked decreases in the amounts of both the mRNA (up to 90%) and protein (up to 60%) of ADH4 and CYP2E1. Similar results were obtained following 24h or 8days of treatm...
Source: Toxicology in Vitro - June 30, 2017 Category: Toxicology Authors: Attignon EA, Distel E, Le-Grand B, Leblanc AF, Barouki R, de Oliveira E, Aggerbeck M, Blanc EB Tags: Toxicol In Vitro Source Type: research

Nrf2 mediates the protective effects of homocysteine by increasing the levels of GSH content in HepG2 cells.
In conclusion, the antioxidant transcriptional factor Nrf2 was demonstrated to mediate the Hcy‑induced increase in GSH expression levels and cellular protection in HepG2 cells. PMID: 28560453 [PubMed - as supplied by publisher]
Source: Molecular Medicine Reports - June 2, 2017 Category: Molecular Biology Tags: Mol Med Rep Source Type: research

Exploring a common mechanism of alcohol-induced deregulation of RNA Pol III genes in liver and breast cells.
Abstract Alcohol intake is associated with numbers of different human cancers, such as hepatocellular carcinoma (HCC) and breast cancer. However, the molecular mechanism remains to be elucidated. RNA polymerase III-dependent genes (Pol III genes) deregulation elevates cellular production of tRNAs and 5S rRNA, resulting in an increase in translational capacity, which promote cell transformation and tumor formation. To explore a common mechanism of alcohol-associated human cancers, we have comparably analyzed that alcohol causes deregulation of Pol III genes in liver and breast cells. Our results reveal that alcohol...
Source: Gene - May 25, 2017 Category: Genetics & Stem Cells Authors: Yi Y, Huang C, Zhang Y, Tian S, Lei J, Chen S, Shi G, Wu Z, Xia N, Zhong S Tags: Gene Source Type: research

A MicroRNA-124 Polymorphism is Associated with Fracture Healing via Modulating BMP6 Expression
Conclusion: These data proved the expression of miR-124-3p was associated with the healing of metaphysealfracture of distal tibia, and could be recognized as a biomarker to predict the healing of metaphysealfracture of distal tibia.Cell Physiol Biochem 2017;41:2161 –2170
Source: Cellular Physiology and Biochemistry - April 25, 2017 Category: Cytology Source Type: research

SIRT3 Acts As a Negative Regulator of Autophagy Dictating Hepatocyte Susceptibility to Lipotoxicity
Conclusion: our data identified SIRT3 to be a novel negative regulator of autophagy, whose activation by SFAs contributes to lipotoxicity in hepatocytes and suggest that restraining SIRT3 overactivation can be a potential therapeutic choice for the treatment of NAFLD as well as other metabolic disorders, with lipotoxicity being the principal pathomechanism. This article is protected by copyright. All rights reserved.
Source: Hepatology - April 24, 2017 Category: Internal Medicine Authors: Songtao Li, Xiaobing Dou, Hua Ning, Qing Song, Wei Wei, Ximei Zhang, Chen Shen, Jiaxin Li, Changhao Sun, Zhenyuan Song Tags: Steatohepatitis and Metabolic Liver Disease Source Type: research