The mechanism of gentamicin-inhibited insulin release by isolated islets.
These experiments were performed in order to determine the mechanism of action of the aminoglycoside antibiotic gentamicin on insulin release by isolated islets. Gentamicin significantly reduced the insulin release in the absence as well as in the presence of increasing concentrations of glucose. This effect was immediate and promptly reversible. In the presence of glucose plus high concentrations of K+ the antibiotic did not affect insulin secretion. Gentamicin did not change 86Rb efflux from perifused islets or the glucose metabolism in incubated islets. These data show that gentamicin does not alter the recognition and subsequent metabolism of glucose, and the system responsible for insulin secretion. We suggest that gentamicin reduces glucose-induced insulin release by blocking the entry of Ca2+ into the B-cells.
Boschero
A C
AC
Delattre
E
E
D000818:Animals; D005839:Gentamicins / Q000494:pharmacology*; D005947:Glucose / Q000378:metabolism / Q000494:pharmacology; D066298:In Vitro Techniques; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D007473:Ion Channels / Q000187:drug effects; D007515:Islets of Langerhans / Q000187:drug effects* / Q000378:metabolism; D010477:Perfusion; D011188:Potassium / Q000494:pharmacology; D011868:Radioisotopes; D051381:Rats; D011919:Rats, Inbred Strains; D012413:Rubidium
D005839:Gentamicins; D007328:Insulin; D007473:Ion Channels; D011868:Radioisotopes; D005947:Glucose; D012413:Rubidium; D011188:Potassium