La composition cytologique du pancréas endocrine foetal dans les conditions normales et pathologiques

Assche, F.A. Van; Gepts, W

doi:10.1007/bf01212059

Cited by 45 publications

(22 citation statements)

References 28 publications

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“…Blood glucose and insulin during OGTT in 1-4 and 5-9-year-old infants of gestational diabetic mothers (IGDM) as compared to those of pregestational insulin-dependent diabetic mothers (IDM) enhanced glucose tolerance in these neonates [22,23], which is believed to be due to a "conditioning" of the pancreatic beta cells in utero, leading to enhanced secretion of insulin to a glycaemic stimulus. Accordingly, Van Assche et al [24] described hyperplasia of the beta cells in newborns of diabetic mothers. However, the question remains whether and how this enhanced glucose tolerance in the neonate of a gestational diabetic mother is transformed into IGT in later life.…”

Section: Discussionmentioning

confidence: 99%

Glucose tolerance and insulin secretion in children of mothers with pregestational IDDM or gestational diabetes

et al. 1997

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Since Pedersen's fundamental work [1] the metabolic situation in infants of mothers with diabetes mellitus during pregnancy has been investigated in a number of studies [2][3][4]. While most authors focussed on altered glucose homeostasis during neonatal life, it remains unclear if these alterations do persist or resolve in later life. Clinical investigations during childhood indicated elevated frequencies of impaired glucose tolerance (IGT) in the offspring of mothers with diabetes during pregnancy [5,6]. Some authors reported alterations of insulin secretion such as hyperinsulinaemia [6,7] which is known to play a key role in the development of metabolic and cardiovascular disturbances in adulthood [8]. Experimental studies in rats displayed long-term alterations of glucose tolerance and insulin secretion due to the induction of maternal gestational hyperglycaemia which leads to fetal and neonatal hyperinsulinism [9][10][11][12][13].However, only a very small number of studies are available which compared glucose metabolism and Diabetologia (1997Diabetologia ( ) 40: 1094Diabetologia ( -1100 Glucose tolerance and insulin secretion in children of mothers with pregestational IDDM or gestational diabetes Summary The offspring of mothers with diabetes mellitus during pregnancy are presumed to develop altered glucose homeostasis. We analysed metabolic parameters at birth and glucose tolerance and insulin secretion during oral glucose tolerance tests at 1-9 years of age in 129 children born to mothers with pregestational insulin-dependent diabetes (IDDM) and 69 infants of gestational diabetic mothers. Newborns of IDDM mothers displayed higher insulin (p < 0.001), glucose (p < 0.05), and insulin/glucose ratios (p < 0.002) than newborns of gestational diabetic mothers. During childhood, frequencies of impaired glucose tolerance (IGT) rose in infants of IDDM mothers from 9.4 % at 1-4 years to 17.4 % at 5-9 years of age, while in children of gestational diabetic mothers an increase from 11.1 % up to 20.0 % was observed. Offspring of gestational diabetic mothers displayed higher stimulated blood glucose (p < 0.025) than infants of IDDM mothers, while children of IDDM mothers showed higher stimulated insulin (p < 0.025), accompanied by increased fasting and stimulated insulin/glucose ratios (p < 0.05 and p < 0.02, respectively). Stimulated insulin in childhood was positively correlated to insulin at birth (p < 0.05). Furthermore, insulin/glucose ratio in childhood showed a positive correlation to insulin (p < 0.01) and insulin/glucose ratio at birth (p < 0.005). In conclusion, a pathogenetic role of fetal and neonatal hyperinsulinism for the development of IGT in both groups of infants of diabetic mothers is suggested, in particular for early induction of insulin resistance in the offspring of mothers with pregestational IDDM. [Diabetologia (1997)

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Section: Discussionmentioning

confidence: 99%

Glucose tolerance and insulin secretion in children of mothers with pregestational IDDM or gestational diabetes

et al. 1997

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“…It was confi rmed that fetal hyperinsulinism was due to B cell hyperplasia and the hypothesis was put forward that hyperactivity of the fetal B cells might result in reduced secretory capacity in later life. Furthermore, an intact hypothalamic structure was needed to induce B cell hyperplasia, predicting the role of the hypothalamus in perinatal programming [50] . D ö rner was among the fi rst to provide evidence that exposure to a diabetic intra-uterine environment increases the risk of developing diabetes in the offspring.…”

