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. 2017 Jan;149(1):75–84. doi: 10.1085/jgp.201611653

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© 2017 Remedi et al.

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms/). After six months it is available under a Creative Commons License(Attribution–Noncommercial–Share Alike 4.0 International license, as described at https://creativecommons.org/licenses/by-nc-sa/4.0/).

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Figure 2. — Increased blood glucose in Kir6.1-GOF mice. (A–C, left) Representative intrinsic GFP fluorescence in freshly isolated islets from transgenic mice. High fluorescence in transgenic islets indicates the presence of the Kir6.1 transgene (Kir6.1[x], Control), and loss of fluorescence in transgenic β cells within islets after Cre-recombination (Rip-Kir6.1[x]) indicates actual expression of the transgene specifically in these cells. Bars, 10 µm. (right) Fed blood glucose over time after weaning in Rip-Kir6.1[WT] (A, black), single mutant Rip-Kir6.1[GD] (B, green), and double mutant Rip-Kir6.1[GD,QR] (C, red) with respect to their control littermates (white). Data represent mean ± SEM, n = 8–10 animals in each group. Significant differences (*, P < 0.05) between transgenic and control littermate mice are indicated (t test).