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R. R. Beck

Bio: R. R. Beck is an academic researcher. The author has contributed to research in topic(s): Fetus & Hydrocortisone. The author has an hindex of 1, co-authored 1 publication(s) receiving 7 citation(s).
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Journal ArticleDOI
TL;DR: The 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, which could have effects both on maturational events in the fetus that are accelerated by glucoc Corticosterone and on the ability to respond to stress.
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.

7 citations


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Journal ArticleDOI
TL;DR: It is demonstrated that GDM affects the maternal and neonatal lipid profiles as well as different key players of placental cholesterol transfer from the maternal to the fetal circulation, depending on the maternal BMI.
Abstract: Gestational diabetes mellitus (GDM) is a common complication of pregnancy that is characterized by glucose intolerance, leads to dyslipidemia, and is aggravated by obesity. Cholesterol is taken up by the placenta as part of lipoproteins through the scavenger receptor class B type I receptor (SRBI), low-density lipoprotein receptor (LDLR), and very low density lipoprotein receptor (VLDLR), and its efflux is then mediated by ABCA1 and ABCG1. PCSK9 is involved in the degradation of LDLR and VLDLR. The goal of this study was to evaluate the impact of GDM and prepregnancy body mass index (BMI) on cholesterol transport through the modulation of the expression of several key players. Human full-term placenta, maternal, and venous cord blood samples were obtained at delivery from normal-weight women without GDM (n = 10), normal-weight women with GDM (n = 6), and overweight/obese women with GDM (n = 6). Lipids (total cholesterol, high-density lipoprotein, low-density lipoprotein, triglycerides, free fatty acids, apolipoprotein A1, apolipoprotein B100) levels were evaluated in blood samples. Messenger RNA and protein expression levels (LDLR, VLDLR, SRBI, ABCA1, ABCG1, proprotein convertase subtilisin/kexin type 9, liver x receptors, peroxisome proliferator-activated receptors) were assessed in human full-term placenta, respectively, by real-time RT-PCR and Western blots. Lipoprotein lipase activity was evaluated using a commercial kit on tissue homogenates. Overall, our study demonstrates that GDM affects the maternal and neonatal lipid profiles as well as different key players of placental cholesterol transfer from the maternal to the fetal circulation, depending on the maternal BMI. These changes could affect the fetal metabolism and predispose the fetus to future metabolic diseases.

51 citations


Journal ArticleDOI
TL;DR: The results indicate that alloxan-induced diabetes alters adrenocortical steroid metabolism which may contribute to changes in the pattern of steroid secretion noted by other investigators.
Abstract: Studies were carried out to determine if diabetes mellitus influenced the activities of adrenal steroidogenic enzymes. Adult male rabbits were made diabetic by an i.v. infusion of alloxan (100 mg/kg) and were killed 1 or 2 months later. Mitochondrial cytochrome P-450 concentrations were not affected by diabetes but steroid 11β-hydroxylase activity was greater in the diabetics than in controls after both 1 and 2 months. The type I spectral change produced by 11-deoxycorticosterone, the substrate for 11β-hydroxylation, was also greater in mitochondria from diabetics. By contrast, mitochondrial cholesterol side-chain cleavage activity was similar in controls and diabetics. Microsomal cytochrome P-450 concentrations were unaffected by diabetes but 21-hydroxylase activity was significantly lower in adrenal microsomes from diabetics than from controls. The results indicate that alloxan-induced diabetes alters adrenocortical steroid metabolism which may contribute to changes in the pattern of steroid secretion noted by other investigators.

