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Wfs1 loss-of-function disrupts the composition of mouse pancreatic endocrine cells from birth and impairs Glut2 localization to cytomembrane in pancreatic β cells.
- Source :
-
Biochemical & Biophysical Research Communications . May2023, Vol. 658, p80-87. 8p. - Publication Year :
- 2023
-
Abstract
- Wfs1 is an endoplasmic reticulum (ER) membrane located protein highly expressed in pancreatic β cells and brain. Wfs1 deficiency causes adult pancreatic β cells dysfunction following β cells apoptosis. Previous studies mainly focus on the Wfs1 function in adult mouse pancreatic β cells. However, whether Wfs1 loss-of-function impairs mouse pancreatic β cell from its early development is unknown. In our study, Wfs1 deficiency disrupts the composition of mouse pancreatic endocrine cells from early postnatal day 0 (P0) to 8 weeks old, with decreased percentage of β cells and increased percentage of α and δ cells. Meanwhile, Wfs1 loss-of-function leads to reduced intracellular insulin content. Notably, Wfs1 deficiency impairs Glut2 localization and causes the accumulation of Glut2 in mouse pancreatic β cell cytoplasm. In Wfs1 -deficient mice, glucose homeostasis is disturbed from early 3 weeks old to 8 weeks old. This work reveals that Wfs1 is significantly required for the composition of pancreatic endocrine cells and is essential for Glut2 localization in mouse pancreatic β cells. • Wfs1 deficiency disrupts the composition of mouse pancreatic endocrine cells from P0 to 8 weeks old. • Wfs1 deficiency causes the reduction of intracellular insulin content. • Wfs1 loss-of-function impairs Glut2 localization to cytomembrane. • Wfs1 -deficient mice show disturbances in glucose tolerance from 3 weeks old. [ABSTRACT FROM AUTHOR]
- Subjects :
- *MICE
*MEMBRANE proteins
*ENDOPLASMIC reticulum
*HOMEOSTASIS
*ENDOCRINE cells
Subjects
Details
- Language :
- English
- ISSN :
- 0006291X
- Volume :
- 658
- Database :
- Academic Search Index
- Journal :
- Biochemical & Biophysical Research Communications
- Publication Type :
- Academic Journal
- Accession number :
- 163144839
- Full Text :
- https://doi.org/10.1016/j.bbrc.2023.03.074