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  • pregnant rats  (2)
  • Slight gestational hyperglycaemia  (1)
  • 1
    ISSN: 1432-0428
    Schlagwort(e): Glucose infusion ; pregnant rats ; fetus ; plasma insulin ; fetal body weight ; lipid synthesis
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary Mild hyperglycaemia was induced in unrestrained pregnant rats from day 20.5 to day 23.5 of pregnancy, using a continuous glucose infusion. Control rats were infused with distilled water. In post-mature fetuses from glucose-infused rats, raised plasma glucose and insulin concentrations were related to increased body weight (6.03±0.07 g) and total carcass fat (2.02±0.04% of fresh weight) compared with control fetuses of the same age (5.35±0.07 and 1.5±0.04 g, respectively). Concurrently, the rate of lipogenesis in the carcass, estimated from the incorporation of tritium from tritiated water into fatty acids, was significantly increased in fetuses from glucose infused rats compared with control rats (6.00±0.34 versus 2.62±0.27 and 3H2O · h-1 · g tissue-1, respectively).
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 2
    ISSN: 1432-0428
    Schlagwort(e): Slight gestational hyperglycaemia ; high gestational hyperglycaemia ; fetus ; insulin release ; perifused pancreas ; leucine ; arginine
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary Unrestrained pregnant rats were infused with glucose during the last week of pregnancy to produce slight or high gestational hyperglycaemia. Control rats were infused with distilled water. Insulin secretion of the fetuses at term was studied in vitro using a perifusion system. Compared with controls, perifused pancreases of slightly hyperglycaemic fetuses showed a similar pattern of insulin secretion in response to 10 mmol/l leucine. Arginine-induced insulin secretion at 20 mmol/1 was higher than in controls. In both groups, 10 mmol/l a-ketoisocaproate had a poor stimulatory effect on insulin release, and 5 mmol/1 D-glyceraldehyde was ineffective in eliciting insulin secretion. In highly hyperglycaemic fetuses all the secretagogues, with the exception of arginine, which induced a sustained monophasic insulin secretory response, had no effect on insulin release. These data show that long-term exposure of fetal B cells to high plasma glucose levels in utero suppresses or alters further insulin secretory response not only to glucose but also to other nutrient secretagogues. The partially spared insulin secretory response to arginine suggests that the defect may concern stimulus-secretion coupling rather than insulin releasing machinery.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 3
    ISSN: 1432-0428
    Schlagwort(e): Glucose infusion ; pregnant rats ; prolonged pregnancy ; fetus ; plasma insulin ; plasma glucagon ; liver phosphoenolpyruvate carboxykinase ; liver glycogen
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary Continuous glucose infusion was used to induce mild hyperglycaemia in unrestrained pregnant rats during the last three days of pregnancy. Control pregnant rats were infused with distilled water. Fetuses were studied after normal or prolonged pregnancy. Fetuses from glucose-infused rats, compared with controls, showed higher plasma glucose levels, increased plasma insulin and lower plasma glucagon concentrations. Pregnancy prolonged until day 23.5 resulted in a rise in the glucagon/insulin ratio from 6.5 to 67 in fetuses from control rats and from 1.3 to 13 in fetuses from glucose-infused rats. Concurrently in fetuses from control rats, liver phosphoenolpyruvate carboxykinase activity increased markedly and liver glycogen stores decreased sharply. In fetuses from glucose-infused rats, liver phosphoenolpyruvate carboxykinase activity rose and glycogen content decreased, but to a lesser extent. These results show that both the A and B cells of the rat fetal pancreas are sensitive to chronic glucose stimulation.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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