http://www.cnr.it/ontology/cnr/individuo/prodotto/ID187810
Dopamine-Mediated Autocrine Inhibitory Circuit Regulating Human Insulin Secretion in Vitro (Articolo in rivista)
- Type
- Label
- Dopamine-Mediated Autocrine Inhibitory Circuit Regulating Human Insulin Secretion in Vitro (Articolo in rivista) (literal)
- Anno
- 2012-01-01T00:00:00+01:00 (literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
- 10.1210/me.2012-1101 (literal)
- Alternative label
Simpson N, Maffei A, Freeby M, Burroughs S, Freyberg Z, Javitch J, Leibel R.L., Harris P.E. (2012)
Dopamine-Mediated Autocrine Inhibitory Circuit Regulating Human Insulin Secretion in Vitro
in Molecular endocrinology (Baltim. Md.)
(literal)
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
- Simpson N, Maffei A, Freeby M, Burroughs S, Freyberg Z, Javitch J, Leibel R.L., Harris P.E. (literal)
- Pagina inizio
- Pagina fine
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
- Rivista
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroFascicolo
- Note
- Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
- Division of Endocrinology (N.S., M.F., S.B., P.E.H.) and Center for Molecular Recognition (Z.F., J.J.), Columbia University Medical College,
The Naomi Berrie Diabetes Center (M.F., R.L.L., P.E.H.), New York, New York 10032;
The Institute of Genetics and Biophysics A. Buzzati-Traverso (A.M.), Consiglio Nazionale delle Ricerche, 80131 Naples, Italy (literal)
- Titolo
- Dopamine-Mediated Autocrine Inhibitory Circuit Regulating Human Insulin Secretion in Vitro (literal)
- Abstract
- We describe a negative feedback autocrine regulatory circuit for glucose-stimulated insulin secretion in purified human islets in vitro. Using chronoamperometry and in vitro glucose-stimulated insulin secretion measurements, evidence is provided that dopamine (DA), which is loaded into insulin-containing secretory granules by vesicular monoamine transporter type 2 in human ?-cells, is released in response to glucose stimulation. DA then acts as a negative regulator of insulin secretion via its action on D2R, which are also expressed on ?-cells. We found that antagonism of receptors participating in islet DA signaling generally drive increased glucose-stimulated insulin secretion. These in vitro observations may represent correlates of the in vivo metabolic changes associated with the use of atypical antipsychotics, such as increased adiposity. (literal)
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