Summary
Oral glucose tolerance tests (OGTT) were performed for two subsequent days in 4 patients with active acromegaly, 2 patients with prolactin-producing pituitary adenomas and one insulinoma patient. Thirty minutes before the second OGTT 250 µg of somatostatin were injected intravenously as a bolus followed by a somatostatin infusion (500 µg) over 2 1/2 hours. The OGTTs were pathologic due to the hGH- and hPRL-induced insulin antagonism; they could not be normalized or improved by somatostatin. Only the peak of the blood sugar curve was shifted from one to two and a half hours after glucose administration; insulin and hGH levels were regularly suppressed after somatostatin whereas hPRL remained unchanged in most instances. Gastrin levels increased in all patients during the OGTT, the increase was suppressed in 4 patients.
These findings show that the pathologic glucose tolerance due to insulin antagonism could not be improved by somatostatin in contrast to the deteriorated glucose tolerance in insulinopenic states.
Zusammenfassung
Bei 4 Patienten mit aktiver Akromegalie, 2 Patienten mit einem Prolaktin-produzierenden Hypophysentumor und einer Patientin mit einem Insulinom wurde an 2 aufeinanderfolgenden Tagen ein oraler Glucosetoleranztest (OGTT) durchgeführt. Während des 2. OGTT wurden 30 min vor Beginn der Glucosebelastung 250 µg Somatostatin als Bolus injiziert, gefolgt von einer Somatostatin-Infusion (500 µg) über 2 1/2 Std. Die durch den Wachstumshormon-bzw. Prolaktin-induzierten Insulinantagonismus bedingte pathologische Glucosebelastung konnte durch Somatostatin nicht normalisiert werden; lediglich das Blutzucker-Maximum verschob sich von 1 auf 2 1/2 Std nach Glucosegabe. Die Insulin- und Wachstumshormonspiegel wurden durch Somatostatin supprimiert, die Prolaktinspiegel hingegen verhielten sich variabel. Der bei allen Patienten beobachtete glucoseinduzierte Anstieg des Serum-Gastrins wurde in 4 Fällen durch Somatostatin gehemmt.
Diese Befunde zeigen, daß die pathologische Glucosetoleranz bei Insulinantagonismus im Gegensatz zu der bei Insulinmangel durch Somatostatin nicht wesentlich beeinflußt werden kann.
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Gottsmann, M., Landgraf, R., Londong, W. et al. Einfluß von Somatostatin auf die orale Glucosetoleranz bei autonomer Mehrsekretion von Wachstumshormon, Prolaktin oder Insulin. Klin Wochenschr 53, 1161–1166 (1975). https://doi.org/10.1007/BF01476456
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DOI: https://doi.org/10.1007/BF01476456