Maternal and fetal adrenocortical function in the diabetic rabbit

Abstract

To investigate whether maternal or fetal glucocorticoid secretion is altered during pregnancy complicated by diabetes mellitus, in vitro production of corticosterone (B) and cortisol (F) was measured on day 28 of gestation in rabbits made alloxan diabetic prior to pregnancy. In addition, plasma B and F were followed throughout the experimental period. Fetuses of diabetic mothers were hyperglycemic and hyperinsulinemic, and mortality was much higher (18%) than that of control animals (1.5%). No significant differences were found in maternal plasma B or F during gestation, whereas F was significantly lower in fetuses of diabetic mothers. In vitro production of both B and F by maternal and fetal adrenals was lower in the diabetic animals, and responses to ACTH or insulin added to the incubation were the same in both groups. These results suggest that the ability of the adrenal cortex to secrete glucocorticoids may be impaired both in the mother and fetus when maternal diabetes is present. This could have effects both on maturational events in the fetus that are accelerated by glucocorticoids and on the ability to respond to stress.

Maternal diabetes and its effect on biochemical and functional development of rabbit fetal lung

“…In our study of severe states of diabetes we have not observed macrosomia. On the contrary, the fetal body weight is reduced (Table I), an observation that is in agreement with previous reports on the effect of severe hyperglycemia (Guleff and Beck 1981;Sirek et al 1963;Gewolb et al 1982).…”

“…The animal model described in this study manifests some of the characteristics of a poorly controlled human diabetic pregnancy: maternal and fetal hyperglycemia and the absence of fetal or neonatal macrosomia. Although in our investigation maternal and fetal insulin levels were not determined, previous studies have demonstrated that hyperinsulinemia exists in the fetuses 9f a diabetic doe (Wellman et al 1969; Guleff and Beck 1981). It has also been demonstrated in the fetuses of diabetic rats (Pitkin and Van Orden 1974;Kevran et al 1978) and in the human offspring of a diabetic mother (Steinke and Driscoll 1965;Obenshain et al 1970;Stubbs and Stubbs 1978).…”

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

“…The finding that maternal adrenalectomy in rats, during the last 3-4 days of gestation, does not reduce maternal corticosterone levels to the same extent as it does in non-pregnant animals (Châtelain, Dupouy & Allaume, 1980;Mulay, Varma & Solomon, 1982) has led to the suggestion by Châtelain et al (1980) that the increase in plasma corticosterone levels in the last 3-4 days of gestation is a result of increased production of corticosterone by the rat fetus. Guleff & Beck (1981) have also reported decreased cortisol levels in fetuses of alloxan-induced diabetic rabbits, but they found no alteration in maternal plasma cortisol and cortico¬ sterone levels. In human diabetic pregnancy maternal and cord blood corticosteroid levels at the time of vaginal delivery or Caesarian section were either similar (Chattoraj, Carroll, Turner, Gillespie, Pinkus & Charles, 1974) or slightly raised (Scholz & Huther, 1970).…”

“…Hyperinsulinaemia is a characteristic feature in human diabetic pregnancy (Steinke & Driscoll, 1965;Sosenko et al 1979). In other experimental models fetal hyperinsulinaemia is present in non-human primates (Mintz et al 1972) and in the alloxan-induced diabetic rabbit some investigators have found no evidence of fetal hyperinsulinaemia (Bose, Manne, D'Ercole & Lawson, 1980;Sosenko, Lawson, Demottaz & Frantz, 1980) whereas others have reported raised fetal plasma insulin levels in the fetuses of alloxan-treated rabbits (Guleff & Beck, 1981).…”

Modulation of Cholesterol Transport by Insulin-Treated Gestational Diabetes Mellitus in Human Full-Term Placenta1

“…Utilization of CHOL by the fetal adrenal glands could also influence the levels of circulating lipoproteins. In diabetic animals, the adrenal function is impaired, which could result in a reduced utilization of circulating LDL [52,53]. However, the increased neonatal levels of FFA and indirectly the increased birth weight in normal-weight women with GDM could be due to the excessive internalization of lipoproteins into the placenta, the increased activity of LPL, and the increased expression of fatty acid carriers, such as CD36 in the case of obesity [54].…”