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  • Title: [Serum immunoreactive insulin after the oral administration of single dose of tolbutamide. I. Peripheral vein immunoreactive insulin in normal subjects and mild diabetics (author's transl)].
    Author: Goto A.
    Journal: Nihon Naibunpi Gakkai Zasshi; 1975 Aug 20; 51(8):676-84. PubMed ID: 1237421.
    Abstract:
    It has been confirmed in numerous studies that the hypoglycemic effect of sulfonyl-ureas is mainly owing to its insulinogenic action. Intravenous administrations of the drugs have been adopted in many of these studies. But the oral administrations of the drugs in a few studies lead to conflicting results concerning its insulinogenic action. In this study, the concentrations of blood glucose, serum immunoreactive insulin (IRI), serum free fatty acid (FFA) and serum tolbutamide were measured following the oral administration of single dose of tolbutamide in six normal and eleven maturity onset mild diabetic subjects. The same parameters were measured after the oral administration of tolbutamide plus sodium bicarbonate in six normal subjects. The changes of these parameters were compared with the changes following the intravenous administration of sodium tolbutamide in six normal subjects. The oral administration of three grams of tolbutamide alone caused a gradual but significant decrease of blood glucose level. Serum FFA response showed an initial decrease, followed by a rebound elevation. In spite of 21 per cent reduction of blood glucose level, serum IRI level did not show any significant change throughout the observation for five hours. Serum tolbutamide concentration rose gradually and reached to 24.4+/-3.9 mg per 100 ml (Mean+/-SEM) at the end of the observation. Almost identical results were obtained in diabetic subjects. Three grams of tolbutamide plus the same dose of sodium bicarbonate were administered orally to the normal subjects. A profound decrease of blood glucose level with a nadir (35 per cent reduction) at 45 minutes and a significant increase of serum IRI level with a peak (273 per cent increase) at 20 minutes were obtained, and associated with a comparatively rapid elevation of serum tolbutamide concentration reached to 31.9+/-3.3 mg per 100 ml after three hours. From these results, it is suggested that slow rise of serum tolbutamide concentration after the oral administration of tolbutamide alone might lead to moderate secretion of insulin and sooner rise might evoke larger secretion into the pancreatic vein, and that an existence of moderate hyperinsulinism in the pancreatic venous blood after the oral administration of tolbutamide alone might cause a decrease of gluconeogenesis in the liver. And the failure of serum IRI response in the peripheral blood in spite of hyperinsulinism in the pancreatic vein might be due to hepatic trapping of the secreted insulin.
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