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. Author manuscript; available in PMC: 2021 Jun 16.
Published in final edited form as: Cell Metab. 2017 Jun 6;25(6):1348–1361.e8. doi: 10.1016/j.cmet.2017.05.006

Figure 2. Expression of Slc38a5 in Intact Islets and α Cells from GCGR Antibody-Treated or Gcgr–/– Mice.

Figure 2.

(A) Differentially regulated genes in intact islets of mice treated with GCGR antibody (10 mg/kg) for 21 days. The gene expression was compared to mice treated with control antibody. Inclusion criteria were average baseline expression > 10 normalized counts, fold change > 1.5, and p < 0.01 (n = 5).

(B) Differentially regulated genes in α cell-enriched fraction of Gcgr−/− mice. Inclusion criteria were as described in (A).

(C) Changes in expression of amino acid transporters in islets of mice treated with GCGR or control antibody for 21 days. Transporters with expression > 1 RPKM were included.

(D) Same as in (C), but gene expression is determined in the α cell-enriched fraction of Gcgr−/− mice. Transporters with expression > 1 RPKM were included.

(E) Immunofluorescence staining of pancreas sections for glucagon (red) and Slc38a5 (green) in mice treated with GCGR or control antibody (3 mg/kg) for 21 days.

(F) Percentage of Slc38a5-positive α and β cells. Data are mean ± SEM. GCGR antibody (95 islets/pancreas from n = 15 pancreata), control antibody (30 islets/pancreas from n = 12 pancreata). ****p < 0.0001.

(G) Immunofluorescence staining of pancreas sections for glucagon (red) and Slc38a5 (green) in Gcgr−/− and wild-type mice.

(H) Percentage of Slc38a5-positive α and β cells in pancreas sections from Gcgr−/− mice. Data are mean ± SEM (20 islets/pancreas from n = 5 pancreata/group). ****p < 0.0001.