Acetaldehyde-Derived Advanced Glycation End-Products Promote Alcoholic Liver Disease

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Acetaldehyde-Derived Advanced Glycation End-Products Promote Alcoholic Liver Disease

BACKGROUND Chronic ingestion of ethanol increases acetaldehyde and leads to the production of acetaldehyde-derived advanced glycation end-products (AA-AGE). We evaluated the toxicity of AA-AGE on hepatocytes and studied the role of AA-AGE in the pathogenesis of alcoholic liver disease (ALD). METHODS Rat hepatocyte cultures were treated with N-ethyllysine (NEL) or AA-AGE and the cell viability...

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Dietary advanced glycation end-products aggravate non-alcoholic fatty liver disease

AIM To determine if manipulation of dietary advanced glycation end product (AGE), intake affects non-alcoholic fatty liver disease (NAFLD) progression and whether these effects are mediated via RAGE. METHODS Male C57Bl6 mice were fed a high fat, high fructose, high cholesterol (HFHC) diet for 33 wk and compared with animals on normal chow. A third group were given a HFHC diet that was high in...

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Neurotoxicity of acetaldehyde-derived advanced glycation end products for cultured cortical neurons.

The Maillard reaction that leads to the formation of advanced glycation end products (AGEs) plays an important role in the pathogenesis of angiopathy in diabetic patients, in aging, and in neurodegenerative processes. We hypothesize that acetaldehyde (AA), one of the main metabolites of alcohol, may be involved in alcohol-induced neurotoxicity in vivo by formation of AA-derived AGEs (AA-AGEs) w...

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Advanced glycation end products

Aging is the progressive accumulation of damage to an organism over time leading to disease and death. Aging research has been very intensive in the last years aiming at characterizing the pathophysiology of aging and finding possibilities to fight age-related diseases. Various theories of aging have been proposed. In the last years advanced glycation end products (AGEs) have received particula...

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Effect of Dietary Advanced Glycation End Products on Mouse Liver

UNLABELLED The exact pathophysiology of non-alcoholic steatohepatitis (NASH) is not known. Previous studies suggest that dietary advanced glycation end products (AGEs) can cause oxidative stress in liver. We aim to study the effects of dietary AGEs on liver health and their possible role in the pathogenesis of NASH. METHODS Two groups of mice were fed the same diet except the AGE content vari...

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ژورنال

عنوان ژورنال: PLoS ONE

سال: 2013

ISSN: 1932-6203

DOI: 10.1371/journal.pone.0070034