الفهرس 
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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
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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.