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Copper-Fructose Interactions: A Novel Mechanism in the Pathogenesis of NAFLD

1,2,*, 3,4 and 1,2,5,6,7
1
Department of Medicine, Division of Gastroenterology, Hepatology and Nutrition, University of Louisville School of Medicine, Louisville, KY 40202, USA
2
Hepatobiology&Toxicology Center, University of Louisville School of Medicine, Louisville, KY 40202, USA
3
Department of Pediatrics, Emory University School of Medicine, Atlanta, GA 30307, USA
4
Children’s Healthcare of Atlanta, Atlanta, GA 30322, USA
5
Department of Pharmacology and Toxicology, University of Louisville School of Medicine, Louisville, KY 40202, USA
6
University of Louisville Alcohol Research Center, University of Louisville School of Medicine, Louisville, KY 40202, USA
7
Robley Rex Veterans Affairs Medical Center, Louisville, KY 40206, USA
*
Author to whom correspondence should be addressed.
Nutrients 2018, 10(11), 1815; https://doi.org/10.3390/nu10111815
Received: 18 October 2018 / Revised: 8 November 2018 / Accepted: 16 November 2018 / Published: 21 November 2018
(This article belongs to the Special Issue Fructose and Glucose for Human Health)
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PDF [1603 KB, uploaded 21 November 2018]
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Abstract

Compelling epidemiologic data support the critical role of dietary fructose in the epidemic of obesity, metabolic syndrome and nonalcoholic fatty liver disease (NAFLD). The metabolic effects of fructose on the development of metabolic syndrome and NAFLD are not completely understood. High fructose intake impairs copper status, and copper-fructose interactions have been well documented in rats. Altered copper-fructose metabolism leads to exacerbated experimental metabolic syndrome and NAFLD. A growing body of evidence has demonstrated that copper levels are low in NAFLD patients. Moreover, hepatic and serum copper levels are inversely correlated with the severity of NAFLD. Thus, high fructose consumption and low copper availability are considered two important risk factors in NAFLD. However, the causal effect of copper-fructose interactions as well as the effects of fructose intake on copper status remain to be evaluated in humans. The aim of this review is to summarize the role of copper-fructose interactions in the pathogenesis of the metabolic syndrome and discuss the potential underlying mechanisms. This review will shed light on the role of copper homeostasis and high fructose intake and point to copper-fructose interactions as novel mechanisms in the fructose induced NAFLD. View Full-Text
Keywords: copper; fructose; kupffer cell (KC); iron; non-alcoholic fatty liver disease (NAFLD); metabolic syndrome; gut microbiota copper; fructose; kupffer cell (KC); iron; non-alcoholic fatty liver disease (NAFLD); metabolic syndrome; gut microbiota
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Song, M.; Vos, M.B.; McClain, C.J. Copper-Fructose Interactions: A Novel Mechanism in the Pathogenesis of NAFLD. Nutrients 2018, 10, 1815.

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