Use of Streptozotocin as Diabetic Agent in Pregnant Rats

Sybulski, S.; Maughan, G.B.

doi:10.1210/endo-89-6-1537

Cited by 44 publications

(34 citation statements)

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“…On the other hand, the retardation of fetal growth was also evident in diabetic mother rats (Sybulski and Maughan, 1971;Love et al, 1964). In the present experiment, the degree of diabetes was relatively severe, at least as judged by maternal weight gain and blood glucose level.…”

Section: Discussionsupporting

confidence: 51%

Changes in the Cholesterol Level in the Tissues of Streptozotocin-Induced Diabetic Mother Rats and Their Infants During the Early Postpartum Period

Fujimoto

Fujii

1974

Endocrinol Japon

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SynopsisA diabetes-like state was induced by intravenous injection of a single dose of streptozotocin (SZ), 45mg/kg, in pregnant rats and the cholesterol level in the tissues of. the mothers and their infnats was examined during the early postpartum period.The following results were obtained. 1) The infants of the diabetic mothers were smaller than the infants of normal mothers and were markedly hyperglycemic. 2) Serum cholesterol was markedly increased on day 21 of pregnancy both in normal and diabetic groups. The concentration, however, declined nearly to the nonpregnant normal level on the 1st day after delivery in normal mothers, while it decreased stepwise until day 7 in diabetic mothers.3) The cholesterol contents in the adrenal, liver and serum of infants of normal and diabetic groups increased progressively during the early postpartum period. However, the cholesterol level in these tissues was always lower in the infants of diabetic mothers than in normal infants; the concentration in the liver was considerably lower. 4) The adrenal cholesterol concentration decreased abruptly in the normal mother on day 1 after delivery and it returned to approximately normal level on day 7. On the other hand, no alteration in the cholesterol concentration was observed in the daibetic mother after parturition. In addition, the adrenal weight of the diabetic mother was heavier than that of the normal control mother at all stages examined.These results suggest impairment of the steroidogenesis in the maternal adrenal in response to endogenous ACTH during the parturition in a diabetic state. Moreover, it was clearly demonstrated that SZ-induced hyperglycemia in pregnant rats affected the cholesterol metabolism in the adrenal and liver in newborns.

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Section: Discussionsupporting

confidence: 51%

Changes in the Cholesterol Level in the Tissues of Streptozotocin-Induced Diabetic Mother Rats and Their Infants During the Early Postpartum Period

Fujimoto

Fujii

1974

Endocrinol Japon

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“…In addition to malformations, the offspring of diabetic rats also display growth retardation at birth (5,6,(16)(17)(18)(19), as well as during the embryonic period (20). Our study therefore also aimed to search for maternal parameters correlating with the embryonic-fetal growth retardation in diabetic pregnancy, parameters not necessary identical to those associated with embryonic malformations.…”

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confidence: 99%

Correlations between Maternal Metabolism and Deranged Development in the Offspring of Normal and Diabetic Rats

et al. 1995

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In an attempt to define the pathogenesis of congenital malformations in diabetic pregnancy, a number of serum factors were determined in normal and diabetic pregnant rats and correlated to the outcome of gestation with the aid of multivariate linear regression analysis. The animals were from two different lines of Sprague-Dawley rats with documented differences in rates of fetal dysmorphogenesis in diabetic pregnancy. The diabetic rats increased less in body weight than the normal rats, yet displayed increased liver and kidney weights. The serum concentrations of glucose, P-hydroxybutyrate, triglycerides, the branched-chain amino acids, and asparagine, proline, alanine, citrulline, tyrosine, and ornithine were increased by diabetes. In contrast, IGF-I, glutamic acid, glutamine, cystine, and lysine were decreased in the serum of the diabetic pregnant rats. The maternal metabolic imbalance exerted profound effects on embryonic development. Thus, the embryos of the diabetic rats were smaller, had fewer somites, and contained less DNA and protein than the control embryos. In addition, the resorption and malformation rates were increased in the embryos of the diabetic rats. The regression analysis of the data revealed significant interrelationships between adverse embryonic outcome (rates of malformations and resorptions) and the maternal serum concentrations of glucose, triglycerides, P-hydroxybutyrate, branched-I---Diabetic pregnancy is associated with an increased risk of fetal maldevelopment (1-3). The pathogenesis of congenital malformations in the offspring of diabetic mothers is unknown. In previous clinical and experimental studies, strict metabolic control of the mother has been shown to diminish the risk of fetal maldevelopment, especially if the improved control is initiated in early pregnancy (4-7) or before conception (8).chain amino acids, and creatinine. This suggests that the maternal metabolism of the three major classes of nutrients covariates with the embryonic development in diabetic rat pregnancy. The monitoring of only one of these maternal parameters, e.g. the serum glucose concentration, may therefore not adequately predict the developmental status of the offspring. Our results suggest that the pathogenesis of fetal malformations in diabetic pregnancy is multifactorial. Thus, maintaining metabolites from all nutrient classes at a normal level may be important in preventing adverse fetal outcome. Maintenance of normal serum glucose levels alone, however, does not seem to completely protect the fetus from malformations (9). Other disturbed metabolic processes in the mother, reflected by alterations in serum levels of associated metabolites, may therefore have pathogenic roles in the teratogenicity of diabetic pregnancy. In previous studies of an animal model for diabetic pregnancy, w e found increased rates of fetal malformations and resorptions among the offspring of streptozotocin-diabetic rats

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“…10 Interestingly, human ␤ cells are resistant to SZ. 11 A robust dose of SZ in rats induces permanent hyperglycemia and hypoinsulinemia within 48 hours, 12,13 which has been used by numerous research groups, including ours, as a model for type 1 diabetes during pregnancy. 14,15 We have also studied pregnancies in spontaneously diabetic biobreeding rats, which develop an autoimmune form of type 1 diabetes.…”

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confidence: 99%

Is Low-Dose streptozotocin in Rats an Adequate Model for Gestational Diabetes Mellitus?

Caluwaerts¹,

Holemans²,

Bree³

et al. 2003

Journal of the Society for Gynecologic Investigation

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Use of Streptozotocin as Diabetic Agent in Pregnant Rats

Cited by 44 publications

References 0 publications

Changes in the Cholesterol Level in the Tissues of Streptozotocin-Induced Diabetic Mother Rats and Their Infants During the Early Postpartum Period

Changes in the Cholesterol Level in the Tissues of Streptozotocin-Induced Diabetic Mother Rats and Their Infants During the Early Postpartum Period

Correlations between Maternal Metabolism and Deranged Development in the Offspring of Normal and Diabetic Rats

Is Low-Dose streptozotocin in Rats an Adequate Model for Gestational Diabetes Mellitus?

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