Metabolic basis of ethanol-induced hepatic and pancreatic injury in hepatic alcohol dehydrogenase deficient deer mice

Bhopale, Kamlesh K.; Wu, Haoming; Boor, Paul J.; Popov, Vsevolod L.; Ansari, Ghulam; Kaphalia, Bhupendra S.

doi:10.1016/j.alcohol.2006.09.005

Cited by 49 publications

(86 citation statements)

References 44 publications

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“…Metabolism via CYP2E1 releases free radicals which diminishes defense systems against oxidative stress [34]. Furthermore, non-oxidative metabolism of ethanol to FAEEs, a marker of fat accumulation and organ damage may contribute to pathophysiology of ALD [23].…”

Section: Discussionmentioning

confidence: 99%

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TGF-β enhances alcohol dependent hepatocyte damage via down-regulation of alcohol dehydrogenase I

Ciuclan

Ehnert

Ilkavets

et al. 2010

Journal of Hepatology

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Section: Discussionmentioning

confidence: 99%

“…(Supplementary Fig. 4) [23,24]. TGF-b decreases ADH1 expression in mouse and human hepatocytes as measured by semi-quantitative real-time PCR ( Fig.…”

Section: Tgf-b Decreases Adh1 Expression In Hepatocytesmentioning

confidence: 99%

TGF-β enhances alcohol dependent hepatocyte damage via down-regulation of alcohol dehydrogenase I

Ciuclan

Ehnert

Ilkavets

et al. 2010

Journal of Hepatology

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“…A strain of deer mice (Peromyscus maniculatus) naturally deficient in ADH [180] has been used to study various aspects of ethanol metabolism [181,182]. In animals fed a 4% ethanol diet for 60 days, these studies demonstrated increased nonoxidative metabolism of ethanol to fatty acid ethyl esters in ADH-/-versus WT animals, in addition to increased mortality and histological changes to the liver and pancreas.…”

Section: Adh (Knock-out) Modelsmentioning

confidence: 99%

Utility of Genetically Modified Animal Models for Drug Metabolism and Drug Transporters

Bessire

Youdim

Hurst

et al. 2012

Encyclopedia of Drug Metabolism and Interactions

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Genetically modified animals (GEMA) provide in vivo tools to understand the role of enzymes, transcriptional factors, and transporters in drug disposition and drug toxicities. Several phase I and II enzymes, transcriptional factors, and the clinically relevant drug transporters have been reviewed in this chapter by highlighting how the animal models have elucidated or validated their role in drug disposition, endogenous substrate regulation, or drug toxicities. The utility of animal models in research and drug development provides in vivo tools to gain a better understanding of the role of drug‐metabolizing enzymes, transcriptional factors, and transporters in the absorption, disposition, metabolism, and drug‐related toxicities.

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“…2 The liver is an organ with a wide range of functions, including the detoxication of metabolites, drugs, and xenobiotics.…”

Section: Introductionmentioning

confidence: 99%

“…4 Chronic ethanol abuse may subsequently be associated with morbidity and mortality. 2 The use of drugs in the treatment of ethanol-induced liver damage is still limited by the complications associated with their long-term use. 4 Thus, the use of natural products with known bioactive agents and better safety proles has been proposed as a better alternative for treating liver disease.…”

mentioning

confidence: 99%

The in vivo hepato-recovery effects of the polyphenol-rich fermented food Xeniji™ on ethanol-induced liver damage

Zulkawi¹,

Ng²,

Zamberi

et al. 2017

RSC Adv.

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Xeniji is a health food product produced by bacterial lactic acid fermentation. Although fermented foods, including Xeniji, have been widely consumed for various health purposes, including as an antioxidant to improve liver disease, their polyphenol content and in vivo hepato-recovery effects have yet to be evaluated. This study aims to evaluate the polyphenol content of Xeniji and its in vivo hepato-recovery effect on ethanol-induced liver damage. In this study, the polyphenolic acids of Xeniji are quantified by liquid chromatography-mass spectrometry (LCMS). In addition, the recovery effect of Xeniji on ethanolinduced liver damage in mice is evaluated by assessing the serum liver enzyme profile, liver inflammation, liver oxidative stress, and the level of CYP2E1. Xeniji is recorded to contain a high concentration of caffeoylquinic acid and sakuranetin, based on the LCMS-MS quantification results. In terms of the in vivo hepato-recovery study, intake of ethanol induces substantial liver damage indicated by an increase of the serum liver enzyme profile, liver inflammation, liver oxidative stress and the level of CYP2E1. On the other hand, Xeniji promotes recovery from ethanol-induced liver damage by restoring antioxidant levels, enhancing the metabolism of ethanol in the liver and suppressing inflammation in a dosage-dependent manner. Xeniji is a fermented functional food that possesses hepato-recovery effects on ethanol-induced liver damage.

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Metabolic basis of ethanol-induced hepatic and pancreatic injury in hepatic alcohol dehydrogenase deficient deer mice

Cited by 49 publications

References 44 publications

TGF-β enhances alcohol dependent hepatocyte damage via down-regulation of alcohol dehydrogenase I

TGF-β enhances alcohol dependent hepatocyte damage via down-regulation of alcohol dehydrogenase I

Utility of Genetically Modified Animal Models for Drug Metabolism and Drug Transporters

The in vivo hepato-recovery effects of the polyphenol-rich fermented food Xeniji™ on ethanol-induced liver damage

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