Journal ArticleDOI
TL;DR: It seems unlikely that an increase in maternal adrenal steroid concentrations is necessary for the development of amiloride-sensitive Na+ transport in rabbit blastocysts, as there were no pregnancy-specific alterations in circulating adrenal steroids concentrations during the preimplantation stages of embryonic development.
Abstract: Plasma aldosterone, corticosterone, and cortisol were measured during the first week of pseudopregnancy or pregnancy in New Zealand White rabbits to determine whether any sustained elevations of adrenal steroids occur. There were no pregnancy-specific alterations in circulating adrenal steroid concentrations during the preimplantation stages of embryonic development. Elevation of plasma aldosterone in vivo did not induce amiloride-sensitive Na+ transport across the embryonic trophectoderm. It therefore seems unlikely that an increase in maternal adrenal steroid concentrations is necessary for the development of amiloride-sensitive Na+ transport in rabbit blastocysts. Sodium efflux from Day 6 post coitum (p.c.) blastocysts was lower than Na+ influx. By day 7 p.c. Na+ efflux was equivalent in magnitude to the component of Na+ influx not inhibited by amiloride. This suggests that between Days 6 and 7 p.c. the amiloride-sensitive component of Na+ influx becomes essential for blastocyst expansion.

7 citations


Journal ArticleDOI
Raimund Hummelink1, Philip L. Ballard1Institutions (1)
TL;DR: In the rabbit, increases in plasma cortisol and nuclear receptor-cortisol complex are not temporally associated with the major events of lung development as in other species.
Abstract: Corticosteroid treatment of the fetus, which accelerates lung maturation, may mimic a modulating role of endogenous corticoids in normal development. To investigate this question, we determined the developmental pattern of plasma corticoids and their binding proteins in the rabbit, a commonly used species for studies of lung differentiation. The concentration of cortisol, the most potent glucocorticoid in the rabbit, was maximal at 23 days gestation (1.89 μg/dl), declining to 0.54 μg/dl at term (31 days). Levels of plasma corticosterone were always lower than those of cortisol. The adrenal content of corticoids, expressed per adrenal DNA or g BW, decreased during late gestation. Corticosteroid-binding globulin in fetal plasma decreased strikingly between day 23 (36 fig cortisol bound/dl) and day 31 (4.4 μg/dl; P < 0.001), whereas maternal levels increased about 10-fold during this time. Free cortisol in the fetus increased between 21 and 23 days (0.041 μg/dl) and then decreased somewhat until after day 29...

21 citations


Journal ArticleDOI
Ira H Gewolb1, Joseph B Warshaw1Institutions (1)
TL;DR: Delayed fetal lung maturation observed in fetuses of streptozotocindiabetic rats is associated with a decrease in total circulating corticosteroid levels late in gestation, but it is likely that other mechanisms may be responsible for the observed delay in lung development in Fetuses of diabetic pregnancies.
Abstract: Delayed fetal lung development is a feature of the diabetic pregnancy. Since fetal glucocorticoids are important in the regulation of lung maturation, we measured corticosterone and corticosteroid-binding globulin binding capacity in streptozotocin-diabetic pregnant rats and their fetuses. Previous studies have demonstrated delayed fetal lung maturation in this animal model. In control fetuses, total corticosterone concentration increased through day 20 of gestation, then declined until day 22 (term). The unbound steroid, which accounted for 5-10% of the total, increased approximately 3-fold from day 18 to term. Corticosteroid-binding globulin binding capacity peaked on day 19 after which it decreased. Maternal total and unbound corticosterone levels and corticosteroid-binding globulin binding capacity remained relatively constant throughout the final week of normal gestation. When compared to controls, fetuses from diabetic pregnancies had significantly lower total corticosterone from day 19 through 22. Corticosteroid-binding globulin binding capacity was also significantly decreased in these fetuses for the last 4 days of gestation. Similar differences were noted in maternal samples. However, no significant differences in unbound, biologically active, corticosterone were seen when diabetic and control groups were compared. Thus, delayed fetal lung maturation observed in fetuses of streptozotocin-diabetic rats is associated with a decrease in total circulating corticosteroid levels late in gestation. However, since unbound corticosteroid levels were similar in fetuses of control and diabetic animals, it is likely that other mechanisms may be responsible for the observed delay in lung development in fetuses of diabetic pregnancies.

15 citations


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Author's H-index: 1

No. of papers from the Author in previous years
YearPapers
19811