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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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Ginger (Zingiber officinale) Attenuates Obesity and Adipose Tissue Remodeling in High-Fat Diet-Fed C57BL/6 Mice.

TL;DR: In this paper, the role of ginger in modulating adipocyte metabolism is largely unknown, but the authors hypothesized that ginger supplementation inhibits high-fat (HF)-diet-mediated obesity and investigated whether ginger modulates adipocyte remodeling.
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Pathophysiological mechanisms involved in non-alcoholic steatohepatitis and novel potential therapeutic targets

TL;DR: Physiopathology of NAFL and NASH and their progression to cirrhosis involve several parallel and interrelated mechanisms, such as, insulin resistance, lipotoxicity, inflammation, oxidative stress, and recently the gut-liver axis interaction has been described.
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Earliest evidence of caries lesion in hominids reveal sugar-rich diet for a Middle Miocene dryopithecine from Europe.

TL;DR: This study investigates the caries lesion in the 12.5 Ma old type specimen of Dryopithecus carinthiacus Mottl 1957 (Primates, Hominidae), and challenges the model of a step-wise increase in dietary quality during hominid evolution and support the uricase hypothesis.
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Natural Progression of Non-Alcoholic Steatohepatitis to Hepatocellular Carcinoma.

TL;DR: An updated review of the pathogenic mechanisms leading from NASH to HCC as well as an exploration of the role of biomarkers and screening are provided.
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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