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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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Diet-induced obesity leads to pro-inflammatory alterations to the vitreous humour of the eye in a rat model.

TL;DR: DIO-related metabolic disturbances disrupt VH homeostasis in a manner that reflects development of a pro-inflammatory environment and may lead to overt pathologies with compromised eye function.
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Cytochrome c release from rat liver mitochondria is compromised by increased saturated cardiolipin species induced by sucrose feeding

TL;DR: The results suggest that both intra- and extramitochondrial H2O2 are involved in cytochrome c release, but the persisting difference between C and SF levels can be attributed to the differences in cardiolipin compositions.
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β-Sitosterol mitigates the development of high-fructose diet-induced nonalcoholic fatty liver disease in growing male Sprague–Dawley rats

TL;DR: In this article, β-Sitosterol (Bst), a naturally occurring phytosterol, has antihyperlipidaemic and hepatoprotective properties, and has been shown to have anti-hyperlipidemic properties.
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Extra fructose in the growth medium fuels lipogenesis of adipocytes.

TL;DR: Cells developed lipid vesicles much earlier with fructose and showed altered kinetics of the expression of mRNAs involved in lipogenesis and hexose uptake, and adiponectin secretion peaked earlier in fructose containing media than in media with glucose only.
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Mitigative effects of the bioactive flavonol fisetin on high‐fat/high‐sucrose induced nonalcoholic fatty liver disease in rats

TL;DR: Worldwide growing rates of obesity are correlated with the rising prevalence of nonalcoholic fatty liver disease (NAFLD) with limited available therapeutics.
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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