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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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Journal ArticleDOI

High-fat/high-carbohydrate-diet short- and middle-term effects on gerbil adrenal zona fasciculata histology.

TL;DR: A histological study of the adrenal was performed in gerbils receiving a high-fat/high-carbohydrate-diet (HFC) for 8 or 12 weeks as mentioned in this paper .
Journal Article

Comparative effect of a high fat with or without high levels of sucrose diets on peripheral neuropathy in c57bl/6j mice.

TL;DR: In this article , the effect of feeding mice a high fat and high sucrose diet on neuropathy compared to mice fed only a high-fat diet and mice fed a high diet and treated with streptozotocin was evaluated.
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Effects of Dietary Supplementation with Myo-inositol on Hepatic Expression of Glycolytic and Fructolytic Enzyme Genes in Rats Fed a High-sucrose Diet

TL;DR: In this article, the effects of a major lipotrope, myo-inositol, on the expression of primary glycolytic (glucokinase and phosphofructokinase) and fructolytic enzyme (ketohexokinase [KHK] and aldolase B) genes in the livers of rats fed a control diet, high-sucrose diet, or high sucrose Diet supplemented with 0.5% myo inositol for 14 d.
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Daily Consumption of Angelica Keiskei Juice Attenuated Hyperlipidaemia and Hepatic Steatosis Caused by Western Diet in C57BL/6J Mice

TL;DR: It is suggested that daily consumption of AK juice may have potentials to prevent WD-induced NAFLD development through mitigating intestinal barrier damage, intestinal lipid absorption, and hepatic ER oxidative stress.
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Early-life metabolic dysfunction impairs cognition and mitochondrial function in mice.

TL;DR: In this article , the authors evaluated the relationship between peripheral metabolic and bioenergetic changes induced by a two-hit protocol and their impact on cognitive function in juvenile mice and found that exposure to HFD+STZ early in life has a detrimental impact on the metabolic and mitochondrial function of tissues with metabolic and thermogenic activities.
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.
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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