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.

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Thirty patients with gastric ulcer and thirty-threegastrectomized patients were studied for the investigation of glucose metabolism in gastrectomized patients and for the elucidation of the mechanism of it's abnormality, or of its relation to diabetes mellitus.
They received 100 g oral glucose tolerance test, glucose tolerance test by puodenal tubing or intravenous glucose tolerance test. Blood sugar, serum IRI and NEFA were determined.
The following are the results of the present investigation:
1) The respnses of blood sugar after 100 g oral glucose loading in thirty patients with gastric ulcer were diabetic in fourteen cases, borderline hyperglycemic in thirteen cases and normoglycemic in only three cases.
2) The falling rate of blood sugar was significantly lower in the group with gastric ulcer than in the normal one. This finding suggests that the rate of utlization of glucose in the body is lower in the former group.
3) The response of blood sugar after glucose loading in gastrectomized patients was oxyhyperglycemic, and this tendency was more exaggerated in the patients more than three months than in those less than three months (after gastrectomy). There was no significant differerence in the response of blood sugar of the patients gastrectomized between by Billroth I and II methods, and in the patients elapsed many years after gastrectomy, no one showed prolonged hyperglycemic response of blood sugar.
4) The response of blood sugar in glucose tolerance test by duodenal tubing in the normal subjects showed more oxyhyperglycemic pattern than in oral glucose one, but the falling rate of blood sugar was not so rapid as in gastrectomized patients.
5) The change of serum IRI after glucose loading in gastrectomized patients was similar to that of blood sugar level. The level of serum IRI increased immediately after glucose loading and then decreased rapidly, and there was no significant difference in the response of serum IRI in the subjects operated between by Billroth I and II methods.
6) In gastrectomized patients, the response of serum insulin became higher in parallel with the development of the level of blood sugar among normal, oxyhyperglycemic and diabetic types. However, in diabetic subjects, the response of serum insulin became lower contrary to the increase of blood sugar.
7) The falling rate of NEFA after glucose loading ingastrectomized group was similar to that of normal one, but the value of NEFA in the former one began to increase already two hours after glucose loading.

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The serum insulin response of diabetic subjects is reported to be higher than that of nondiabetic ones, and there are also studies which reported lower insulin response in diabetics.
In order to clarify this discrepancy or changes from high insulin response to low one, the relationship between glucose tolerance curve and serum insulin response was investigated.
Two hundred and fourteen males and one hundred and thirty-two females, untreated diabetic or obese, were studied. As controls eleven males and fourteen females, healthy and non-obese, were used.
One hundred glucose was administered orally, and serum sample were obtained at fasting, half, one, one and half, two and three hours after administrati on.
Serum blood sugar, FFA and IRI were determined.
The results are as follows:
1) The IRI response of borderline hyperglycemic subjects was higher and more delayed than that of normal ones. The patterns of responses of blood sugar and IRI are quite similiar each other.
2) The IRI response of diabetic subjects with fasting blood sugar level of less than 119 mg/dl was highest among tested, and the peak rise of insulin was retarded till two hours after glucose loading.
3) The IRI response became lower little by little, coincidently with the progress of decrease of glucose tolerance. Especially, diabetics with fasting blood sugar level of more than 160 mg/dl showed very low insulin response in comparison with those of less blood sugar value.
4) In subjects with same glucose tolerance, obese group showed higher insulin response than non-obese one. Both had lower insulin response with the progress of decrease of glucose tolerance.
5) The ratio ΔIRI/Δ Blood Sugar during initial thirty minutes after glucose loading decreased with the lowering of glucose tolerance.
6) Fasting levels of FFA in serums of diabetic, borderline and normal subjects were high in this order, but there was no significant difference in their falling rate after glucose loading.

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