Morphological changes in pancreatic islets of KATP channel-deficient mice:The involvement of KATP channels in the survival of insulin cells and the maintenance of islet architecture

Citation
A. Winarto et al., Morphological changes in pancreatic islets of KATP channel-deficient mice:The involvement of KATP channels in the survival of insulin cells and the maintenance of islet architecture, ARCH HIST C, 64(1), 2001, pp. 59-67
Citations number
38
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Medical Research Diagnosis & Treatment
Journal title
ARCHIVES OF HISTOLOGY AND CYTOLOGY
ISSN journal
0914-9465 → ACNP
Volume
64
Issue
1
Year of publication
2001
Pages
59 - 67
Database
ISI
SICI code
0914-9465(200102)64:1<59:MCIPIO>2.0.ZU;2-6
Abstract
The ATP-sensitive potassium channel (KATP channel) is an essential ion chan nel involved in glucose-induced insulin secretion. The KATP channel is comp osed of an inwardly rectifying potassium channel, Kir6.2, and the sulfonylu rea receptor (SUR 1); in the pancreas it is reported to be shared by all en docrine cell types. A previous study by our research group showed that Kir 6.2-knockout mice lacked KATP channel activities and failed to secrete insu lin in response to glucose, but displayed normal blood glucose levels and o nly mild impairment in glucose tolerance at younger ages, In some aged knoc kout mice, however, obesity and hyperglycemia were recognizable. The presen t study aimed to reveal morphological changes in pancreatic islets of Kir 6 .2-knockout mice throughout life. At birth, there were no significant diffe rences in the islet cell arrangement between the knockout mice and controls . At 14 postnatal weeks glucagon cells appeared in the central parts of isl ets, and this image became more pronounced with aging. In animals older tha n 50 weeks insulin cells decreased in numbers and intensity of insulin immu noreactivity; most islets in 70- and 80-week-old mice were predominantly co mposed of glucagon cells and peptide YY (PYY)-containing cells. Staining of serial sections and double staining of single sections from these old mice demonstrated the frequent coexpression of glucagon and PYY, which is a phe notype for the earliest progenitor cells of pancreatic endocrine cells, The se findings suggest that the KATP channel is important for insulin cell sur vival and also regulates the differentiation of islet cells.