1970 年 13 巻 3 号 p. 245-254
Insulinoma, a typical case of hyperinsulinism, has engendered an interest in order to understand better the regulation of insulin release.
The studies on insulin responses after administrationof various insulin releasers or inhibitors were carriedout in three patients with insulinoma (bening adenomahistologically). And also, ultrastracture of beta-cells of insulinoma were observed electronmicroscopically.
1) The fasting serum insulin levels in three cases with insulinoma were found to be greater than thatobserved in normal subjects. After oral administrationof glucose or 1-leucine and intravenous abministration of glucagon, serum insulin levels elevated markedly. However these excesive rises were not in paralled with the content of insulin in the tumors.
2) The increase of serum insulin level during glucose loading was depressed markedly, but not during glucagon loading, by the administration of adrenaline or propranolol (a beta adrenergic receptor blocking agent).
In vitro experiments using tumor slices, beta adrenergic stimalators accelerated the insulin release from tumor. The insulin release were found to be unchanged in alpha adrenergic stimulated condition prodused by both administration of adrenaline and propranolol. The findings in here, both clinical or experimental studies, indicating that insulin release is stimulated by betaadrenergic stimulator and inhibited by aIpha-adrenergic stimulator in inslinomas as same rs in normal subjects, suggest that neurohumoral regulation would be undertaken in insulinoma in which tumor is in benign.
3) Electronmicroscopically, it was observed that beta granules of beta cells in insulinoma were generally scanty. The cores of beta-granules were generally round with a little variation, while there were mixed forms in normal ones; being round, rectangle and tri-angle.
These findings suggest that storage form of insulin in beta cells of insulinoma may be different from that in normal beta cells.