Field Of Vision
Copyright ©2012 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Gastroenterol. Sep 7, 2012; 18(33): 4478-4480
Published online Sep 7, 2012. doi: 10.3748/wjg.v18.i33.4478
Opposite fates of fructose in the development of metabolic syndrome
Marta Alegret, Juan C Laguna
Marta Alegret, Juan C Laguna, Department of Pharmacology and Therapeutic Chemistry, School of Pharmacy, University of Barcelona, Institute of Biomedicine, 08028 Barcelona, Spain
Marta Alegret, Juan C Laguna, Biomedical Network Research Centre, Physiopathology of Obesity and Nutrition (CIBERobn), 08028 Barcelona, Spain
Author contributions: Alegret M and Laguna JC contributed equally to the writing of this manuscript.
Correspondence to: Dr. Juan C Laguna, Department of Pharmacology and Therapeutic Chemistry, School of Pharmacy, University of Barcelona, Institute of Biomedicine, Avda. Diagonal 643, 08028 Barcelona, Spain. jclagunae@ub.edu
Telephone: +34-93-4024530 Fax: +34-93-4035982
Received: June 27, 2012
Revised: August 13, 2012
Accepted: August 16, 2012
Published online: September 7, 2012
Abstract

This short review comments on the recently published work of Ishimoto et al regarding the opposing effects of fructokinase C and A isoforms on fructose-induced metabolic syndrome in mice. The framework for the commentary is the preexisting background of epidemiological and experimental data regarding the association between ingestion of fructose, as present in sweetened beverages, and the development of metabolic syndrome. The work of Ishimoto et al clearly confirms the negative effect of fructose on lipid and glucose metabolism, independently from the amount of energy provided by the ingested sugar. It also confirms the absolute requirement of liver fructose metabolism, driven by fructokinase activity, in order to develop the full spectrum of metabolic syndrome alterations.

Keywords: Lipid metabolism; Fatty liver; Obesity; Hyperglycemia; Dyslipidemia