Opposite effects of 5-hydroxytryptophan and 5-hydroxytryptamine on the function of microdissected ob/ob-mouse pancreatic islets

Lindström, Per; Sehlin, Janove

doi:10.1007/bf00275948

Cited by 18 publications

(6 citation statements)

References 32 publications

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“…The alkalinizing effect of glucose appears not to be secondary to increased insulin release. Both theophylline (Malaisse et al, 1967;Hellman et al, 1974) and L-5-hydroxytryptophan (Lindstr6m & Sehlin, 1983; see the Results section above) are strong potentiators of glucose-induced insulin…”

Section: Discussionmentioning

confidence: 97%

“…The [14C]DMO uptake at high glucose was further increased by 4mM-L-5-hydroxytryptophan to an apparent pHi of 7.53. We have previously shown that L-5-hydroxytryptophan is a strong potentiator of glucose-induced insulin release in experiments using bicarbonate-buffered media (Lindstr6m & Sehlin, 1983). In separate experiments we found that this is the case also in media devoid of bicarbonate buffer.…”

Section: Preincubation Mediummentioning

confidence: 99%

“…We have re-investigated the effects of glucose on the pHi in pancreatic f-cells by measuring the accumulation of [14C]DMO in fl-cell-rich pancreatic islets Qf ob/ob mice. A preliminary account of these results has been presented elsewhere (Lindstrom & Sehlin, 1983).…”

mentioning

confidence: 92%

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Effect of glucose on the intracellular pH of pancreatic islet cells

Lindström¹,

Sehlin²

1984

Biochemical Journal

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To characterize the effect of glucose on the intracellular pH (pHi) of pancreatic islet cells, we measured the accumulation of 14C-labelled 5,5-dimethyloxazolidine-2,4-dione ( [14C]DMO) in beta-cell-rich islets from ob/ob mice. D-Glucose (20 mM) stimulated insulin release and enhanced the [14C]DMO equilibrium uptake corresponding to an increase of pHi by about 0.15 unit. The glucose effect on DMO uptake was concentration-dependent, with half-maximal effect at about 4 mM-glucose and maximum effect at about 10 mM-glucose. It was inhibited by 20 mM-mannoheptulose and potentiated by 4 mM-L-5-hydroxytryptophan, but not affected by 2 mM-theophylline. Mannoheptulose is an inhibitor and L-5-hydroxytryptophan and theophylline are potentiators of glucose-stimulated insulin release. The glucose-induced increase in pHi appeared rapidly (7 min) and persisted for at least 30 min and it was observed both in bicarbonate/CO2-buffered and in Hepes [4-(2-hydroxyethyl)-1-piperazine-ethanesulphonic acid]-buffered media. Addition of extracellular bicarbonate buffer lowered the pHi, but did not affect basal insulin release, whereas 5 mM-NH4+ increased pHi and induced a 4-fold increase of basal insulin release. We conclude that, in contrast with previous assumptions, glucose increases intracellular pH in the islet cells. This effect may be coupled to the glucose metabolism and associated with triggering of insulin release.

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Section: Discussionmentioning

confidence: 97%

Section: Preincubation Mediummentioning

confidence: 99%

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Effect of glucose on the intracellular pH of pancreatic islet cells

Lindström¹,

Sehlin²

1984

Biochemical Journal

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“…SDAT has been suggested to be a gener-alized disease (34,35) and our present findings support this suggestion. Cholinergic and catecholaminergic substances play an important role in the modulation of insulin and glucagon release (33,36,37) which might explain the elevated insulin levels in our patients with SDAT.…”

Section: Discussionmentioning

confidence: 89%

Changes in Blood Glucose and Insulin Secretion in Patients with Senile Dementia of Alzheimer Type

Bucht

Adolfsson

Lithner

et al. 1983

Journal of Internal Medicine

129

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A retrospective study of 839 hospital records with various dementia diagnoses showed that 63 cases had a diagnosis of diabetes mellitus as well. None of these were found in the group of patients with senile dementia of Alzheimer type (SDAT). Oral glucose tolerance tests (OGTT) were performed in patients with SDAT, multiinfarct dementia (MID), cerebrovascular disease (CVD), hospitalized control patients (Chosp) and healthy elderly persons (Celd). Fasting blood sugar was significantly lower and the areas under the OGTT curves were significantly smaller in the SDAT group than in the CVD and the Chosp group. SDAT patients had higher insulin levels than Celd during the OGTT and on a statistically significant level 90 min after ingestion of sugar. Our findings suggest that SDAT and diabetes mellitus may not co‐exist and that patients with SDAT have decreased blood sugar concentrations and elevated serum insulin levels. It is discussed whether this is an effect of the transmitter deficiencies in SDAT or may serve to explain these deficiencies.

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“…Previous studies have indicated that monoamines, such as 5-HT, DA, epinephrine, and norepinephrine, can inhibit glucose-mediated insulin secretion in human, golden hamster, rat, and mouse pancreatic islet B cells (Porte and Williams 1966;Feldman and Lebovitz 1970;Feldman et al 1971;Aleyassine and Gardiner 1975;Lindstrom and Sehlin 1983). The catecholamines, epinephrine and norepinephrine, can regulate insulin secretion directly (Porte et al 1976).…”

Section: Discussionmentioning

confidence: 99%

Immunohistochemical Localization of Monoamine Oxidase Type B in Pancreatic Islets of the Rat

Huang

Ito

Arai

2005

J Histochem Cytochem.

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S U M M A R Y Monoamine oxidase (MAO) is regarded as a mitochondrial enzyme. This enzyme localizes on the outer membrane of mitochondria. There are two kinds of MAO isozymes, MAO type A (MAOA) and type B (MAOB). Previous studies have shown that MAOB activity is found in the pancreatic islets. This activity in the islets is increased by the fasting-induced decrease of plasma glucose level. Islet B cells contain monoamines in their secretory granules. These monoamines inhibit the secretion of insulin from the B cells. MAOB is active in degrading monoamines. Therefore, MAOB may influence the insulinsecretory process by regulating the stores of monoamines in the B cells. However, it has not been determined whether MAOB is localized on B cells or other cell types of the islets. In the present study, we used both double-labeling immunofluorescence histochemical and electron microscopic immunohistochemical methods to examine the subcellular localization of MAOB in rat pancreatic islets. MAOB was found in the mitochondrial outer membranes of glucagon-secreting cells (A cells), insulin-secreting cells (B cells), and some pancreatic polypeptide (PP)-secreting cells (PP cells), but no MAOB was found in somatostatin-secreting cells (D cells), nor in certain other PP cells. There were two kinds of mitochondria in pancreatic islet B cells: one contains MAOB on their outer membranes, but a substantial proportion of them lack this enzyme. Our findings indicate that pancreatic islet B cells contain MAOB on their mitochondrial outer membranes, and this enzyme may be involved in the regulation of monoamine levels and insulin secretion in the B cells.

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Opposite effects of 5-hydroxytryptophan and 5-hydroxytryptamine on the function of microdissected ob/ob-mouse pancreatic islets

Cited by 18 publications

References 32 publications

Effect of glucose on the intracellular pH of pancreatic islet cells

Effect of glucose on the intracellular pH of pancreatic islet cells

Changes in Blood Glucose and Insulin Secretion in Patients with Senile Dementia of Alzheimer Type

Immunohistochemical Localization of Monoamine Oxidase Type B in Pancreatic Islets of the Rat

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