Mouse islets were used to study how glucose modulates arginine stimulation of insulin release. At 3 mmol/l glucose, arginine (20 mmol/l) decreased the resting membrane potential of B cells by about 10 mV, but did not evoke electrical activity. This depolarisation was accompanied by a slight but rapi
The effect of glucose, tolbutamide, and arginine on C-peptide release during remission in type I diabetes mellitus
β Scribed by U. Vetter; E. Heinze; A. Thon; W. Beischer; W. Teller
- Publisher
- Springer
- Year
- 1983
- Tongue
- English
- Weight
- 506 KB
- Volume
- 140
- Category
- Article
- ISSN
- 0340-6997
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β¦ Synopsis
The insulin secretory capacity was examined in diabetic children at the time of partial clinical remission during which their condition could be managed with low insulin therapy (less than 0.5 U insulin/kg body weight) and no urinary glucose excretion. The extent of the residual beta cell function in 26 children was assessed either by an i.v. arginine test, a combined i.v. glucose-i.v. arginine test, a combined i.v. tolbutamide-i.v. arginine test, or a combined oral glucose-i.v. arginine test determining the C-peptide response by calculating the area under the curve above baseline levels. Two of the children were tested repeatedly. Under the above conditions i.v. glucose and i.v. tolbutamide did not release C-peptide in diabetic children. In contrast, C-peptide secretion during arginine infusion following i.v. glucose or i.v. tolbutamide was significantly enhanced compared to the C-peptide secretion observed during arginine infusion alone. The C-peptide response to oral glucose was sluggish with no effect on the following arginine infusion. The results indicate that during remission in juvenile onset diabetes i.v. glucose and i.v. tolbutamide without themselves being an appropriate signal for C-peptide release amplify the response to a subsequent arginine infusion under appropriate conditions.
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