Effects of glucose,chloromercuribenzene-p-sulphonic acid and 4-acetamido-4′-isothiocyanostilbene-2,2′- disulphonic acid on phosphate efflux from pancreatic islets

Collagenase-isolated pancreatic islets of non-inbred ob/ob mice, containing more than 90% β-cells, were labelled with radioactive orthophosphate (³²P or ³³P) and then subjected to non-recirculating perifusion. The basal D-glucose concentration in the perifusion medium was 2.8 mM. When the concentration was suddenly raised to 5.6, 8.3 or 16.7 mM, D-glucose promptly elicited a transient and dose-dependent release of radiophosphate. In the presence ot 2.8 mM D-glucose, 0.1 mM of the poorly permeating sulphydryl blocker, chloromercuribenzene-p-sulphonic acid, also evoked a phosphate flush resembling the one induced by d-glucose. The basal radiophosphate release was partially inhibited by 1 mM 4-acetamido-4′-isothiocyanostilbene-2,-2′-disulphonic acid. However, the phosphate flush induced by 16.7 mM d-glucose was not noticeably inhibited by 4-acetamido-4′-isothiocyanostilbene-2,-2′-disulphonic acid. It is concluded that the phosphate flush emanates from β-cells and that membrane sulphydryl groups may participate in its regulation. Although at least the basal phosphate release may in part represent transmembrane transport through 4-acetamido-4′-isothiocyanostilbene-2,2′-disulphonic acid-sensitive anion channels, other mechanisms are also likely to participate in the glucose-induced phosphate flush.