Glucagon secretion and alpha-cell sensitivity to somatostatin in genetically diabetic mice C57BL/KsJ-mdb.
In previous studies in C57BL/KsJ mdb/mdb mice, we observed alterations in glucose-induced insulin secretion in vitro, and a defective inhibitory effect of somatostatin on insulin secretion. In this work we studied glucagon secretion patterns under arginine-glucose stimulation, in perifused pancreatic slices from genetically diabetic mice aged 20 to 90 days. We also explored whether alpha-cells present a diminished sensitivity to somatostatin. Results showed that: a) in mdb/mdb mice aged 20 to 90 days, glucagon secretion patterns exhibited basal hypersecretion and a diminished first peak; b) somatostatin inhibited stimulated-glucagon secretion below baseline values in mdb/mdb mice aged 20 to 30 days. In later stages (40 to 90 days), somatostatin exerted a lower inhibitory effect since glucagon levels remain above basal values. This could indicate a progressive impairment in alpha-cell sensitivity to somatostatin, as it was previously observed in beta-cells.
Karabatas
L M
LM
Fundación Laboratorio de Investigaciones Pediátricas, Hospital General de Niños, Dr. Pedro de Elizalde, Buenos Aires.
Arata
M
M
Pivetta
O H
OH
Basabe
J C
JC
D000367:Age Factors; D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000503:physiopathology*; D005260:Female; D005934:Glucagon / Q000378:metabolism*; D007515:Islets of Langerhans / Q000187:drug effects*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D010179:Pancreas / Q000378:metabolism; D010477:Perfusion; D013004:Somatostatin / Q000494:pharmacology*
D013004:Somatostatin; D005934:Glucagon