Abstract:
:Insulin secretion by beta-cells of pancreatic islets is regulated by various soluble factors including glucose and hormones. The importance of direct cell-cell communication among beta-cells or between beta-cells and other cell types for such regulation has remained unclear, however. Transmembrane proteins Src homology 2 domain-containing protein tyrosine phosphatase substrate-1 (SHPS-1) and its ligand CD47 interact through their extracellular regions and contribute to intercellular communication. We now show that both SHPS-1 and CD47 are prominently expressed in beta-cells of the pancreas. The plasma insulin level in the randomly fed state was markedly reduced in mice that express a mutant form of SHPS-1 lacking most of the cytoplasmic region compared with that in wild-type (WT) mice, although the blood glucose concentrations of the two types of mice were similar. This reduction in the plasma insulin level of SHPS-1 mutant mice was even more pronounced in animals maintained on a high-fat diet. Glucose tolerance was also markedly impaired in SHPS-1 mutant mice on a high-fat diet, whereas both peripheral insulin sensitivity and the insulin content of the pancreas in the mutant animals were similar to those of WT mice. Glucose-stimulated insulin secretion was similar for islets isolated from WT or SHPS-1 mutant mice. The impaired glucose tolerance of SHPS-1 mutant mice was ameliorated by treatment with the alpha2-adrenergic antagonist yohimbine. These results suggest that SHPS-1 promotes insulin secretion from beta-cells and thereby protects against diabetes. Preventing of alpha2-adrenergic receptor-mediated inhibition of insulin secretion may partly participate in such a function of SHPS-1.
journal_name
Endocrinologyjournal_title
Endocrinologyauthors
Kobayashi M,Ohnishi H,Okazawa H,Murata Y,Hayashi Y,Kobayashi H,Kitamura T,Matozaki Tdoi
10.1210/en.2008-0236subject
Has Abstractpub_date
2008-11-01 00:00:00pages
5662-9issue
11eissn
0013-7227issn
1945-7170pii
en.2008-0236journal_volume
149pub_type
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