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  • Growth hormone  (1)
  • Key words Hyperglycemia  (1)
  • 1
    Digitale Medien
    Digitale Medien
    Springer
    Pediatric nephrology 14 (2000), S. 567-571 
    ISSN: 1432-198X
    Schlagwort(e): Key words Hyperglycemia ; Glucose intolerance ; Diabetes ; Metabolic effects ; Insulin-like growth factors ; Growth
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract  Overexpression of insulin-like growth factor-1 binding protein (IGFBP-1) in transgenic mice has provided insight into the physiological role of this binding protein in modulating the metabolic and growth-promoting effects of the IGFs. IGFBP-1 transgenic mice demonstrate both intrauterine and postnatal growth retardation. Organ weight was proportionately reduced relative to body weight in most organs, with the exception of the brain, which was disproportionately small in transgenic mice. There were no gross neurological manifestations of the reduction in brain size. Transgenic mice also demonstrated fasting hyperglycemia, impaired glucose tolerance, and modest insulin resistance in skeletal muscle and hepatic tissue. From these data, we can conclude that overexpression of IGFBP-1 results in inhibition of IGF action and in profound impairment of brain development, modest inhibition of fetal and postnatal growth, and inhibition of the metabolic effects of the IGFs. Increased expression of IGFBP-1 has been documented in a variety of situations, such as fetal nutritional deprivation and hypoxia, and has been considered to be a marker of metabolic disturbances that cause fetal growth retardation. The observations in IGFBP-1 transgenic mice suggest expression of IGFBP-1 may itself contribute to the growth retardation and impaired fetal brain development.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 2
    ISSN: 1432-0428
    Schlagwort(e): Growth hormone ; insulin ; insulin-like growth factor-I ; diabetes ; growth ; somatomedin
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary Although growth hormone is known to be the main regulator of insulin-like growth factor-I, insulin has also been shown to play a role in regulating serum insulin-like growth factor I levels in diabetic animals. While this effect is thought to be due to correction of metabolic perturbations, some studies have suggest that insulin may have a direct effect on growth and/or insulin-like growth factor-I levels. We have examined the effects of acute and chronic insulin administration to non-diabetic, pituitary-intact and hypophysectomised rats. Rats were injected intraperitoneally with insulin as an acute bolus (10 U) or a chronic subcutanious infusion (low dose; 2.4 U/day, high dose; 12 U/day) over 5 days. Insulin-like growth factor-I mRNA was quantitated by Northern and slot blots of RNA from various tissues. A small (less than 2-fold) but significant increase (p〈0.05) was seen in hepatic insulin-like growth factor-I mRNA abundance in pituitary-intact rats following acute insulin injection and chronic low dose insulin infusion. An increase in insulin-like growth factor-I mRNA levels was also seen in other tissues including diaphragm, lung, kidney and heart. A significant increase (p〈0.05) in serum insulin-like growth factor-I levels was also observed 6 h after insulin injection. In contrast, in pituitary-intact rats which received high dose insulin infusion and were hypoglycaemic at the time of death, tissue levels of insulin-like growth factor-I mRNA were reduced compared to saline-treated control groups. Similarly in the hypophysectomised rats neither acute nor chronic insulin administration had any consistent effect on insulin-like growth factor-I mRNA abundance in any of the tissues examined. This data suggests that insulin has no direct effect in regulating insulin-like growth factor-I gene expression. The small effects demonstrable in pituitary-intact rats may result from a synergistic action of insulin with growth hormone or other pituitary factors.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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