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. Author manuscript; available in PMC: 2021 Jan 1.
Published before final editing as: J Endocrinol. 2019 Jul 1:JOE-19-0182.R2. doi: 10.1530/JOE-19-0182

Figure 1. Glis3Δpanc mice exhibit a loss of insulin-producing beta cells.

Figure 1.

Figure 1.

Figure 1.

(A) Schematic of wild type and recombinant Glis3 allele. A conditional knockout allele for the Glis3 gene was generated in C57BL/6 mice containing loxP sites (triangles) surrounding exon 5 of Glis3. Exons 4–6 encode the DNA-binding domain (DBD). Mice were bred with a strain expressing Cre recombinase under the control of the Pdx1 promoter. (B) Random blood glucose levels of mice at 8-weeks of age. Glis3Δpanc mice were grouped as either Euglycemic (<250 mg/dL) or Hyperglycemic (>250 mg/dL) and compared to control littermates (WT) (N=11 WT, N=5 Glis3Δpanc euglycemic, N=4 Glis3Δpanc hyperglycemic). Immunofluorescence staining revealed a reduction in the number of INS+PDX1+ beta cells (C) and pancreatic polypeptide+ cells (D), with no apparent effect on (E) glucagon or (F) somatostatin expression. Nuclei were visualized by DAPI staining. Representative images are shown. * indicates p<0.05.