Ischemic heart disease is an important cause of death for both sexes.
Risk factors include dyslipidernia, glucose intolerance and hyperinsulinemia
(Granberry and Fonseca. 1999). The incidence of ischemic heart disease
is more in mole than female in the reproductive period of life due to
the well known protective mechanism of estrogen. The androgen role is
still controversiaL
This study was designed to investigate the protective role of endogenous
estrogen and aruirogen on cardiovascular risk factors in insulin resistance
induced rats. Four groups of albino rats were used in this study.
Each group is subdivided into sub-group A (males) and subgroup B (females)
Group)': served as a control group. Group II: received solution of
10% sucrose in water, instead of drinking water for induction of insulin
resistance. Group III: received solution of 10% sucrose and injected IP by
anti-estrogen at a dose 1 mg /Kg/ day. Group IV: received solution of 10%
sucrose and given anti-androgen orally at a dose 67.5 mg / kg /day. Blood
samples were collected by decapitation after 12 weeks of experiment,
and the following were estimated in animal sera: Fasting blood sugar.
fasting insulin, cholesterol, triglycerides. LDL and HDL.
Insulin resistance increases cardiovascular risk factors in mole arui female
rats with more effect on female. The cause of increase risk in insulin
resistance induced female is hyperandrogenism while the cause in insulin
resistance induced mole is decrease androgen level with increase estrogen!
androgen ratio.
We conclude that both endogenous estrogen and androgen have a pro-
781
Ashraf Belal and Mohamed Nabih
tective role against ischemic heart disease, but estrogen is more protective
in females and androgen is more protective in males. A balance between
estrogen and androgen in males and females is essential for this
protective role. Any defect in estrogen / androgen balance increase cardiovascular
risk factors. |
