E. Karlsson et S. Sandler, Islet amyloid polypeptide promotes beta-cell proliferation in neonatal ratpancreatic islets, DIABETOLOG, 44(8), 2001, pp. 1015-1018
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 2
1. 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/mug o
f DNA 6 h) (control 1% FCS: 3634 +/- 662; 1 nmol/1 6347 +/- 1535; 10 nmol/l
5157 +/- 769; p < 0.05 islet amyloid polypeptide vs control). In accordanc
e with this, a doubling of the autoradiographic labelling index was seen in
immunocytochemically stained islet beta cells after exposure to 1 and 10 n
mol/l islet amyloid polypeptide. Islet amyloid polypeptide at I nmol/l incr
eased 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 th
ese changes did not attain statistical difference. Islet amyloid polypeptid
e did not have any marked effect on the islet cell death frequency, suggest
ing that islet amyloid polypeptide is a more potent promoter of proliferati
on than of programmed cell death.
Conclusion/interpretation. Our data indicate islet amyloid polypeptide is a
potential regulator of proliferation in neonatal pancreatic islet cells, a
n effect which can partly be attributed to the proliferation of beta cells.