[Hyperinsulinism induced with glucocorticoid--a study on using a perifusion system of isolated islets in rats (author's transl)].
In order to elucidate the mechanism of hyperinsulinism following a treatment with glucocorticoid, insulin secretion induced with glucose or tolbutamide was investigated by a perifusion experiment on isolated islets of rats. The results are summarized as follows: 1. The fasting blood glucose level was significantly higher on the 2nd day (174.0 +/- 11.8 mg/dl) and 3rd day (179.6 +/- 9.5 mg/dl) in the glucocorticoid treated rats, than it was in the control rats (129.0 +/- 12.0 mg/dl). The serum insulin levels began to increase from the first day following the glucocorticoid treatment (17.2 +/- 1.3 microU/ml in the control rats, 27.6 +/- 2.1 microU/ml on the 1st day, 32.4 +/- 3.9 microU/ml on the 2nd day, and 34.5 +/- 1.4 microU/ml on the 3rd day). 2. The insulin content of the islets decreased with the glucocorticoid treatment (765.6 +/- 34.5 microU/islet in the control rat, 576.6 +/- 25.0 microU/islet on the 1st day, 629.2 +/- 36.9 microU/islet on the 2nd day, and 482.0 +/- 43.5 microU/islet on the 3rd day). 3. In the perifusion experiment, a biphasic pattern of insulin secretion was demonstrated with the stimulation of glucose in the control and glucocorticoid treated rats. A remarkable enhancement of insulin secretion was observed by the stimulation of 100 mg/dl glucose. The amount of insulin secretion at the first phase (up to 7 min. after the glucose stimulation) was 2.9 +/- 0.5 microU/islet on the 1st day, 2.7 +/- 0.3 microU/islet on the 2nd day and 3.8 +/- 0.1 microU/islet on the 3rd day; these amounts were high compared with that of 1.8 +/- 0.1 microU/islet in the control rat. The amount of insulin secretion at the second phase (8 to 60 min. after the glucose stimulation) was 28.5 +/- 2.5 microU/islet on the 1st day, 37.1 +/- 3.3 microU/islet on the 2nd day and 41.3 +/- 1.8 microU/islet on the 3rd day; these amounts were higher when compared with that of 24.7 +/- 0.7 microU/islet in the control rat. 4. The monophasic insulin secretion from isolated islets by the stimulation of tolbutamide was enhanced with the treatment of glucocorticoid. These results indicate that glucocorticoid directly enhances insulin secretion from the pancreatic islets at the physiological concentration of blood glucose, which seems to be an important factor in the occurrence of hyperinsulinemia associated with glucocorticoid therapy.
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D003348:Cortisone / Q000494:pharmacology; D005938:Glucocorticoids / Q000009:adverse effects* / Q000494:pharmacology; D005947:Glucose / Q000494:pharmacology; D006946:Hyperinsulinism / Q000139:chemically induced* / Q000503:physiopathology; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D051381:Rats; D014044:Tolbutamide / Q000494:pharmacology
D001786:Blood Glucose; D005938:Glucocorticoids; D007328:Insulin; D014044:Tolbutamide; D005947:Glucose; D003348:Cortisone