Lipid peroxidation of poly-unsaturated fatty acids in normal and obese adipose tissues

Abstract

Adipose tissues function as the primary storage compartment of fatty acids and as an endocrine organ that affects peripheral tissues. Many of adipose tissue-derived factors, often termed adipokines, have been discovered in recent years. The synthesis and secretion of these factors vary in different depots of adipose tissues. Excessive lipid accumulation in adipocytes induces inflammatory processes by up-regulating the expression and release of pro-inflammatory cytokines. In addition, activated macrophages in the obese adipose tissue release inflammatory cytokines. Adipose tissue inflammation has also been linked to an enhanced metabolism of polyunsaturated fatty acids (PUFAs). The non-enzymatic peroxidation of PUFAs and of their 12/15-lipoxygenase-derived hydroperoxy metabolites leads to the generation of the reactive aldehyde species 4-hydroxyalkenals. This review shows that 4-hydroxyalkenals, in particular 4-hydroxynonenal, play a key role in lipid storage homeostasis in normal adipocytes. Nonetheless, in the obese adipose tissue an increased production of 4-hydroxyalkenals contributes to the inflamed phenotype.

Keywords::

• Adipose tissue
• diabetes
• 4-hydroxydodecadienal
• 4-hydroxynonenal
• inflammation
• lipid peroxidation
• lipoxygenase
• obesity
• PLA₂

Acknowledgements

The authors dedicate this article to the memory of Dr. Margarita Lorenzo who passed away in 2010. This article is based on a lecture and discussions that were conducted at an In Memoriam Seminar of Margarita Lorenzo on “Obesity, inflammation and insulin resistance” that took place at the University Complutense of Madrid, Spain, on 11 November 2010.

This study was supported, in part, by grants from the Larry Adler Foundation for Diabetes Research, the Dr. Adolf and Klara Brettler Center for Research in Molecular Pharmacology and Therapeutics at the Hebrew University and the David R. Bloom Center for Pharmacy at the Hebrew University. S. Sasson is affiliated with both centres. G. Cohen and Y. Riahi received fellowships from the Hebrew University Center for Diabetes Research.

Declaration of interest

The authors report no conflicts of interest. The authors alone are responsible for the content and writing of this article.

Notice of correction: This paper was published online on 11 March 2011 containing an incorrect version of Figure 1. The paper in it’s present form is correct. The authors and publishers would like to apologize for any inconvenience caused.