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alcohol dehydrogenase/lihavuus
Linkki tallennetaan leikepöydälle
Sivu 1 alkaen 24 tuloksia
Interaction between high-fat diet and alcohol dehydrogenase on ethanol-elicited cardiac depression in murine myocytes.
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OBJECTIVE
Consumption of high-fat diet and alcohol is associated with obesity, leading to enhanced morbidity and mortality. This study was designed to examine the interaction between high-fat diet and the alcohol metabolizing enzyme alcohol dehydrogenase (ADH) on ethanol-induced cardiac
Transcriptomic identification of ADH1B as a novel candidate gene for obesity and insulin resistance in human adipose tissue in Mexican Americans from the Veterans Administration Genetic Epidemiology Study (VAGES).
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Type 2 diabetes (T2D) is a complex metabolic disease that is more prevalent in ethnic groups such as Mexican Americans, and is strongly associated with the risk factors obesity and insulin resistance. The goal of this study was to perform whole genome gene expression profiling in adipose tissue to
[Changes in the pattern of substance use after bariatric surgery: report of one case].
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Even though the benefits of bariatric surgery are supported by scientific evidence, its indications and contraindications must be revised to avoid its indiscriminate use. Substance use is more common in patients subjected to bariatric surgery than in the general population. After surgery, an
Development and validation of a 96-well cellular assay for the discovery of ALDH1A1 inhibitors.
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Retinoic acid, the active metabolite of vitamin A, plays important roles in various physiological and pathological processes. The two-step production of retinoic acid from vitamin A (retinol) is catalyzed by alcohol dehydrogenases and aldehyde dehydrogenases, which are potential therapeutic targets
MEHP/ethanol co-exposure favors the death of steatotic hepatocytes, possibly through CYP4A and ADH involvement
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Liver steatosis has been associated with various etiological factors (obesity, alcohol, environmental contaminants). How those factors work together to induce steatosis progression is still scarcely evaluated. Here, we tested whether phthalates could potentiate death of steatotic hepatocytes when
[Role of alcohol-metabolizing enzymes gene polymorphisms and environmental exposure on colorectal cancer: a case-only study].
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OBJECTIVE
This study was designed to explore the interactions of alcohol dehydrogenase 1B (ADH1B) rs1229984, aldehyde dehydrogenase 2 (ALDH2)(rs671) and cytochrome P4502E1(CYP2E1)rs1329149 with environmental factors and the interactions between genetic factors in the susceptibility of colorectal
ADH2 and CYP2E1 genetic polymorphisms: risk factors for alcohol-related birth defects.
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Considerable variation in offspring outcome occurs following intrauterine ethanol exposure. The mechanism underlying this varying susceptibility may involve genetic differences in ethanol metabolism catalyzed by alcohol dehydrogenase (ADH) and cytochrome P450 2E1 (CYP2E1). A recent population study
Metabolic syndrome, diabetes and atherosclerosis: influence of gene-environment interaction.
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Despite remarkable progress in diagnosis and understanding of risk factors, cardiovascular disease (CVD) remains still the leading cause of morbidity and mortality in the world's developed countries. The metabolic syndrome, a cluster of risk factors (visceral obesity, insulin resistance,
Translational Implications of the Alcohol-Metabolizing Enzymes, Including Cytochrome P450-2E1, in Alcoholic and Nonalcoholic Liver Disease.
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Fat accumulation (hepatic steatosis) in alcoholic and nonalcoholic fatty liver disease is a potentially pathologic condition which can progress to steatohepatitis (inflammation), fibrosis, cirrhosis, and carcinogenesis. Many clinically used drugs or some alternative medicine compounds are also known
Ethanol Extract of Pinus koraiensis Leaf Ameliorates Alcoholic Fatty Liver via the Activation of LKB1-AMPK Signaling In Vitro and In Vivo.
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Although Pinus koraiensis leaf (PKL) was reported for its anti-diabetes, anti-obesity and anticancer effects as a folk remedy, the inhibitory effect of PKL on alcoholic fatty liver has never been elucidated yet. This study investigated the molecular mechanisms of PKL on alcoholic fatty liver in
Hepatic mitochondrial dysfunction induced by fatty acids and ethanol.
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Understanding the key aspects of the pathogenesis of alcoholic fatty liver disease particularly alterations to mitochondrial function remains to be resolved. The role of fatty acids in this regard requires further investigation due to their involvement in fatty liver disease and obesity. This study
p53-Inducible DHRS3 is an endoplasmic reticulum protein associated with lipid droplet accumulation.
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The transcription factor p53 plays a critical role in maintaining homeostasis as it relates to cellular growth, proliferation, and metabolism. In an effort to identify novel p53 target genes, a microarray approach was utilized to identify DHRS3 (also known as retSDR1) as a robust candidate gene.
[Alcoholic liver disease: the roles of genetic-epigenetic factors and the effect of abstinence].
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The pathogenesis of alcoholic liver disease depends not only on the toxic effects of alcohol, but also on the complex interaction of host's and environmental factors. Thus, the genetic pre-disposition, co-morbidities and behavioral factors all play a role in the individual variations in the disease
Determinants of alcohol use and abuse: Impact of quantity and frequency patterns on liver disease.
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More than 70% of alcohol is consumed by 10% of the population in the United States. Implicit in this statistic is that tremendous variation in the pattern of drinking (quantity, frequency, and duration) exists among alcohol consumers. Individuals who are binge or chronic drinkers will have different
Alcoholic fatty liver: its pathogenesis and mechanism of progression to inflammation and fibrosis.
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Liver disease in the alcoholic is due not only to malnutrition but also to ethanol's hepatotoxicity linked to its metabolism by means of the alcohol dehydrogenase and cytochrome P450 2E1 (CYP2E1) pathways and the resulting production of toxic acetaldehyde. In addition, alcohol dehydrogenase-mediated
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