Influence of streptozotocin-induced diabetes in pregnant rats on plasma corticosterone and progesterone levels and on cytoplasmic glucocorticoid receptors in fetal tissues

Abstract

Administration of a dose of 45 mg streptozotocin/kg on day 2 of gestation produced a diabetic state in pregnant rats and was associated with fetal hyperinsulinaemia. Although there was no evidence of fetal macrosomia, the ratio of fetal liver and lung weight to body weight was greater in fetuses of diabetic rats, suggesting an increase in the size of these organs relative to the body weight. Maternal and fetal plasma corticosterone levels of diabetic rats between 19 and 22 days of gestation was significantly lower than the corresponding control values. Maternal plasma progesterone levels of diabetic rats were lower than controls on days 19 and 20 of gestation, but higher than controls on day 21 of gestation. The absence of pregnancy-related changes in maternal and fetal plasma corticosterone levels and maternal progesterone levels in diabetic rats suggest that adrenocortical function as well as ovarian and/or placental function may be impaired, which may in turn be related to the observed delay in parturition of approximately 18 h as well as to the low survival rate of the pups. There was a small increase in the cytoplasmic glucocorticoid receptor concentration in the lung but not in the liver of fetuses of diabetic mothers when compared with fetuses of controls, suggesting that the increased receptor concentration may be a compensatory mechanism to overcome the effect of decreased corticosterone levels and increased insulin levels in the fetuses of diabetic rats.

Influence of streptozotocin‐diabetes on the pharmacokinetics, placental transfer and tissue localization of dexamethasone in rats

“…Streptozotocin-diabetes in rats has been viewed as an appropriate model for studies on foetal and placental development (Farrell et al, 1982). Effects of a moderate dose of streptozotocin used in this study on the mother, foetus and placenta (Table 1) are similar to those reported elsewhere (Mulay & Solomon, 1983). Unlike the previous study (Varma & Yue, 1984), animals in this study were fed a normal laboratory chow instead of a semi-synthetic diet of comparable composition and dexamethasone was quantitated on the basis of radioactivity rather than by radioimmunoassay; these two differences did not appreciably alter the results.…”

“…This cannot be attributed to any differences in maternal or foetal serum protein-dexamethasone binding. Streptozotocindiabetes in rats causes a decrease in maternal and foetal plasma corticosterone levels and either no change or an increase in foetal lung and liver cytoplasmic glucocorticoid receptor levels (Mulay & Solomon, 1983); if anything, both these effects of diabetes will tend to increase rather than decrease the localization of dexamethasone in foetal tissues.…”

“…Diabetes in nonpregnant (3 weeks prior to the study) and pregnant (day 1-2 of gestation) rats was induced by intravenous injections of 150 l tmol kgstreptozotocin dissolved freshly in saline-citrate buf-fer; controls were injected with the buffer (Mulay & Solomon, 1983). Animals had free access to tap water and a normal Purina rat chow instead of the semi-synthetic diet used in the previous study (Varma & Yue, 1984).…”

Effect of Streptozotocin Administration to Pregnant Mice on Serum Glucose, Glycosylated Hemoglobin and Weight of Organs of the Mother Mice and Their Pups

“…There are numerous findings in rats with regard to the influence of diabetes on the gestation, the fetus and infant (8)(9)(10)(11)(12)(13)(14); however, there have been only a few reports on the effects of STZ treatment in pregnant mice (15). Namely, in the Swiss strain of mice STZ (200 mg/kg, i.p.)…”

“…The prenatal period of mouse and rat can be divided into 3 stages: 1) implantation stage (mouse: 0-5 days, rat: 0-7 days), 2) organ formation stage (mouse: 6-13 days, rat: [8][9][10][11][12][13][14][15] days), and fetal growth stage (mouse: 14-20 days, rat: 16-22 days) (16).…”