Aims/hypothesis:  

We aimed to clarify the role of islet amyloid polypeptide, which is expressed at early embryonic onset, in the proliferation and cell death of neonatal islet cells.

Methods:  

Fetal islets were prepared from pregnant rats on gestational day 21. Islets were cultured in RPMI 1640 (11.1 mmol/l glucose) + 10 % fetal calf serum (FCS) for 48 h, followed by a 24-h culture period in RPMI 1640 (5.6 mmol/l glucose) + 1 % FCS. The islets were then exposed to rat islet amyloid polypeptide (1–10 nmol/l) for 24 h.

Results:  

Iselt amyloid polypeptide increased islet DNA synthesis (dpm/μg of DNA · 6 h) (control 1 % FCS: 3634 ± 662; 1 nmol/l 6347 ± 1535; 10 nmol/l 5157 ± 769; p < 0.05 islet amyloid polypeptide vs control). In accordance with this, a doubling of the autoradiographic labelling index was seen in immunocytochemically stained islet beta cells after exposure to 1 and 10 nmol/l islet amyloid polypeptide. Islet amyloid polypeptide at 1 nmol/l increased the islet insulin content (202 ± 25 % of control; p < 0.01) and the 24-h medium insulin concentration (1 nmol/l islet amyloid polypeptide: 143 ± 19 % of control; p < 0.05) but at 10 nmol/l islet amyloid polypeptide these changes did not attain statistical difference. Islet amyloid polypeptide did not have any marked effect on the islet cell death frequency, suggesting that islet amyloid polypeptide is a more potent promoter of proliferation than of programmed cell death.

Conclusion/interpretation:  

Our data indicate islet amyloid polypeptide is a potential regulator of proliferation in neonatal pancreatic islet cells, an effect which can partly be attributed to the proliferation of beta cells. [Diabetologia (2001) 44: 1015–1018]