Aim: 

To further characterise osmotically-induced insulin secretion.

Methods: 

We compared response of freshly isolated rat pancreatic islets and INS-1 and INS-1E tumour cell lines to 15 mmol/l glucose, 30% hypotonic medium and 20% hypertonic medium using static incubations and perifusion by Ca²⁺containing or depleted medium.

Results: 

In Ca²⁺containing medium glucose induced insulin release in all three cell types. Hypotonicity induced insulin secretion from islets and INS-1 cells but not from INS-1E cells, in which secretion was inhibited despite a significant increase in cell volume. GdCl₃ (100 mmol/l) did not affect insulin response from INS-1E cells to hypotonic challenge. Hypertonic medium inhibited glucose-induced insulin secretion from islets but not from tumour cells. Noradrenalin (1 mmol/l) inhibited glucose-induced but not swelling-induced insulin secretion from INS-1 cells. Surprisingly, perifusion with Ca²⁺depleted medium showed distinct secretory response of INS-1E cells to hypotonicity that was even higher than that of INS-1 cells.

Conclusion: 

Functioning glucose-induced insulin secretion is not sufficient prerequisite for hypotonicity-induced response in INS-1E cells suggesting that swelling-induced exocytosis is not essential step in the mechanism mediating glucose-induced insulin secretion. Both cell lines are resistant to inhibitory effect of hyperosmolarity on glucose-induced insulin secretion. Response of INS-1E cells to hypotonicity is inhibited by the presence of Ca²⁺in medium.

Acknowledgements:

The work was supported by the project 2/6158/26 of the Grant Agency of Ministry of Education of the Slovak republic and Slovak Academy of Sciences (VEGA), project APVV 0235-06 and project of CE SAV CENDO