Section: Fetal Environment and Increased Fetal Growth Human Datamentioning

confidence: 99%

Fetal growth and developmental programming

Galjaard

Devlieger²,

Assche³

2012

Journal of Perinatal Medicine

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The environment in utero and in early neonatal life may induce a permanent response in the fetus and the newborn, leading to enhanced susceptibility to later diseases. This review concentrates on the role and mechanisms of events during the antenatal and immediate postnatal period resulting in later life diseases, concentrating on abnormal growth patterns of the fetus. Fetal overgrowth is related to exposure to a diabetic intra uterine environment, increasing the vulnerability to transgenerational obesity and hence an increased sensitivity to more diabetic mothers. This effect has been supported by animal data. Fetal growth restriction is complex due to malnutrition in utero , catch up growth due to a high caloric intake and low physical activity in later life. Metabolic changes and a transgenerational effect of intra uterine malnutrition has been supported by animal data. In recent years the discovery of alterations of the genome due to different infl uences during embryonic life, called epigenetics, has led to the phenomenon of fetal programming resulting in changing transgenerational metabolic effects.

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“…From the results of the differential cell counting it is assumed that type IV cells together with D cells [ll, 13] may belong to a heterogenous A 1 cell group [1], because there was a striking correspondence, when the percentages of D and type IV cells, found in the electron microscope, were summed (43%), and compared with the percentage of the A 1 cells (42%), light microscopically determined.…”

Section: Discussionmentioning

confidence: 99%

Morphometric and ultrastructural studies in an infant with leucine-sensitive hypoglycemia, hyperinsulinism and islet hyperplasia

et al. 1974

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Summary.Morphometrie and ultrastruetural studies were performed on biopsy material from the pancreas of an infant with severe leucine-sensitive hypoglycemia and hyperinsulinism, in whom no insulinoma had been found. Qualitatively many large B cells were observed within the pancreatic islets. Quantitatively an about two fold increase of islet tissue proportion (4.2 %) was demonstrated, compared with controls of approximately the same age (1.8%). Differential islet cell counting revealed an increase in A 1 cells whereas the percentage of A 2 and B cells appeared to be unchanged. Ultrastructurally in addition to A, B, and D cells a fourth islet cell type was demonstrated in unusual frequency. Its general function and its particular significance for the hypoglycemic syndrome are unknown. The findings correspond well with recent observations on the islet cell system in cases of neonatal hypoglycemia with leucine-sensitivity and hyperinsulinism.Key words: Neonatal hypoglycemia, hyperinsulinism, leucine-sensitivity, islet hyperplasia, ultrastructure, A, B, D and type IV cells.Reports concerning histopathology [3,4,8,9,16,17,18] or ultrastructure [26] of the pancreatic islets in idiopathic neonatal hypoglycemia are rare. Most of the examined pancreata showed a regular islet system [18], whereas only few exhibited islet hyperplasia. Moreover, as quantitative methods were only rarely applied to islet examination in infants, the diagnosis of islet hyperplasia as a cause of neonatal hypoglycemia remained often doubtful.A recent report of Misugi and coworkers [26] renewed the interest in the islet system in neonatal hypoglycemia. The anthers described islet cell hyperp/asia in three infants with leucine-sensitive hypoglycemia [4] and hyperinsulinism. The ultrastruetural examination revealed a fourth islet cell type in addition to A, B and D cells. The present report of a ease of leucine-sensitive neonatal hypoglycemia confirms the findings of Misugi and associates, and briefly discusses the significance of the observations on the basis of the literature on this subject.

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La composition cytologique du pancréas endocrine foetal dans les conditions normales et pathologiques

Cited by 45 publications

References 28 publications

Glucose tolerance and insulin secretion in children of mothers with pregestational IDDM or gestational diabetes

Glucose tolerance and insulin secretion in children of mothers with pregestational IDDM or gestational diabetes

Fetal growth and developmental programming

Morphometric and ultrastructural studies in an infant with leucine-sensitive hypoglycemia, hyperinsulinism and islet hyperplasia

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