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World J Gastroenterol. Feb 21, 2014; 20(7): 1807-1821
Published online Feb 21, 2014. doi: 10.3748/wjg.v20.i7.1807
Published online Feb 21, 2014. doi: 10.3748/wjg.v20.i7.1807
Diet high in fructose leads to an overexpression of lipocalin-2 in rat fatty liver
Salamah Mohammad Alwahsh, Hatice Ali Seyhan, Shakil Ahmad, Sabine Mihm, Giuliano Ramadori, Frank Christian Schultze, Department of Gastroenterology and Endocrinology, University Medical Center Goettingen, 37075 Goettingen, Germany
Min Xu, Department of General, Visceral and Pediatric Surgery, University Medical Center Goettingen, 37075 Goettingen, Germany
Author contributions: Alwahsh SM designed, wrote the paper, and performed the research; Seyhan HA, Ahmad S and Xu M participated in performing the research, and data analysis; Ramadori G designed the research and data interpretation; Mihm S and Schultze FC provided critical improvement of the study, data interpretation, and final approval of the version to be published.
Correspondence to: Frank Christian Schultze, MD, Department of Gastroenterology and Endocrinology, University Medical Center Goettingen, Robert-Koch-Str. 40, 37075 Goettingen, Germany. f.schultze@med.uni-goettingen.de
Telephone: +49-551-398932 Fax: +49-551-396921
Received: August 15, 2013
Revised: September 13, 2013
Accepted: October 14, 2013
Published online: February 21, 2014
Revised: September 13, 2013
Accepted: October 14, 2013
Published online: February 21, 2014
Core Tip
Core tip: Both Lieber-DeCarli (LDC) and LDC + 70% cal fructose (L-HFr) models featured fatty liver. Fructose-enriched regimen induced metabolic syndrome in the corresponding rats. Lipocalin-2 (LCN-2) was strikingly increased in the liver and serum of the L-HFr group. In this group, the increase of LCN-2 synthesis was associated with inflammation at week 4, whereas the peak value of LCN-2 at week 8 was mainly accompanied by impairment of the mitochondrial function. Nevertheless, an interaction coexists between both processes. The indicators of stress conditions and apoptosis were elevated at both time points. Evidently, the expression of LCN-2 was correlated to inflammatory and metabolic processes.