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. 2016 Mar 1;30(5):502–507. doi: 10.1101/gad.273821.115

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© 2016 Arnes et al.; Published by Cold Spring Harbor Laboratory Press

This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genesdev.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.

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Figure 2. — βlinc1 knockout mice are glucose-intolerant and have defects in endocrine specification. (A) βlinc1^−/− 16-wk-old mice are mildly glucose-intolerant. (AUC) Area under the curve. (B) Plasma insulin levels in 16-wk-old βlinc1^−/− mice (green) (n = 10) and littermate βlinc1^+/+ control mice (blue) (n = 7) at 0 and 30 min after glucose injection. (C) Immunofluorescence analysis of pancreas development at E15.5 showing a reduction of β cells and an increase of somatostatin-producing δ cells in βlinc1^−/− mice compared with βlinc1^+/+ and βlinc1^+/− mice. There are no apparent morphological defects in the exocrine compartment, which was visualized by immunostaining against CPA1. Images are representative of n > 3 mice. Bar, 50 µm. (D) Quantification of hormone-producing cells in E15.5 pancreata. n = 4. Error bars represent ±SEM. (*) P < 0.05 βlinc1^−/− versus βlinc1^+/+; (#) P < 0.05 βlinc1^−/− versus βlinc1^+/−, Student's t-test.