Overexpression of Monocarboxylate Transporter-1 (Slc16a1) in Mouse Pancreatic β-Cells Leads to Relative Hyperinsulinism During Exercise

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FIG. 1.
FIG. 1.

A: Transgenic mouse strain for β-cell–specific, inducible expression of MCT1. MCT1 transgenic mice bearing Mct1 and firefly luciferase (Luc) cDNA under the control of a bidirectional tetracycline-regulated promoter (TRE) (22) were crossed with RIP7-rtTA mice in which the reverse tetracycline transactivator (rtTA) is expressed under control of the rat insulin promoter (RIP). In DT offspring, treatment with doxycycline induces expression of luciferase and MCT1 selectively in β-cells. B: Regulation of transgene expression is shown in islets isolated from DT mice. Islets from a single mouse were divided and cultured in the presence (+Dox) or absence (−Dox) of 5 μg/mL doxycycline for 48 h. Six size-matched islets were lysed, and luciferase activity was measured. Data are presented as mean ± SEM (n = 3). C: Immunofluorescence of pancreatic slices showing islets from ST control and DT mice, both treated with doxycycline, visualized with anti-insulin antibodies. Increased MCT1 staining is visible in DT mice. Scale bar = 50 μm. D: Quantification of immunofluorescence showing intensity of α-MCT1 signal within insulin-positive regions as mean ± SEM. E: Mct1 mRNA quantified by quantitative RT-PCR in tissues prepared from DT mice treated with (+Dox) or without (−Dox) doxycycline (n = 3). *P < 0.05 by Student t test; **P < 0.01 by Student t test. Sk., skeletal. (A high-quality digital representation of this figure is available in the online issue.)

This Article

  1. Diabetes vol. 61 no. 7 1719-1725