High‐fat and high‐sucrose (western) diet induces steatohepatitis that is dependent on fructokinase
Takuji Ishimoto,Miguel A. Lanaspa,Christopher J. Rivard,Carlos A. Roncal-Jimenez,David J. Orlicky,Christina Cicerchi,Rachel H. McMahan,Manal F. Abdelmalek,Hugo R. Rosen,Matthew R. Jackman,Paul S. MacLean,Christine P. Diggle,Aruna Asipu,Shinichiro Inaba,Tomoki Kosugi,Waichi Sato,Shoichi Maruyama,Laura G. Sánchez-Lozada,Yuri Y. Sautin,James O. Hill,David T. Bonthron,Richard J. Johnson +21 more
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TLDR
The protection in fructokinase knockout mice suggests a key role for fructose (from sucrose) in this development of steatohepatitis, and emphasize the important role of fructose in the development of fatty liver and nonalcoholic steato hepatitis.About:
This article is published in Hepatology.The article was published on 2013-11-01 and is currently open access. It has received 252 citations till now. The article focuses on the topics: Fructokinase & Steatohepatitis.read more
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Toxic AGE (TAGE) Theory for the Pathophysiology of the Onset/Progression of NAFLD and ALD
TL;DR: The pathophysiological roles of GA-AGESs and AA-AGEs (toxic AGEs, TAGE) and a related novel theory for preventing the onset/progression of NAFLD and ALD are discussed.
Journal ArticleDOI
The severity of rat liver injury by fructose and high fat depends on the degree of respiratory dysfunction and oxidative stress induced in mitochondria
Claudia Isabel García-Berumen,Omar Ortiz-Avila,Manuel Alejandro Vargas-Vargas,Bricia A. del Rosario-Tamayo,Clotilde Guajardo-López,Alfredo Saavedra-Molina,Alain R. Rodríguez-Orozco,Christian Cortés-Rojo +7 more
TL;DR: Severity of liver injury induced by fructose or fat was related to the degree of dysfunction and oxidative damage in mitochondria, and attention should be paid on the serious effects observed in the HF + Fr group as the typical Western diet is rich in both fat and carbohydrates.
Journal ArticleDOI
Pathophysiology of NAFLD and NASH in Experimental Models: The Role of Food Intake Regulating Peptides.
Lucia Kořínková,Veronika Pražienková,L Černá,Alena Karnošová,Blanka Železná,Jaroslav Kuneš,Lenka Maletínská +6 more
TL;DR: The role of food intake regulating peptides in NAFLD and NASH mouse models is explored and Glucagon-like peptide-1, another anorexigenic peptide, and GLP-1 receptor agonists (GLP- 1R), represent potential therapeutic agents to preventNAFLD progression to NASH.
Journal ArticleDOI
A Novel Wistar Rat Model of Obesity-Related Nonalcoholic Fatty Liver Disease Induced by Sucrose-Rich Diet.
Maria Luiza Pereira Lima,Laura Hora Rios Leite,Carolina Rosa Gioda,Fabiola de Oliveira Paes Leme,Claudia Alves Couto,Cândido C. Coimbra,Virginia Hora Rios Leite,Teresa C. A. Ferrari +7 more
TL;DR: In conclusion, a sucrose-rich diet induced obesity, insulin resistance, oxidative stress, and NAFLD in rats.
Journal ArticleDOI
Tissue-Specific Fructose Metabolism in Obesity and Diabetes.
Robert N. Helsley,Francois Moreau,Manoj K. Gupta,Aurelia Radulescu,Brian J. DeBosch,Samir Softic,Samir Softic +6 more
TL;DR: An increase in sugar intake, particularly fructose, has been associated with the development of obesity and its complications, and inhibition of fructose utilization in tissues primary responsible for its metabolism alters consumption in other tissues, which have not been traditionally regarded as important depots of fructose metabolism.
References
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Evolution of inflammation in nonalcoholic fatty liver disease: The multiple parallel hits hypothesis†
TL;DR: Endoplasmic reticulum stress and related signaling networks, (adipo)cytokines, and innate immunity are emerging as central pathways that regulate key features of NASH.
Journal ArticleDOI
Fructose consumption as a risk factor for non-alcoholic fatty liver disease
Xiaosen Ouyang,Pietro Cirillo,Yuri Y. Sautin,Shannon J. McCall,James L. Bruchette,Anna Mae Diehl,Richard J. Johnson,Manal F. Abdelmalek +7 more
TL;DR: The pathogenic mechanism underlying the development of NAFLD may be associated with excessive dietary fructose consumption, and fructose resulted in dose-dependent increase in KHK protein and activity.
Journal ArticleDOI
Nonalcoholic steatohepatitis, insulin resistance, and metabolic syndrome: Further evidence for an etiologic association
Gianfranco Pagano,Giovanni Pacini,Giovanni Musso,Roberto Gambino,Fabio Mecca,Nadia Depetris,Maurizio Cassader,Ezio David,Paolo Cavallo-Perin,Mario Rizzetto +9 more
TL;DR: Hyperinsulinemia and insulin resistance occur frequently in patients with NASH; these conditions do not stem from a reduced hepatic insulin extraction but from an enhanced pancreatic insulin secretion compensatory to reduced insulin sensitivity.
Journal ArticleDOI
Dietary habits and their relations to insulin resistance and postprandial lipemia in nonalcoholic steatohepatitis
Giovanni Musso,Roberto Gambino,Franco De Michieli,Maurizio Cassader,Mario Rizzetto,Marilena Durazzo,Emanuela Fagà,Barbara Silli,Gianfranco Pagano +8 more
TL;DR: Dietary habits may promote steatohepatitis directly by modulating hepatic triglyceride accumulation and antioxidant activity as well as indirectly by affecting insulin sensitivity and postprandial triglyceride metabolism.
Journal ArticleDOI
The role of fructose in the pathogenesis of NAFLD and the metabolic syndrome.
TL;DR: Excessive dietary fructose consumption may underlie the development of nonalcoholic fatty liver disease and the metabolic syndrome, and it is postulate that NAFLD and alcoholic fatty Liver disease share the same pathogenesis.
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