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 sedentary (r)evolution: Have we lost our metabolic flexibility?
TL;DR: It is argued that the metabolic disease epidemic is largely based on a deficit in metabolic flexibility, and can be reversed by re-cultivating suppressed metabolic programs, which became obsolete in an affluent environment, particularly the ability to easily switch to ketone body and fat oxidation.
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The Angiogenesis Inhibitor ALS-L1023 from Lemon-Balm Leaves Attenuates High-Fat Diet-Induced Nonalcoholic Fatty Liver Disease through Regulating the Visceral Adipose-Tissue Function.
TL;DR: Analysis of VAT function revealed that HFD-ALS led to fewer CD68-positive macrophage numbers and lower expression of inflammatory cytokines compared with HFD, suggesting that angiogenesis inhibitors could aid in the treatment and prevention of obesity-induced human NAFLD.
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Small-Molecule Kinase Inhibitors for the Treatment of Nononcologic Diseases.
TL;DR: In this article, the authors discuss a number of kinases and their small-molecule inhibitors for the treatment of diseases in non-oncologic therapeutic fields and highlight the opportunities and challenges in developing such inhibitors.
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An Overview of Mouse Models of Nonalcoholic Steatohepatitis: From Past to Present
TL;DR: The most important NAFLD/NASH mouse models that have been developed over the years are summarized and briefly highlight the pros and cons.
Journal ArticleDOI
The role of the gut microbiome and diet in the pathogenesis of non-alcoholic fatty liver disease
TL;DR: Current evidence supporting an association between NAFLD and the gut microbiome and dietary factors is summarized and potential underlying mechanisms underpinning these associations are explored and whether manipulation of the Gut microbiome is a potential therapeutic strategy to prevent or treatNAFLD.
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.
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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.
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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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