Smail Leila, Berdja Sihem, Neggazi Samia, Hamlat Nadjiba, Boumaza Saliha, Sahraoui Abdelhamid, Benazzoug Yasmina, Kacimi Ghouti, Haffaf E Mahdi and Aouichat Bouguerra Souhila
It was established that the sand rat Psammomys obesus is an experimental model of type diabetes 2 and dyslipidemia, in this in vivo study the sand rats were submitted to natural diet associated with fat (10%) and sucrose (20%) enriched diet /rat per day for 6 months.
The initial time and once of the months, plasma parameters were evaluated and at 6th month aortic morphology were examined. To simulate hyperinsulinemic stress, the effects of high dose of insulin 10 UI/ml during 6 h were investigated on subcultured aortic control fibroblasts which were implicated in extracellular matrix remodeling during the atherosclerosis process. In this work report, the proliferation rates, morphological aspects of apoptosis, few markers of oxidative stress (malonaldehyde and nitric oxid) and type I and III collagen contained in extracellular compartment were evaluated. Others animals received a high fat high sucrose diet showed hyperglycemia associated with hyperinsulinemia, dyslipidemia, hyperproteinemia, increase of cardiac markers, low and very low density lipoproteins and decrease high density lipoprotein versus control group. The aortas of diabetic ranimals were exhibited an important disorganization and remodeling of vascular extracellular matrix. In vitro results indicated a
decrease in cellular proliferation rate, the apparition of some morphological characters of apoptosis (hypertrophy fibroblasts, hypercondensation chromatin, oncosis) and increase of malonaldehyde, total nitrite production in intracellular compartment and increase of total proteins, type I and III collagen especially type III were observed in extracellular compartment. The high fat high sucrose diet induced diabetes associated with hyperinsulinemia and development of extracellular matrix remodeling in sand rats similar to human advanced atherosclerotic lesions. The high insulin dose induced an increase of both some markers of oxidative stress caused apoptosis and extracellular type III collagen especially.
