| First Author | Bathina S | Year | 2023 |
| Journal | Biomolecules | Volume | 13 |
| Issue | 3 | PubMed ID | 36979475 |
| Mgi Jnum | J:352971 | Mgi Id | MGI:7449395 |
| Doi | 10.3390/biom13030540 | Citation | Bathina S, et al. (2023) Normal beta-Cell Glut2 Expression Is not Required for Regulating Glucose-Stimulated Insulin Secretion and Systemic Glucose Homeostasis in Mice. Biomolecules 13(3) |
| abstractText | OBJECTIVE: Glucose transporter 2 (GLUT2) is expressed in the pancreatic beta-cell, intestine, liver, and kidney in mice. Although GLUT2 is considered as a major regulator of insulin secretion, in vivo contribution of beta-cell Glut2 to glucose-stimulated insulin secretion and systemic glucose homeostasis is undefined. Therefore, the main objective of this study is to determine the role of beta-cell Glut2 in regulating insulin secretion and blood glucose levels in mice. METHODS: We produced mice in which we can knock down Glut2 at a desired time specifically in beta-cells (beta-Glut2 KD) by crossing Glut2(LoxP/LoxP) mice with Ins1(CreERT2) mouse strain and using the Cre-Lox recombination technique. We measured fasting blood glucose levels, glucose tolerance, and glucose-stimulated insulin secretion in the beta-Glut2 KD mice. We used qRT-PCR and immunofluorescence to validate the deficiency of beta-cell Glut2 in beta-Glut2 KD mice. RESULTS: We report that both male and female beta-Glut2 KD mice have normal glucose-stimulated insulin secretion. Moreover, the beta-Glut2 KD mice exhibit normal fasting blood glucose levels and glucose tolerance. The beta-Glut2 KD mice have upregulated GLUT1 in islets. CONCLUSIONS: Our findings demonstrate that normal beta-cell Glut2 expression is not essential for regulating glucose-stimulated insulin secretion and systemic glucose homeostasis in mice. Therefore, the currently assumed role of beta-cell GLUT2 in regulating insulin secretion and blood glucose levels needs to be recalibrated. This will allow an opportunity to determine the contribution of other beta-cell glucose transporters or factors whose normal expression may be necessary for mediating glucose stimulated insulin secretion. |
