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Open AccessJournal ArticleDOI

High‐fat and high‐sucrose (western) diet induces steatohepatitis that is dependent on fructokinase

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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.
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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.

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Citations
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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.
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The severity of rat liver injury by fructose and high fat depends on the degree of respiratory dysfunction and oxidative stress induced in mitochondria

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.
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Pathophysiology of NAFLD and NASH in Experimental Models: The Role of Food Intake Regulating Peptides.

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.
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Tissue-Specific Fructose Metabolism in Obesity and Diabetes.

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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Journal ArticleDOI

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

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

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.
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Dietary habits and their relations to insulin resistance and postprandial lipemia in nonalcoholic steatohepatitis

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.
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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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