Fig. 4: HTR2B receptor agonist treatment increases β-cell proliferation in vitamin B6-deficient dams and normalizes glucose tolerance at GD 16.5. | Communications Biology

Fig. 4: HTR2B receptor agonist treatment increases β-cell proliferation in vitamin B6-deficient dams and normalizes glucose tolerance at GD 16.5.

From: Vitamin B6 deficiency disrupts serotonin signaling in pancreatic islets and induces gestational diabetes in mice

Fig. 4

Shown in (A) is representative ×20 immunofluorescent images of GD 12.5 pancreases from PBS and HTR2B agonist injected control and vitamin B6-deficient (VB6D) mice. Proliferating β-cells are identified using MCM-2 and Insulin antibodies and calculated as percentage of total β-cells (B). Glucose AUC for PBS and HTR2B agonist-treated control and VB6D dams at GD 16.5 is shown in (C). Data for panels A and B are based on 40–50 islets per mouse (N = 3 mice), while panel C represents 5–7 mice. Two-way ANOVA tests performed in panels B and C revealed a diet × treatment interaction effect and post hoc Tukey’s multiple comparison tests were subsequently performed. *p ≤ 0.05, **p < 0.01, ****p < 0.0001.

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