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Open AccessJournal ArticleDOI

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

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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Combination of Alcohol and Fructose Exacerbates Metabolic Imbalance in Terms of Hepatic Damage, Dyslipidemia, and Insulin Resistance in Rats

TL;DR: Evidence is provided for the coaction of ethanol and fructose with a high-fat-diet on dyslipidemia and insulin resistance-accompanied liver damage and the L-EF diet significantly elevated blood glucose, insulin, and total-cholesterol levels.
Journal ArticleDOI

Adipokines in Liver Cirrhosis.

TL;DR: The Child-Pugh score and the model of end-stage liver disease score have been established to assess residual liver function in patients with liver cirrhosis, and studies having analyzed these proteins in systemic blood in cirrhotic patients are listed to identify adipokines that are comparably changed in the different cohorts of patients.
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Neuronal deletion of ghrelin receptor almost completely prevents diet-induced obesity

TL;DR: Novel findings suggest that suppressing central ghrelin signaling may serve as a unique antiobesity strategy and that neuronal GHS-R is a crucial regulator of energy metabolism and a key mediator of DIO.
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Metabolic syndrome: F stands for fructose and fat

TL;DR: It emerges that mice that cannot metabolize fructose are healthier when placed on carbohydrate-rich diets.
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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