Stimulation of insulin secretion by beta-endorphins (I-27 & I-31)
1987; Elsevier BV; Volume: 40; Issue: 21 Linguagem: Inglês
10.1016/0024-3205(87)90097-x
ISSN1879-0631
AutoresD. L. Curry, Leslie L. Bennett, Choh Hao Li,
Tópico(s)Pain Mechanisms and Treatments
ResumoSynthetic human beta-endorphin potentiates insulin secretion by the isolated perfused rat pancreas when glucose is present in the perfusate at concentrations of either 125 or 200 mg/dl, whereas it fails to exert any effect on insulin secretion in the presence of a substimulatory concentration of 100 mg/dl. Similar potentiation of insulin secretion occurred in response to the 1–27 fragment (beta-endorphinI-27) of beta-endorphin. This transient potentiation lasts only 3 to 4 minutes, whereupon secretion returns toward control levels. Thus beta-endorphin produces only a transient spike-like secretory profile similar to the first phase of glucose-induced insulin secretion and it fails to produce any chronic insulin secretory response comparable to the second phase of insulin secretion. The insulinotropic effect of beta-endorphins occurred at concentrations varying from 0.1 to 5.0 ug/ml. These data suggest that beta-endorphin and beta-endorphinI-27 potentiate insulin secretion via a common beta cell opioid receptor, and that beta-endorphin may exert a paracrine control of insulin secretion. However, any such regulation appears to be via short-term alterations in the secretory process per se.
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