PARTIAL PANCREATECTOMY IN THE RAT AND SUBSEQUENT DEFECT IN GLUCOSE-INDUCED INSULIN RELEASE
PARTIAL PANCREATECTOMY IN THE RAT AND SUBSEQUENT DEFECT IN GLUCOSE-INDUCED INSULIN RELEASE
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DOI:
10.1172/jci110910
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发表时间:
1983-01-01
影响因子:
15.9
通讯作者:
WEIR, GC
中科院分区:
文献类型:
--
作者:
BONNERWEIR, S;TRENT, DF;WEIR, GC
To define the consequences of a known reduction of .beta.-cell mass in rats, 90% partial pancreatectomies were performed. For the 6 wk following surgery moderate hyperglycemia was maintained in the fed state but there were no differences in body wt or plasma insulin concentrations compared with sham-pancreatectomized controls. Following surgery (8-10 wk) regeneration of the remnant was evident with remnant weight being 26%, .beta.-cell mass being 42% and non-.beta.-cell mass being 47% of values found for control whole pancreas. There were comparable increases in the remnant content of insulin, glucagon and somatostatin. Following meal challenges, i.p. and i.v. glucose tolerance tests and i.v. arginine challenge given 6-7 wk after surgery, the insulin responses to glucose were blunted or absent but the responses following the meals or arginine were intact. Similarly, when the pancreatic remnant was perfused in vitro, insulin release after challenge with 300 mg/dl glucose was markedly reduced whereas intact responsiveness to 10 mM arginine was retained. The chronic stimulation of a reduced .beta.-cell mass can lead to a selective loss of glucose-induced insulin secretion.