scispace - formally typeset
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.
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.

read more

Citations
More filters
Journal ArticleDOI

Dietary fructose as a risk factor for non-alcoholic fatty liver disease (NAFLD)

TL;DR: Understanding of how fructose intake can favor these pathological processes is crucial for the development of appropriate noninvasive diagnostic and therapeutic approaches to detect and treat these metabolic effects.
Journal ArticleDOI

Perspective: A Historical and Scientific Perspective of Sugar and Its Relation with Obesity and Diabetes

TL;DR: It is suggested that fructose-induced obesity is driven by engagement of a "fat switch" and provide novel insights into new approaches for the prevention and treatment of these important diseases.

The Sweet Path to Metabolic Demise: Fructose and Lipid

TL;DR: It is shown that hepatic insulin resistance develops from diacylglycerol-PKCɛ-mediated impairment of insulin signaling and possibly additional mechanisms, and initiatives that decrease fructose consumption and therapies that block fructose-mediated lipogenesis will be necessary to avert future metabolic pandemics.
References
More filters
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.
Related Papers (5)