Next Article in Journal / Special Issue
Immunological Mechanisms in the Pathophysiology of Non-Alcoholic Steatohepatitis
Previous Article in Journal
Cytokines, Chaperones and Neuroinflammatory Responses in Heroin-Related Death: What Can We Learn from Different Patterns of Cellular Expression?
Previous Article in Special Issue
Relationship between Serum Osteocalcin Levels and Non-Alcoholic Fatty Liver Disease in Adult Males, South China
Int. J. Mol. Sci. 2013, 14(10), 19846-19866; doi:10.3390/ijms141019846
Review

Development of Nonalcoholic Hepatopathy: Contributions of Oxidative Stress and Advanced Glycation End Products

1,†
, 1,2
, 1,†
, 3
 and 1,4,*
1 Institute of Chemistry and Biotechnology, Federal University of Alagoas (IQB/UFAL), Maceio, Alagoas 57072-900, Brazil 2 Federal Institute for Education, Science and Technology of Alagoas, Maceio, Alagoas 57020-600, Brazil 3 Faculty of Nutrition, Federal University of Alagoas (FANUT/UFAL), Maceio, Alagoas 57072-970, Brazil 4 Northeast Biotechnology Network (RENORBIO), Federal University of Alagoas (UFAL), Maceio, Alagoas 57072-900, Brazil These authors contributed equally to this work.
* Author to whom correspondence should be addressed.
Received: 24 July 2013 / Revised: 7 September 2013 / Accepted: 10 September 2013 / Published: 1 October 2013
(This article belongs to the Special Issue Non-Alcoholic Fatty Liver Disease Research)
View Full-Text   |   Download PDF [724 KB, uploaded 19 June 2014]   |   Browse Figures

Abstract

Advanced glycation end products (AGEs) are generated spontaneously in cells; however, under conditions of hyperglycemia and lipid peroxidation, their levels are higher than usual, which contribute to the development of diseases such as the nonalcoholic fatty liver disease (NAFLD). NAFLD is associated with oxidative stress (OS), which is linked to the transition of steatosis to steatohepatitis due to lipid peroxidation. The AGE-receptor interaction in hepatic stellate cells leads to an increase in reactive oxygen species and enhances the proliferation and activation of these cells, worsening liver fibrosis and disease progression. In this vicious cycle, there is production of (carboxymethyl)lysine, a biomarker for products of advanced glycation and lipid peroxidation, being a shared component between the two pathways. In this review, we aim to compile evidence to support the basic molecular mechanisms of AGEs and OS generation and their influence, independently or combined, on the evolution of NAFLD. The deeper understanding of the interrelations of AGEs + OS may help to elucidate the pathogenic pathways of NAFLD and to devise rational therapeutic interventions for this disease, with an expected positive impact on quality of life of patients.
Keywords: oxidative stress; liver; AGEs; nonalcoholic fatty liver disease; molecular mechanism of biological activity oxidative stress; liver; AGEs; nonalcoholic fatty liver disease; molecular mechanism of biological activity
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Share & Cite This Article

Export to BibTeX |
EndNote


MDPI and ACS Style

Santos, J.C.F.; Valentim, I.B.; de Araújo, O.R.P.; Ataide, T.R.; Goulart, M.O.F. Development of Nonalcoholic Hepatopathy: Contributions of Oxidative Stress and Advanced Glycation End Products. Int. J. Mol. Sci. 2013, 14, 19846-19866.

View more citation formats

Related Articles

Article Metrics

Comments

Citing Articles

[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert