Normal and Abnormal Foetal Weight Gain

Jj, Hoet

doi:10.1002/9780470719688.ch12

Cited by 22 publications

(7 citation statements)

References 67 publications

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“…The reasons for this discrepancy remain unclear; the short duration of pregnancy in the rat and the poor development of adipose tissue in term fetuses (approximately 1%) compared to that of human babies (averaging 16%) could account for the difference between rats and humans. In contrast growth retardation is reported in infants of women with longstanding and complicated diabetes [21]. In severely diabetic rats the fetal growth retardation observed by us and others [6,22,23] may be due to decreased basal plasma insulin levels [5,6 and Fig.…”

Section: Discussionmentioning

confidence: 91%

The endocrine pancreas of the fetus from diabetic pregnant rat

1978

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Diabetes was induced in female rats by streptozotocin administration prior to mating. Pregnant rats were divided into "severe diabetics" (blood glucose concentration above 300 mg/100 ml) and "mild diabetics" (blood glucose ranging from 100 to 200 mg/100 ml). When compared to control fetuses, fetuses from severely diabetic mothers showed a slight decrease of body weight on days 20.5 and 21.5. Fetal pancreatic insulin stores and plasma insulin concentrations were decreased at 19.5, 20.5 and 21.5 days. The insulin response to glucose was impaired both in vivo and in vitro. In contrast, fetuses from mildly diabetic females showed no change in body weight. Pancreatic and plasma insulin concentrations were increased at 19.5, 20.5 and 21.5 days. The response of the beta cells of term fetuses of mild diabetics to glucose stimulation was enhanced in vitro. These results are consistent with the hyperglycaemia-hyperinsulinaemia theory with regard to the fetuses from mildly diabetic rats and with an impairment of insulin biosynthesis and release in fetuses from severely diabetic females.

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Section: Discussionmentioning

confidence: 91%

The endocrine pancreas of the fetus from diabetic pregnant rat

1978

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“…Other follow-up studies have demonstrated a high percentage of abnormal or borderline glucose tolerance tests (1 3). The subsequent growth in children of diabetic mothers has also attracted great interest and both normal and abnormal growth patterns have been reported (4, 10, [14][15][16].…”

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confidence: 99%

Follow‐up of Children of Insulin Dependent (Type I) and Gestational Diabetic Mothers

1984

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Fifty-three children of insulin dependent (IDM) and 20 children of gestational diabetic mothers (IGDM) representing 80 and 91%, respectively, of all surviving infants of diabetic mothers born between 1969 and 1972 at Sabbatsberg's hospital, Stockholm, participated in the follow-up study. The first follow-up examination was performed when the children had reached approximately 5 years of age and included measurement of height and weight, insulin response to intravenous glucose, and HLA typing. When the children were approximately 11 years old, a search was performed in the national register for type I diabetes in children in order to ascertain the frequency of type I diabetes mellitus in the total series (n = 88). The majority of children had a normal height for age and desirable weight for height. At the first follow-up all children had normal glucose disappearance rates (kt) and the insulin response including the early insulin response to glucose were not different between IDM and IGDM groups. The frequency distribution of HLA antigens (A, B, C) was not different from normal and there was no association between HLA B 8 and/or B 15 and early insulin response or kt values. At the second follow-up, two children of type I diabetic mothers had acquired type I diabetes, both were HLA B 15 positive, had normal kt values at the first follow-up, one with low, one with a high early insulin response. The frequency of type I diabetes in offspring of insulin dependent diabetic mothers was 3%.

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“…A major clinical feature of anencephaly is prolonged gestation (3). Infants with anencephaly are of normal proportions but are generally under the 50th percentile for weight (4). Pathological studies reveal hypoplastic pituitaries and small adrenals, deficient in a fetal zone (5,6).…”

Section: Introductionmentioning

confidence: 99%

Endocrine Studies in Anencephaly

Hayek¹,

Driscoll²,

Warshaw³

1973

J. Clin. Invest.

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A B S T R A C T Endocrine function has been investigated in four anencephalic neonates to determine the influence of absence of cortical and hypothalamic tissue and of hypoplasia of the pituitary. Intravenous glucose administration resulted in higher peak values for blood sugar and more rapid glucose disposal rates than reported in normals. Intravenous insulin tolerance tests on two of the infants failed to evoke elevations in plasma growth hormone, and the infants showed a remarkable resistance to the hypoglycemic effect of insulin. Administration of lysine-vasopressin caused an active growth hormone release. Similarly, there was a large increase in serum thyrotropin after administration of synthetic thyrotropinreleasing hormone. Basal levels of both thyrotropin and growth hormone were low as compared with values reported for normal newborns. Prolactin values obtained on three of the infants were in the normal range. The results strongly suggest that anterior pituitary function mediated by the hypothalamus and its releasing factors is deficient in anencephaly. However, the anterior pituitary can release growth hormone and thyrotropin when stimulated directly and, in the case of thyrotropin release, may function autonomously. The normal prolactin values presumably reflect the absence of the hypothalamic prolactin inhibitory factor.

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Normal and Abnormal Foetal Weight Gain

Cited by 22 publications

References 67 publications

The endocrine pancreas of the fetus from diabetic pregnant rat

The endocrine pancreas of the fetus from diabetic pregnant rat

Follow‐up of Children of Insulin Dependent (Type I) and Gestational Diabetic Mothers

Endocrine Studies in Anencephaly

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