The effect of monooleoylglycerol on insulin secretion from isolated perifused rat islets
Diabetologia, ISSN: 0012-186X, Vol: 32, Issue: 6, Page: 360-364
1989
- 13Citations
- 1Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations13
- Citation Indexes13
- 13
- CrossRef8
- Captures1
- Readers1
Article Description
The effect of monooleoylglycerol on cholecystokinin-and tolbutamide-induced insulin secretion was examined in isolated perifused rat islets. In the presence of 5.5 mmol/l glucose, addition of 10 nmol/l cholecystokinin or 50 μmol/l tolbutamide had practically no effect on insulin secretion. Combined tolbutamide and cholecystokinin led to a biphasic insulin secretory response which was significantly enhanced by addition of 50 μmol/l monooleoylglycerol, an inhibitor of diacylglycerol kinase. Monooleoylglycerol (50 μmol/l) alone had a minimal stimulatory effect on insulin release in the presence of 5.5 mmol/l glucose. Perifusion of islets with 1 μmol/l forskolin had no significant effect on basal insulin secretion in the presence of 5.5 mmol/l glucose, but markedly enhanced the responses to both cholecystokinin plus tolbutamide, and to the combination of cholecystokinin, tolbutamide and monooleoylglycerol. Lowering the glucose level to 2.75 mmol/l abolished the profound stimulatory effect to these agonist combinations on insulin release. Finally, monooleoylglycerol also enhanced the first and second phase insulin secretory responses induced by 20 mmol/l glucose. These results are discussed in relationship to the possible role of protein kinase C in mediating insulin secretion. © 1989 Springer-Verlag.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0024380844&origin=inward; http://dx.doi.org/10.1007/bf00277259; http://www.ncbi.nlm.nih.gov/pubmed/2668083; http://link.springer.com/10.1007/BF00277259; https://dx.doi.org/10.1007/bf00277259; https://link.springer.com/article/10.1007/BF00277259; http://www.springerlink.com/index/10.1007/BF00277259; http://www.springerlink.com/index/pdf/10.1007/BF00277259
Springer Science and Business Media LLC
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