Possible modulatory role of non-activated lymphocytes on insulin secretion.

In order to study the probable physiological role of non-activated lymphocytes on islet B-cells, we incubated and perfused rat pancreatic islets in the presence of low (2.8 mM) and high (16.7 mM) glucose concentrations after pre-exposure for 60 min to rat lymphocytes or to substances secreted by lymphocytes. Insulin secretion and 86Rb+, 45Ca2+ and [3H]-phosphoinositide metabolite fluxes were lower compared to controls when islets were pre-exposed to lymphocytes but were not different when islets were pre-exposed to substances secreted by lymphocytes. These alterations in isotope flux suggest that, when lymphocytes and islets are in contact, closure of potassium channels and a paradoxical effect of glucose load on insulin release occur in the presence of low glucose concentrations. The alterations observed are probably due to a swift and direct action of lymphocyte secretion perhaps induced by a direct of islet cells.

Possible modulatory role of non-activated lymphocytes on insulin secretion

In order to study the probable physiological role of non-activated lymphocytes on islet B-cells, we incubated and perfused rat pancreatic islets in the presence of low (2.8 mM) and high (l6.7 mM) glucose concentrations after pre-exposure for 60 min to rat lymphocytes or to substances secreted by lymphocytes. Insulin secretion and 86Rb+, 45Ca2+ and [3H]-phosphoinositide metabolite fluxes were lower compared to controls when islets were pre-exposed to lymphocytes but were not different when islets were pre-exposed to substances secreted by lymphocytes. These alterations in isotope flux suggest that, when lymphocytes and islets are in contact, closure of potassium channels and a paradoxical effect of glucose load on insulin release occur in the presence of low glucose concentrations. The alterations observed are probably due to a swift and direct action of lymphocyte secretion perhaps induced by a direct contact of islet cells.