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Abstract During the last decades, corroborating data from clinical and experimental studies revealed that, besides their pivotal role in sexual development and reproduction, estrogens contribute to glucose homeostasis. Supporting the beneficial effect of estrogens on insulin action and glucose homeostasis, insulin sensitivity was demonstrated to be higher in women before the menopause than in age-matched men. In addition, it is well recognized that the menopause favors visceral fat deposition and insulin resistance, leading to a significant increase in type 2 diabetes risk. This study was planned to determine the effects of estrogen deficiency with diabetes and to evaluate the association of inflammatory, endothelial dysfunction markers with cardiovascular risk factor in ovarectomized STZ-diabetic rats. The present study was performed on 80 healthy female adult albino rats allocated into four groups. 1. Control sham-operated group: 20 rats, subjected to all surgical procedures of ovariectomy except for removal of ovaries. 20 day later, they received a single intraperitoneal (i.p.) injection of citrate buffer and were studied 2 weeks later. 2. Sham-operated streptozotocin diabetic group (STZ): 20 rats, subjected to all surgical procedures of ovariectomy except for removal of ovaries. 20 day later, they were rendered diabetic by single i.p. injection of Nicotinamide (120 mg/kg, i.p.) 15 min. before the injection of Streptozotocin (60 mg/kg, i.p.). dissolved in normal salin, citrate buffer (PH 4.5), respectively then studied 2 weeks later. Summary and conclusion 140 3. Ovariectomized group (OVX): 20 rats, subjected to bilateral ovariectomy, 20 day after the operation, they received a single i.p. injection of citrate buffer and were studied 2 weeks later. 4. Ovariectomized STZ diabetic group (OVX–STZ): 20 rats, subjected to bilateral ovariectomy. 20 day after the operation, they were rendered diabetic then studied 2 weeks later. Results encountered in this study showed that diabetes caused marked hyperglycemia. Dyslipidemia in the form of significant elevation of plasma triglycerides, total cholesterol, LDL-c and atherogenic index and decreased HDL-c was found, together with significant elevation of inflammatory markers evidenced by high serum hs-CRP, TNF-α levels and marked endothelial dysfunction in form of significant decrease in serum Nitric Oxide. Ovariectomy resulted in unfavorable changes in Lipid profile showed in the form of significant elevation of serm triglycerides, total cholesterol, LDL-c and atherogenic index and decrease of HDL-c, together with significant increase in inflammatory markers hs-CRP and TNF-α was recorded. In addition to observable endothelial dysfunction (significant decrease in serum nitric oxide). Combination of estrogen deficiency and diabetes in ovariectomized diabetic group resulted in aggravation of the above mentioned metabolic derangements in the form of further elevation of blood glucose even more than diabetic group, serum lipids especially triglycerides, total cholesterol and LDL-c were further elevated more than in ovariectomy or diabetes alone, together with aggravation of inflammatory markers. It is worth mentioning here that the highly significant negative correlation was found between serum levels of Nitric oxid and each of plasma triglycerides, total cholesterol, LDL-c, atherogenic index, hs-CRP and TNF-α pointing to the deleterious effects of estrogen deficiency on endothelial dysfunction and its association with dyslipidemia and inflammation. Also, significant positive correlation was found between serum Nitric oxide and HDL-c a result that shed light on the effect of estrogen deficiency on increasing the incidence of developing diabetes mellitus. |