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  • HPA axis  (1)
  • Key words NIDDM, insulin secretion, fetal growth, programming.  (1)
  • 1
    Digitale Medien
    Digitale Medien
    Springer
    Diabetologia 37 (1994), S. 592-596 
    ISSN: 1432-0428
    Schlagwort(e): Key words NIDDM, insulin secretion, fetal growth, programming.
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary Recent studies suggest that NIDDM is linked with reduced fetal and infant growth. Observations on malnourished infants and studies of experimental animals exposed to protein energy or protein deficiency in fetal or early neonatal life suggest that the basis of this link could lie in the detrimental effects of poor early nutrition on the development of the beta cells of the islets of Langerhans. To test this hypothesis we have measured insulin secretion following an IVGTT in a sample of 82 normoglycaemic and 23 glucose intolerant subjects who were born in Preston, England, and whose birthweight and body size had been recorded at birth. The subjects with impaired glucose tolerance had lower first phase insulin secretion than the normoglycaemic subjects (mean plasma insulin concentrations 3 min after intravenous glucose 416 vs 564 pmol/l, p =0.04). Insulin secretion was higher in men than women (601 vs 457 pmol/l, p =0.02) and correlated with fasting insulin level (p =0.04). However, there was no relationship between insulin secretion and the measurements of prenatal growth in either the normoglycaemic or glucose intolerant subjects. These results argue against a major role for defective insulin secretion as a cause of glucose intolerance in adults who were growth retarded in prenatal life. [Diabetologia (1994) 37: 592–596]
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 2
    Digitale Medien
    Digitale Medien
    Springer
    European journal of pediatrics 157 (1997), S. S7 
    ISSN: 1432-1076
    Schlagwort(e): Key words Fetal growth ; Blood pressure ; Glucose tolerance ; Programming ; HPA axis
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract There is now a large body of evidence to support the hypothesis that events in fetal life permanently alter the structure or function of an individual, programming later adult disease. Reduced birth weight is associated with higher blood pressure in childhood and adult life, and thinness at birth with glucose intolerance and non-insulin dependent diabetes mellitus. Programming of the hypothalamo-pituitary-adrenal (HPA) axis is an attractive hypothesis linking fetal experience and later disease, as an excess of glucocorticoids may be associated with hypertension and glucose intolerance. Moreover, animal data support this hypothesis. Exposing fetal rats to glucocorticoid reduces birth weight and leads to raised blood pressure, as well as to alterations in the HPA axis. Data on the long-term effects of exposure to glucocorticoids in human subjects are limited. Recently, however, reduced size at birth was found to be associated with higher fasting 9 a.m. plasma cortisol concentrations in adults. Raised plasma cortisol concentrations were, in turn, associated with higher blood pressure, and inversely related to measures of glucose tolerance. Conclusion Programming of the HPA axis by events in fetal life may be one of the mechanisms linking reduced size at birth with raised blood pressure and glucose intolerance in later life. Studies of the effects of antenatal and neonatal dexamethasone administration on later blood pressure and glucose tolerance may be warranted.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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