Publications of Faculty of Medicine:THE EFFECT OF ESTROGEN AND TESTOSTERONE HORMONES ON GLUCOSE TOLERANCE AND LIPID PROFILE IN FRUCTOSE-INDUCED INSULIN RESISTANCE IN RATS: Abstract

Title:
THE EFFECT OF ESTROGEN AND TESTOSTERONE HORMONES ON GLUCOSE TOLERANCE AND LIPID PROFILE IN FRUCTOSE-INDUCED INSULIN RESISTANCE IN RATS
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Abstract:

This study was designed to evaluate the effect of estrogen and testosterone hormones on glucose tolerance and lipid profile in Fructoseinduced insulin resistant rats. Eighty rats (40 males and 40 females) were used in this study and were divided into 4 groups of 10 male and 10 female rats. Group (1) served as a control group and was allowed to grow on chow diet and water. Group (2) was grown on chow diet and fructose solution 10% instead of drinking water. Group (3) was grown as group (2) and received daily subcutaneous (s.c.) injections of estradiol benzoate (50 pg /kg) and group (4) was grown as group (2) and received daily s.c. injections of testosterone undecanoate (2 mg /kg). The whole period of the experiment for all groups was 10 weeks. All rats were weighed before and after the experiment and the percent of the weight gain was calculated for each rat. The following parameters were estimated; fasting plasma insulin (Fl), intraperitoneal glucose tolerance test (IPGTT), plasma triglycericles (TG), total cholesterol (PC), high-density lipoproteincholesterol (HDL-c) and low- density lipoprotein-cholesterol (LDL-c). In group (2) there was sign!ficant hyperinsulinemia, impaired glucose tolerance and abnormal lipid profile as compared to control group. These abnormalities were more significant in male than female rats. In group (3) estrogen treatment improved most of these abnormalities in male and female rats while in group (4) testosterone treatment could ameliorate some of the abnormalities in lipid profile in female rats. It could be concluded that estrogen and testosterone hormones may have a role in ameliorat-trig some of the metabolic abnormalities associated with fructose-induced insulin resistance syndrome and may have important metabolic homeostatic functions that need further clarification.