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Original Research

Atherosclerosis and atherosensitivity in two southwest Algerian desert rodents, Psammomys obesus and Gerbillus gerbillus, and in Rattus norvegicus

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Pages 337-345 | Published online: 18 Sep 2012
 

Abstract

Cardiovascular disease, including atherosclerosis, is the leading cause of death in patients with diabetes worldwide; thus, it is a major medical concern. The endothelium contributes to the control of many vascular functions, and clinical observations show that it is a primary target for diabetic syndrome. To get better insight into the mechanisms underlying atherosclerosis, we studied the interspecific differences in the arterial metabolisms of two, Psammomys obesus and Gerbillus gerbillus, as well as Rattus norvegicus (Wistar rat), well known for its atheroresistance. Twenty-two enzymatic activities and six macromolecular substances were histochemically compared in the two desert species and in Wistar aortas (abdominal and thoracic) and arteries (femoral and caudal) embedded in a common block. In the healthy adult rodents, enzyme activities were very intense. They demonstrated that aortic myocytes are capable of various synthesis and catabolism processes. However, considering the frequency of atherosclerosis and its phenotypes, significant differences appeared between the species studied. Our comparative study shows that aortic atherosensitive animals have several common metabolic characteristics, which are found in Psammomys rich in metachromatic glycosaminoglycans (involved in the inhibition of lipolysis and in calcification of the organic matrix), reduced activity in enzymes related to the Krebs cycle (weakening energetic power), and low lipolytic enzyme, adenosine triphosphatase, and adenosine diphosphatase activities. However, the most fundamental pathophysiological difference is the low lipolytic power of the aorta of Psammomys when compared to Wistar rats. This characteristic determines its atherosensitivity and makes this animal model more applicable to the experimental development of atherosclerosis.

Acknowledgments

We are very grateful to Prof Colin J Marsden for reviewing and correcting the English in this manuscript ([email protected]). Thanks to our coworkers in Béni-Abbès, where our research originated, and to our coworkers at CPMC, CHU Mustapha-Bacha of Algiers. This research is supported by the “DGRSDT-MESRS” of Algeria. All authors approved the final version to be published.

Disclosure

The authors report no conflict of interest in this work.