ISSN:
1432-0428
Keywords:
Insulin secretion
;
golden hamsters
;
pancreatic islets
;
norepinephrine
;
dopamine
;
serotonin
;
monoamine oxidase
;
DL-threo-dihydroxyphenylserine
;
L-3,4-dihydroxyphenylalanine
;
5-hydroxytryptophan
;
tranylcypromine
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Summary The purpose of this study was to determine if increased concentrations of pancreatic islet norepinephrine, dopamine, or serotonin alter insulin secretion. Golden hamsters received intraperitoneal injections of the norepinephrine precursor DL-threo-dihydroxyphenylserine, the dopamine precursor L-3,4-dihydroxyphenylalanine, or the serotonin precursor 5-hydroxytryptophan with and without pretreatment of the hamsters with the monoamine oxidase inhibitor tranylcypromine. Administration of the monoamine precursors to animals pretreated with tranylcypromine resulted in a mean increase in plasma glucose of 192% and a mean decrease in plasma insulin of 58%. Using a collagenase isolation technique, islets from control and treated animals were evaluated for monoamine content and insulin secretory capacity. The monoamine concentrations in control islets, in μmol/kg wet weight, were: norepinephrine 42±8; dopamine 8±2; and serotonin 26±9. Administration of the appropriate precursor to control hamsters resulted in a 1.9-fold (norepinephrine), 6-fold (dopamine), and 22-fold (serotonin) increase in monoamines. There was no alteration in the glucose (16.3 mmol/l)-stimulated in vitro insulin secretion from islets obtained from these hamsters. Administration of the precursors to hamsters pretreated with tranylcypromine resulted in a 3.5-fold (norepinephrine), 22-fold (dopamine), and 59-fold (serotonin) increase in monoamines. Glucose-stimulated in vitro insulin secretion from islets obtained from these hamsters was completely blocked. This study suggests that high concentrations of norepinephrine, dopamine, and serotonin in the pancreatic islets can decrease glucose-stimulated insulin secretion.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00251017
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