C-Peptide Levels in Amniotic Fluid in Experimental Fetal Growth Retardation

Prins, F. De; Assche, Ado Van; Milner, R. D. G.

doi:10.1159/000241626

Cited by 14 publications

(7 citation statements)

References 8 publications

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“…Positive relationships therefore exist between fetal body size and the levels of insulin and somatomedin in the blood as seen from the significant correlation between body weight or length and somatomedin activity in the present experiments, and our previous findings that immunoassayable levels of insulin Cpeptide in amniotic fluid were reduced compared to control animals and showed positive correlation with body weight in the Wigglesworth model (37). These studies suggest that nutrient supply may become a limiting factor in the release of both insulin and somatomedin in the rat fetus, and hence in its growth.…”

Section: Discussionsupporting

confidence: 88%

Reduced Plasma Somatomedin Activity and Costal Cartilage Sulfate Incorporation Activity during Experimental Growth Retardation in the Fetal Rat

et al. 1984

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ABSTRACT. In this study, the experimental model of Wigglesworth was used to limit the maternal blood supply to the rat fetus and induce intrauterine growth retardation. The associated changes in plasma somatomedin activity, insulin, glucose, and cartilage metabolic activity are reported. The mean body weight (f SEM) of 108 fetuses in ligated uterine horns was significantly lower than that of 146 control fetuses (ligated, 2820 f 50 mg; control, 3180 MSA, multiplication-stimulating activityThe growth hormone-dependent peptide growth factors, the somatomedins, have a major role in the growth and development of skeletal and somatic tissues in postnatal life (1). Somatomedins also are present in the fetus and a positive correlation between circulating levels and fetal body size led us and others to hypothesize that somatomedins providean important anabolic stimulus to development in utero (2-5). However, the factors controlling circulating levels of somatomedins in the fetus are not understood. Growth hormone does not appear to be important since decapitation of the fetal rabbit and hypophysectomy of the lamb in utero did not lower somatomedin bio-and radioreceptor

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Section: Discussionsupporting

confidence: 88%

Reduced Plasma Somatomedin Activity and Costal Cartilage Sulfate Incorporation Activity during Experimental Growth Retardation in the Fetal Rat

et al. 1984

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“…The degree of growth retardation, approximately 10%, in delivered pups was small compared to what has been observed in utero 1-3 days following surgery [27,29,41,42] . There was, however, a considerable reduction of litter size in IUGR.…”

Section: Discussionmentioning

confidence: 61%

Experimental Intrauterine Growth Retardation in the Rat Causes a Reduction of Pancreatic B-Cell Mass, Which Persists into Adulthood

et al. 2005

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Background and Objectives: The aim of this study was to investigate the possibility that intrauterine growth retardation (IUGR) causes alterations of glucose tolerance, insulin secretory response to glucose, and pancreatic B-cell growth, and if such changes may persist into adulthood. Methods: Pregnant rats were operated on day 16 of pregnancy ad modum Wigglesworth to induce IUGR. Operated rats gave birth to viable offspring but litter size was reduced. The mothers nursed their pups, which were subsequently weaned and reared to an age of 3 months in apparent good health. Results: At 1 day of age, IUGR pups were 10% lighter than control newborns whose mothers had been subjected to a sham operation. Pancreatic B-cell mass and insulin content were reduced by 35–40% in newborn IUGR offspring. Postnatal growth did not differ between IUGR and control animals of either sex and the difference in body weight at birth was not apparent from 1 week of age and onwards. Tests performed at 3 months of age could not demonstrate differences in glucose tolerance between IUGR and control animals. In females, but not in males, the peak insulin secretory response to glucose was lower in IUGR animals compared to controls. In the 3-month-old rats, B-cell mass was reduced by 40% in male and by 45% in female IUGR rats compared to controls, a reduction corresponding to a similar decrease in pancreatic insulin content (male reduction 48%, female reduction 45%). Conclusions: In the rat, IUGR causes a diminution of pancreatic B-cell mass which persists into adulthood. Normal glucose tolerance could be maintained but it is conceivable that increasing demands on insulin secretion may not be met by the reduced B-cell mass and that impaired glucose tolerance and even diabetes would hence develop.

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“…IUGR fetuses displayed significantly lower glucose and insulin levels. In addition, C‐peptide levels were reduced in the amniotic sac of the growth‐retarded fetuses (De Prins et al 1983).…”

Section: Animal Modelsmentioning

confidence: 99%

Lifetime consequences of abnormal fetal pancreatic development

2003

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There is ample evidence that an adverse intrauterine environment has harmful consequences for health in later life. Maternal diabetes and experimentally induced hyperglycaemia result in asymmetric overgrowth, which is associated with an increased insulin secretion and hyperplasia of the insulin-producing B-cells in the fetuses. In adult life, a reduced insulin secretion is found. In contrast, intrauterine growth restriction is associated with low insulin secretion and a delayed development of the insulin-producing B-cells. These perinatal alterations may induce a deficient adaptation of the endocrine pancreas and insulin resistance in later life. Intrauterine growth restriction in human pregnancy is mainly due to a reduced uteroplacental blood flow or to maternal undernutrition or malnutrition. However, intrauterine growth restriction can be present in severe diabetes complicated by vasculopathy and nephropathy. In animal models, intrauterine growth retardation can be obtained through pharmacological (streptozotocin), dietary (semi-starvation, low protein diet) or surgical (intrauterine artery ligation) manipulation of the maternal animal. The endocrine pancreas and more specifically the insulin-producing B-cells play an important role in the adaptation to an adverse intrauterine milieu and the consequences in later life. The long-term consequences of an unfavourable intrauterine environment are of major importance worldwide. Concerted efforts are needed to explore how these long-term effects can be prevented. This review will consist of two parts. In the first part, we discuss the long-term consequences in relation to the development of the fetal endocrine pancreas and fetal growth in the human; in the second part, we focus on animal models with disturbed fetal and pancreatic development and the consequences for later life.

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C-Peptide Levels in Amniotic Fluid in Experimental Fetal Growth Retardation

Cited by 14 publications

References 8 publications

Reduced Plasma Somatomedin Activity and Costal Cartilage Sulfate Incorporation Activity during Experimental Growth Retardation in the Fetal Rat

Reduced Plasma Somatomedin Activity and Costal Cartilage Sulfate Incorporation Activity during Experimental Growth Retardation in the Fetal Rat

Experimental Intrauterine Growth Retardation in the Rat Causes a Reduction of Pancreatic B-Cell Mass, Which Persists into Adulthood

Lifetime consequences of abnormal fetal pancreatic development

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