http://www.cnr.it/ontology/cnr/individuo/prodotto/ID169548
Effect of acute hyperglycemia on insulin secretion in humans (Abstract in rivista)
- Type
- Label
- Effect of acute hyperglycemia on insulin secretion in humans (Abstract in rivista) (literal)
- Anno
- 2002-01-01T00:00:00+01:00 (literal)
- Alternative label
Toschi E., Camastra S., Sironi A.M., Masoni A., Gastaldelli A., Mari A., Ferrannini E., Natali A. (2002)
Effect of acute hyperglycemia on insulin secretion in humans
(literal)
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- Toschi E., Camastra S., Sironi A.M., Masoni A., Gastaldelli A., Mari A., Ferrannini E., Natali A. (literal)
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- Rivista
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- Toschi: Metabolism Unit, CNR Institute of Clinical Physiology, Pisa, Italy - Department of Internal Medicine, University of Pisa, Pisa, Italy - CNR Institute of Clinical Physiology, Via Savi, 8, 56126 Pisa, Italy /
Camastra, Sironi, Masoni, Gastaldelli, Ferrannini, Natali: Metabolism Unit, CNR Institute of Clinical Physiology, Pisa, Italy, Department of Internal Medicine, University of Pisa, Pisa, Italy /
Mari: CNR Institute of Systems Science and Biomedical Engineering, Padova, Italy (literal)
- Titolo
- Effect of acute hyperglycemia on insulin secretion in humans (literal)
- Abstract
- First-phase insulin response to intravenous glucose is impaired both in type 2 diabetic patients and in subjects at risk for the disease. Hyperglycemia can modify ?-cell response by either inhibiting or potentiating both first- and second-phase insulin release. In normal subjects, the effect of acute hyperglycemia on insulin secretion is controversial. We measured (in 13 healthy volunteers) insulin secretion (by deconvolution of plasma C-peptide concentrations) during three consecutive 30-min hyperglycemic steps (2.8, 2.8, and 5.6 mmol/l), followed by an intravenous arginine bolus. First-phase insulin secretion in response to the first hyperglycemic step (456 ± 83 pmol · min-1 · m-2) was significantly larger than that in response to the second step (311 ± 37 pmol · min-1 · m-2, P < 0.01); the subsequent increase in glycemia failed to stimulate first-phase secretion any further (377 ± 60 pmol · min-1 m-2, NS vs. the previous value). This inhibition was also evident when insulin release rates were corrected for the respective increments (absolute or percentage) in plasma glucose levels and was not due to ?-cell exhaustion because the arginine bolus still elicited a large peak of insulin secretion (4,790 ± 2,330 pmol · min-1 · m-1 · M-2). In contrast, second-phase insulin secretion was related to the prevailing glucose levels across the three hyperglycemic steps in a direct quasilinear manner. We conclude that first-phase insulin secretion is inhibited by short-term modest hyperglycemia, whereas the second-phase insulin secretion increases linearly with hyperglycemia. (literal)
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