Insulin release in the Atlantic hagfish Myxine glutinosa in vitro.

Abstract

By using a homologous radioimmunoassay, glucose-stimulated insulin release was studied in isolated islet organs from the Atlantic hagfish. At 16°, glucose (1–5 mM) induced insulin release with a half-maximal response at 3 mM. The efficacy of the glucose response was increased by the addition of the phosphodiesterase inhibitor, 3-isobutyl-1-methylxantine, at a concentration of 1 mM, and omission of Ca2+ from the medium decreased the secretory response. Glucose-induced insulin release was enhanced by lowering the temperature. In perifusion experiments, the time for onset of glucose-induced insulin release was 17 min. Epinephrine (1 mM) inhibited insulin release, whereas a cholinergic drug was without effect. The sulfhydryl reagent chloromercuribenzene-p-sulfonic acid was the most potent insulin secretagogue tested. Unlike the situation in most other investigated species, amino acids did not stimulate insulin release. This finding may be related to the lack of glucagon-producing cells in the hagfish islet parenchyma. Even though the pattern of insulin release in the Atlantic hagfish differs from that of higher animals in both quantitative and qualitative terms, the results indicate that a close connection between insulin release and glucose existed early in vertebrate evolution.