The role of AMP-activated protein kinase in the action of ethanol in the liver

You, Min; Matsumoto, Morio; Pacold, Christine M.; Cho, Won Kyoo; Crabb, David W.

doi:10.1053/j.gastro.2004.09.049

Cited by 425 publications

(386 citation statements)

References 52 publications

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“…Hepatic malonyl-CoA concentrations were measured in neutralized perchloric acid liver extracts at the Mouse Metabolic Phenotyping Center (Yale University School of Medicine, New Haven, CT). 12 Analysis of Hepatic Palmitate Oxidation. The rates of fatty acid oxidation of liver homogenates were analyzed using [1-14 C]-palmitate (Amersham Radiolabeled Chemicals, St. Louis, MO) as described.…”

Section: Methodsmentioning

confidence: 99%

“…13 Primary rat hepatocytes were isolated from fed male Sprague-Dawley rats via collagenase digestion. 12 The rate of oxidation of [1-14 C]-palmitic acid to carbon dioxide was performed as previously described. 12 Maintenance and Differentiation of 3T3-L1 Cells.…”

Section: Methodsmentioning

confidence: 99%

“…12 The rate of oxidation of [1-14 C]-palmitic acid to carbon dioxide was performed as previously described. 12 Maintenance and Differentiation of 3T3-L1 Cells. The 3T3-L1 cells were maintained as subconfluent cultures in Dulbecco's modified Eagle medium (DMEM) supplemented with 10% fetal bovine serum.…”

Section: Methodsmentioning

confidence: 99%

“…Chronic ethanol administration in mice is associated with inhibition of AMP-activated protein kinase (AMPK) and peroxisome proliferator-activated receptor (PPAR) ␣, two critical signaling molecules controlling the pathways of hepatic fatty acid oxidation. [12][13][14][15] These molecules are the major mediators of the metabolic effect of adiponectin. 16,17 Adiponectin is exclusively expressed and secreted from adipose tissue.…”

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confidence: 99%

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Role of adiponectin in the protective action of dietary saturated fat against alcoholic fatty liver in mice

et al. 2005

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The protective effect of dietary saturated fatty acids against the development of alcoholic liver disease has long been known, but the underlying mechanism is not completely understood. We examined the involvement of the adipocyte hormone adiponectin. Circulating adiponectin levels were significantly elevated by chronic ethanol administration to mice consuming a diet high in saturated fat. The increase in circulating adiponectin was associated with the activation a set of hepatic signaling pathways mediated through AMP-activated protein kinase, PPAR-␣, and PPAR-␥ coactivator ␣, which in turn led to markedly increased rates of fatty acid oxidation, prevention of hepatic steatosis, and alleviation of liver enzyme changes. Furthermore, treatment of rat 3T3-L1 adipocytes with saturated fatty acids (palmitic or stearic acids) in the presence of ethanol increased secretion of adiponectin and enhanced activity of a mouse adiponectin promoter. In conclusion, the protective action of saturated fat against the development of alcoholic fatty liver in mice is partially mediated through induction of adiponectin. The present findings suggest a novel paradigm for dietary fatty acids in the pathogenesis of alcoholic liver disease and provide a promising therapeutic strategy-nutritional modulation of adiponectin-in treating human alcoholic fatty liver disease. (HEPATOLOGY 2005;42:568 -577.)

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

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Role of adiponectin in the protective action of dietary saturated fat against alcoholic fatty liver in mice

et al. 2005

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“…AMP kinase, a protein kinase that inhibits lipogenesis and activates fatty acid oxidation, is inhibited by chronic alcohol feeding, which results in increased SREBP-1 activation [26,27]. As a consequence of the alcohol-dependent activation of SREBP-1, a number of lipogenic genes are up-regulated in liver contributing to enhanced lipid synthesis.…”

Section: Introductionmentioning

confidence: 99%

Mitochondrial dysfunction and oxidative stress in the pathogenesis of alcohol- and obesity-induced fatty liver diseases

Mantena

King

Andringa

et al. 2008

Free Radical Biology and Medicine

372

299

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Fatty liver disease associated with chronic alcohol consumption or obesity/type 2 diabetes has emerged as a serious public health problem. Steatosis, accumulation of triglyceride in hepatocytes, is now recognized as a critical "first-hit" in the pathogenesis of liver disease. It is proposed that steatosis "primes" the liver to progress to more severe liver pathologies when individuals are exposed to subsequent metabolic and/or environmental stressors or "second-hits". Genetic risk factors can also influence the susceptibility and severity of fatty liver disease. Furthermore, oxidative stress, disrupted nitric oxide (NO) signaling, and mitochondrial dysfunctional are proposed to be key molecular events that accelerate or worsen steatosis and initiate progression to steatohepatitis and fibrosis. This review article will discuss the following topics regarding the pathobiology and molecular mechanisms responsible for fatty liver disease: 1) the "two-hit" or "multi-hit" hypothesis; 2) the role of mitochondrial bioenergetic defects and oxidant stress; 3) interplay between NO and mitochondria in fatty liver disease; 4) genetic risk factors and oxidative stress responsive genes; and 5) the feasibility of antioxidants for treatment.

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Ethanol Metabolism and Pathogenesis of Alcoholic Liver Injury

Stewart¹,

Day²

2007

Textbook of Hepatology

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The role of AMP-activated protein kinase in the action of ethanol in the liver

Cited by 425 publications

References 52 publications

Role of adiponectin in the protective action of dietary saturated fat against alcoholic fatty liver in mice

Role of adiponectin in the protective action of dietary saturated fat against alcoholic fatty liver in mice

Mitochondrial dysfunction and oxidative stress in the pathogenesis of alcohol- and obesity-induced fatty liver diseases

Ethanol Metabolism and Pathogenesis of Alcoholic Liver Injury

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