Fructose consumption as a risk factor for non-alcoholic fatty liver disease.
By Xiaosen Ouyang, P. Cirillo, Y. Sautin, S. McCall, James L Bruchette, A. Diehl, Richard J. Johnson, M. Abdelmalek. Journal of Hepatology, 2008
829 citations recorded by the source corpus.
Subfields: Endocrinology, Diabetes and Metabolism, Epidemiology, Pathology and Forensic Medicine
View Paper: https://www.semanticscholar.org/paper/fcfa89179b884e307da1db1cff98f1bc96f22694
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In Endocrinology, Diabetes and Metabolism
In Epidemiology
- K. Stanhope
- C. Day
- S. Bellentani
- E. Brunt
- V. Ratziu
- B. Neuschwander‐Tetri
- H. Cortez‐Pinto
- Giulio Marchesini
In Pathology and Forensic Medicine
Citations in the corpus
- The role of fructose in the pathogenesis of NAFLD and the metabolic syndrome (2010, background): “In other case-controlled studies, total fructose consumption was associated with NAFLD in general, and NASH in particular”
- Nonalcoholic fatty liver disease: pathology and pathogenesis. (2010, background): “More recently, studies of NAFLD patients have shown that increased consumption of fructose (79, 80), soft drink”
- Fructose and Sugar: A Major Mediator of Nonalcoholic Fatty Liver Disease (2018, neutral): “Ouyang et al.11 compared individuals with NAFLD, without cirrhosis, to controls that were matched for age, sex and BMI.”
- Sugar consumption, metabolic disease and obesity: The state of the controversy (2015, positive): “There is considerable epidemiological evidence suggesting intake of added sugars and/or sugar-sweetened beverages are associated with the presence of unfavorable lipid levels (6– 8), insulin resistance (9, 10), fatty liver (11, 12), T2DM (13–17), cardiovascular disease (CVD) (18, 19), metabolic synd”
- Increased intestinal permeability and tight junction alterations in nonalcoholic fatty liver disease (2009, neutral): “n 17 18 14 21 Sex (M) 3/14 2/16 NS 3/11 2/19 NS Age 44 (34-53) 41 (32-54) NS 46(32-54) 40 (32-53 NS BMI 24.”
- A position statement on NAFLD/NASH based on the EASL 2009 special conference. (2010, background): “High fructose corn syrup contributes to IR and NAFLD [171], and therefore the consumption of soft drinks should be kept to a minimum as should the consumption of industrial trans-fats (present in many processed foods) which are also associated with the development of NAFLD and hepatic inflammation [”
- INCREASED FRUCTOSE CONSUMPTION IS ASSOCIATED WITH FIBROSIS SEVERITY IN PATIENTS WITH NAFLD (2010, background): “Furthermore, studies have indicated that the development of NAFLD may be associated with excessive dietary fructose consumption.(16,17) Whether increased fructose consumption correlates merely with the development of NAFLD or promotes the transition from NAFLD to NASH and more advanced stages of liv”
- Nonalcoholic fatty liver disease: a precursor of the metabolic syndrome. (2015, background): “[83] Ouyang X, Cirillo P, Sautin Y, et al.”
- Sugar, Uric Acid, and the Etiology of Diabetes and Obesity (2013, background): “The observation that NAFLD subjects may absorb fructose more efficiently is further supported by our observation of higher KHK expression in liver biopsies of NAFLD compared with other liver disease (36) and could be the reason why ATP depletion in response to fructose is greater in NAFLD subjects w”
- Hepatic lipotoxicity and the pathogenesis of nonalcoholic steatohepatitis: The central role of nontriglyceride fatty acid metabolites (2010, background): “Fructose enters the glycolytic pathway to fatty acid synthesis downstream from phosphofructokinase, the rate-limiting enzyme for this pathway, and thus fructose provides an unregulated source of acetyl-CoA as the substrate for DNL.(84,85) Studies in mice have confirmed the importance of dietary suga”