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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Diabetologia 31 (1988), S. 225-227 
    ISSN: 1432-0428
    Keywords: Glucopenia ; insulin ; glucagon ; arginine ; diabetes ; BB/W rats ; perfused pancreas
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To determine if the inhibiting effect of glucopenia on arginine-stimulated insulin secretion is impaired at the onset of autoimmune diabetes, the insulin response to arginine was studied at 5.6 and 2.8 mmol/l glucose in perfused pancreata isolated from BB/W rats on the first day of diabetes and from age-matched diabetes-prone BB/W rats without diabetes. During glucopenia the baseline insulin secretion was reduced by more than 80% in both groups. However, the arginine-stimulated insulin response in the diabetic group was only 16.5% lower during glucopenia compared to 79.1% lower in the nondiabetic controls. Also, enhancement of the arginine-stimulated glucagon response by glucopenia was modest compared to controls. The results indicated that at the onset of this form of autoimmune diabetes the surviving B cells are, for unknown reasons, hyperresponsive to arginine and that, in contrast to the controls, this response is not inhibited by glucopenia.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 2
    ISSN: 1432-0428
    Keywords: Hyperglycaemia ; islet cell function ; insulin ; glucagon ; diabetic remissions ; Type 1 diabetes ; Type 2 diabetes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary It is postulated that hyperglycaemia influences the natural history of Type 1 (insulin-dependent) and Type 2 (non-insulin-dependent) diabetes mellitus. Hyperglycaemia, even when mild, can attenuate the secretory response of pancreatic β and α cells to increments in glucose and can impair insulin-mediated glucose transport, thus impeding its own correction and initiating a cycle of progressive self-exacerbation and metabolic deterioration. Both reduced islet function and insulin action may be the consequence of a generalized down-regulation and/or occupation of glucose transporters by hyperglycaemia so that the islets respond less to further increments in glycaemia. The postulated hyperglycaemic cycle can be initiated by any environmental perturbation that increases insulin demand in previously normoglycaemic patients in whom insulin secretion has already reached a maximum level of compensation for peripheral insulin resistance (as in obese pre-Type 2 diabetes) or for a reduced β-cell mass (as in pre-Type 1 diabetes). Elimination of hyperglycaemia by any means can halt this cycle of progressive metabolic deterioration and may restore transiently metabolic recompensation both in Type 1 and Type 2 diabetes. There is experimental evidence that long-standing severe hyperglycaemia may irreversibly damage β cells.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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