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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The Sweet Path to Metabolic Demise: Fructose and Lipid Synthesis
TL;DR: In this article, the authors link fructose consumption with metabolic disease, an association attributable in part to fructose-mediated lipogenesis, and propose interventions that decrease fructose consumption and therapies that block fructose-induced lipogenesis.
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Dietary Sugars and Endogenous Formation of Advanced Glycation Endproducts: Emerging Mechanisms of Disease.
TL;DR: The most recent reports on the effects of high sugar consumption and diet-derived AGEs on human health suggest the need to limit the dietary sources of A GEs, including added sugars, to prevent the development of metabolic diseases and related comorbidities.
Journal ArticleDOI
Formation of Fructose-Mediated Advanced Glycation End Products and Their Roles in Metabolic and Inflammatory Diseases.
TL;DR: Exogenous and endogenous fructose metabolism, fructose glycation, and in vitro, animal, and human data are summarized to put the fructose-mediated Maillard reaction in the limelight again as a contributing factor in chronic inflammatory diseases and MetS.
Journal ArticleDOI
A splicing switch from ketohexokinase-C to ketohexokinase-A drives hepatocellular carcinoma formation
Xinjian Li,Xu Qian,Li Xia Peng,Yuhui Jiang,Yuhui Jiang,David H. Hawke,Yanhua Zheng,Yan Xia,Jong Ho Lee,Gilbert J. Cote,Hongxia Wang,Liwei Wang,Chao Nan Qian,Zhimin Lu,Zhimin Lu +14 more
TL;DR: A pivotal mechanism underlying the distinct fructose metabolism between HCC cells and normal hepatocytes is revealed and the instrumental role of KHK-A protein kinase activity in promoting de novo nucleic acid synthesis and HCC development is highlighted.
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Diets rich in fructose, fat or fructose and fat alter intestinal barrier function and lead to the development of nonalcoholic fatty liver disease over time
Cathrin Sellmann,Josephine Priebs,Marianne Landmann,Christian Degen,Anna Janina Engstler,Cheng Jun Jin,Stefanie Gärttner,Astrid Spruss,Otmar Huber,Ina Bergheim +9 more
TL;DR: The data suggest that chronic intake of fructose and/or fat may lead to the development of NAFLD over time and that this is associated with an increased translocation of bacterial endotoxin.
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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