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  • 1
    ISSN: 1432-0428
    Keywords: Glucose ; insulin ; glucagon ; glucose metabolism ; A cell ; 2-deoxyglucose ; subtotal pancreatectomy ; ducks
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A possible action of insulin via glucose metabolism on the pancreatic A cell response to glucose, was studied in ducks. 2-Deoxyglucose, a non-metabolizable analogue of glucose was used. In normal ducks, the hyperglycaemia induced by 2-deoxyglucose (IV: 0.5 g/kg) resulted in hyperglucagonaemia, while the same degree of hyperglycaemia, induced by glucose infusion (IV injection 25 mg/kg, and infusion 5 mg/kg/min) immediately suppressed glucagon secretion. In diabetic ducks, two days after subtotal pancreatectomy, glucose responsiveness of the A cell was abolished, but could be restored by insulin treatment before (IM 0.2 U/kg insulin+8 μg/kg glucagon every 6 h) and during (IV 3.6 mU/kg+infusion 0.9 mU/kg/min) the glucose test (IV: 0.5 g /kg). The normal response of the A cell to glucose was not observed in diabetic insulin-treated ducks after the administration of 2-deoxyglucose (IV: 0.5 g/kg). These data suggest an inhibitory effect of the metabolism of glucose on the release of glucagon. In addition, the action of insulin on the A cell may be mediated by its effect on glucose metabolism within the A cell.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 14 (1978), S. 185-190 
    ISSN: 1432-0428
    Keywords: Duck ; adipose tissue ; FFA release ; glucagon ; insulin ; glucose uptake
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The present study was undertaken to determine how free fatty acid (FFA) release by adipose tissue can occur in the absence of pancreatic glucagon, the most potent lipolytic hormone in the duck. Two possible explanations have successively been investigated. Replacement therapy experiments showed that glucose uptake was implicated in the phenomenon; indeed, when pre-operative insulin and glucose levels were restored after total pancreatectomy, plasma FFA progressively fell to a level significantly lower than the pre-operative value. The same effect was observed when the ducks were kept in a continuous state of hyperglycaemia, whereas “normal” levels of insulin or glucose alone were shown to be ineffective. On the other hand a compensatory mechanism for the lack of glucagon, by other lipolytic agents [with the intestine or the anterior pituitary as possible sources] has been excluded by associating the removal of these two organs with pancreatectomy. These experiments suggest that the lack of pancreatic glucagon induced by total pancreatectomy is essentially masked by a failure in glucose uptake due to the operation.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 3
    ISSN: 1432-0428
    Keywords: Glucose ; insulin ; glucagon ; glucose metabolism ; A cell ; 2-deoxyglucose ; subtotal pancreatectomy ; ducks
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A possible action of insulin via glucose metabolism on the pancreatic A cell response to glucose, was studied in ducks. 2-Deoxyglucose, a non metabolizable analogue of glucose was used. In normal ducks, the hyperglycaemia induced by 2-deoxyglucose (IV: 0.5g/kg) resulted in hyper glucagonaemia, while the same degree of hyper glycaemia, induced by glucose infusion (IV injection 25 mg/kg, and infusion 5 mg/kg/min) immediately suppressed glucagon secretion. In diabetic ducks, two days after subtotal pancreatectomy, glucose responsiveness of the A cell was abolished, but could be restored by insulin treatment before (IM 0.2 U/kg insulin + 8 μg/kg glucagon every 6 h) and during (IV 3.6 mU/kg + infusion 0.9 mU/kg/min) the glucose test (IV: 0.5 g /kg). The normal response of the A cell to glucose was not observed in diabetic insulintreated ducks after the administration of 2-deoxyglucose (IV: 0.5 g/kg). These data suggest an inhibitory effect of the metabolism of glucose on the release of glucagon. In addition, the action of insulin on the A cell may be mediated by its effect on glucose metabolism within the A cell.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
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