Article ; Online: Phogrin Regulates High-Fat Diet-Induced Compensatory Pancreatic β-Cell Growth by Switching Binding Partners.
2024 Volume 16, Issue 1
Abstract: The receptor protein tyrosine phosphatase phogrin primarily localizes to hormone secretory granules in neuroendocrine cells. Concurrent with glucose-stimulated insulin secretion, phogrin translocates to pancreatic β-cell plasma membranes, where it ... ...
| Abstract | The receptor protein tyrosine phosphatase phogrin primarily localizes to hormone secretory granules in neuroendocrine cells. Concurrent with glucose-stimulated insulin secretion, phogrin translocates to pancreatic β-cell plasma membranes, where it interacts with insulin receptors (IRs) to stabilize insulin receptor substrate 2 (IRS2) that, in turn, contributes to glucose-responsive β-cell growth. Pancreatic β-cell development was not altered in β-cell-specific, phogrin-deficient mice, but the thymidine incorporation rate decreased in phogrin-deficient islets with a moderate reduction in IRS2 protein expression. In this study, we analyzed the β-cell response to high-fat diet stress and found that the compensatory expansion in β-cell mass was significantly suppressed in phogrin-deficient mice. Phogrin-IR interactions occurred only in high-fat diet murine islets and proliferating β-cell lines, whereas they were inhibited by the intercellular binding of surface phogrin under confluent cell culture conditions. Thus, phogrin could regulate glucose-stimulated compensatory β-cell growth by changing its binding partner from another β-cell phogrin to IR in the same β-cells. |
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| MeSH term(s) | Animals ; Mice ; Diet, High-Fat/adverse effects ; Cell Proliferation ; Cell Culture Techniques ; Cell Cycle ; Glucose |
| Chemical Substances | Glucose (IY9XDZ35W2) |
| Language | English |
| Publishing date | 2024-01-04 |
| Publishing country | Switzerland |
| Document type | Journal Article |
| ZDB-ID | 2518386-2 |
| ISSN | 2072-6643 ; 2072-6643 |
| ISSN (online) | 2072-6643 |
| ISSN | 2072-6643 |
| DOI | 10.3390/nu16010169 |
| Database | MEDical Literature Analysis and Retrieval System OnLINE |
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