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. 2013 May 20;62(6):1904–1912. doi: 10.2337/db12-0769

FIG. 2.

FIG. 2.

Both EP3 expression and PGE2 production are upregulated in a mouse model of T2D. A: qRT PCR was performed on cDNA samples generated from nondiabetic and diabetic BTBR mouse islets. EP3 total, a primer set to a region common in all three splice variants (α, β, and γ). The gene expression of the other EP receptors (EP1, EP2, and EP4), prostaglandin-endoperoxidase synthases (Ptgs1, Ptgs2, and Ptgs3, i.e., COX-1, -2 and -3), and the prostaglandin E synthases (Ptges, Ptges2, and Ptges3) was also determined. Data were normalized within each sample to the Ct of a mouse β-actin primer set. ΔCt values for nondiabetic and diabetic islets were compared by unpaired t test (n = 5; *P < 0.05; **P < 1 × 10−4). NE, not expressed. B: PGE2 production was measured from islets from nondiabetic or diabetic BTBR mice. Islets were cultured for 24 h (hr), and the PGE2 that was secreted into the medium was normalized to the total number of islets. Data were compared by unpaired t test (n = 3. *P < 0.05).