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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.
About
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

Mechanism of preventive effects of exendin-4 and des-fluoro-sitagliptin in a murine model of fructose-induced prediabetes.

TL;DR: In this article , the effects of exendin-4 and des-fluoro-sitagliptin (dipeptidyl peptidase-4 inhibitor) on hepatic disturbances were evaluated in prediabetic rats.
Posted ContentDOI

Early exposure to high-fat diet impairs central and peripheral metabolic function: Impacts on cognition and mitochondrial function

TL;DR: The results indicate that the introduction of a HFD early in life has a detrimental impact on bioenergetic and mitochondrial function of tissues with metabolic and thermogenic activities, which is likely related to hippocampal metabolic changes and cognitive impairment.
Journal ArticleDOI

Moderate Exercise Training Combined With a High-Fat and Sucrose Diet Protects Pancreatic Islet Function in Male C57BL/6J Mice

TL;DR: Exercise training may slow down and/or prevent adverse metabolic effects associated with consuming a westernized diet in mice consuming a high-fat and sucrose diet, and improve glucose tolerance, body mass, insulin sensitivity and GSIS.
Journal ArticleDOI

Osthole Prevents Heart Damage Induced by Diet-Induced Metabolic Syndrome: Role of Fructokinase (KHK)

TL;DR: In this article , the authors tested whether diet-induced metabolic syndrome causes heart disease associated with increased fructose content and metabolism and whether it can be prevented with a fructokinase inhibitor (osthole).
Dissertation

The Dynamic Nature of the POMC Neuron Landscape, and the Impact of POMC Peptides and Body Composition States in Motivated Feeding

Graham Jones
TL;DR: To test whether glutamatergic POMC neurons serve a distinct role in maintaining energy homeostasis, activated Pomc expression Cre-dependently in Vglut2-expressing neurons of mice with conditionally silenced Pomc alleles, indicating that a subpopulation of Pomc neurons must express both neuronal markers.
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.
Journal ArticleDOI

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.
Journal ArticleDOI

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.
Journal ArticleDOI

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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