The Role of Fructose in Non-Alcoholic Steatohepatitis: Old Relationship and New Insights
Autor: | Mario Masarone, Marcello Dallio, Alessandro Federico, Valerio Rosato, Pietro Torre, Mario Romeo, Marcello Persico |
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Přispěvatelé: | Federico, A., Rosato, V., Masarone, M., Torre, P., Dallio, M., Romeo, M., Persico, M. |
Rok vydání: | 2021 |
Předmět: |
0301 basic medicine
medicine.medical_specialty Cirrhosis Sucrose Dietary Sugars Review Fructose 03 medical and health sciences chemistry.chemical_compound 0302 clinical medicine Insulin resistance nutrients Non-alcoholic Fatty Liver Disease Internal medicine medicine Animals Humans TX341-641 Nutrition and Dietetics Metabolism Non-alcoholic steatohepatitis Nutrients Nutrition. Foods and food supply business.industry Lipogenesis Fatty Acids Fatty liver Lipid metabolism Lipid Metabolism medicine.disease Diet Oxidative Stress Phenotype 030104 developmental biology Endocrinology Liver chemistry Disease Progression 030211 gastroenterology & hepatology non-alcoholic steatohepatitis Insulin Resistance Steatosis Steatohepatitis business Non-alcoholic steatohepatiti metabolism Food Science |
Zdroj: | Nutrients Nutrients, Vol 13, Iss 1314, p 1314 (2021) |
ISSN: | 2072-6643 |
Popis: | Non-alcoholic fatty liver disease (NAFLD) represents the result of hepatic fat overload not due to alcohol consumption and potentially evolving to advanced fibrosis, cirrhosis, and hepatocellular carcinoma. Fructose is a naturally occurring simple sugar widely used in food industry linked to glucose to form sucrose, largely contained in hypercaloric food and beverages. An increasing amount of evidence in scientific literature highlighted a detrimental effect of dietary fructose consumption on metabolic disorders such as insulin resistance, obesity, hepatic steatosis, and NAFLD-related fibrosis as well. An excessive fructose consumption has been associated with NAFLD development and progression to more clinically severe phenotypes by exerting various toxic effects, including increased fatty acid production, oxidative stress, and worsening insulin resistance. Furthermore, some studies in this context demonstrated even a crucial role in liver cancer progression. Despite this compelling evidence, the molecular mechanisms by which fructose elicits those effects on liver metabolism remain unclear. Emerging data suggest that dietary fructose may directly alter the expression of genes involved in lipid metabolism, including those that increase hepatic fat accumulation or reduce hepatic fat removal. This review aimed to summarize the current understanding of fructose metabolism on NAFLD pathogenesis and progression. |
Databáze: | OpenAIRE |
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