Abstract
In the dynamics of the disease development, diuresis and glycosuria increase in alloxan-susceptible rats, while in alloxan-resistant rats the increase in the values of these indices is expressed to a lesser extent, and they begin to decrease by day 8 of the disease. In alloxan-susceptible rats, the mass index of adrenal gland is increased, and that of thymus is decreased and corticosterone concentration in blood, adrenal gland and urine as well as alanine and aspartate aminotransferase activities in liver are increased; in alloxan-resistant rats the values of these indices do not differ from those of rats of the control group.
Highlights
It is known from literature that at modeling diabetes mellitus type 1 (DM-I) using alloxan selectively affecting -cells of the islets of Langerhans, experimental animals from heterogeneous groups [1,2] and linear animals [3,4] display different susceptibilities to the diabetogenic effect of alloxan
Some obtained results show that glucocorticoid hormones can play a negative role in exacerbating the severity of experimental DM-I, their excess secretion by adrenal into the bloodstream resulting in the stimulation of gluconeogenesis processes in the target tissues [6,7]
Experimental animals were divided into two groups by blood glucose level 2 weeks after alloxan administration: the first one with glucose level 4-fold exceeded this value in rats of the control group, the second one with glucose level exceeding the control level by 1.3 times
Summary
It is known from literature that at modeling diabetes mellitus type 1 (DM-I) using alloxan selectively affecting -cells of the islets of Langerhans, experimental animals from heterogeneous groups [1,2] and linear animals [3,4] display different susceptibilities to the diabetogenic effect of alloxan. The authors attribute this phenomenon to differences in the oxidative status and the activity of antioxidant systems of animals. Some obtained results show that glucocorticoid hormones can play a negative role in exacerbating the severity of experimental DM-I, their excess secretion by adrenal into the bloodstream resulting in the stimulation of gluconeogenesis processes in the target tissues [6,7].
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