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Journal of Endocrinology (2007) 194, 551-555       DOI: 10.1677/JOE-07-0161
© 2007 Society for Endocrinology
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Rat insulin promoter 2-Cre recombinase mice bred onto a pure C57BL/6J background exhibit unaltered glucose tolerance

Malin Fex1,2,4, Nils Wierup1, Marloes Dekker Nitert1,4, Michael Ristow3 and Hindrik Mulder1,4

1 Department of Experimental Medical Science, Lund University, SE-22184 Lund, Sweden
2 Department of Clinical Science, Unit for Diabetes and Celiac Disease, Clinical Research Centre, Malmö University Hospital, SE-20502 Malmö, Sweden
3 Institute of Nutrition, University of Jena, D-07743 Jena, Germany
4 Lund University Diabetes Centre, SE-22184 Lund, Sweden

(Correspondence should be addressed to M Fex; Email: malin.fex{at}med.lu.se)

ß-Cell-specific gene targeting is a widely used tool when studying genes involved in ß-cell function. For this purpose, several conditional ß-cell knockouts have been generated using the rat insulin promoter 2-Cre recombinase (RIP2-Cre) mouse. However, it was recently observed that expression of Cre alone in ß-cells may affect whole body glucose homeostasis. Therefore, we investigated glucose homeostasis, insulin secretion, and ß-cell mass in our line of RIP2-Cre mice bred onto the C57BL/6J genetic background. We used 12- and 28-week-old female RIP2-Cre mice for analyses of insulin secretion in vitro, glucose homeostasis in vivo and ß-cell mass. Our mouse line has been backcrossedfor14generationstoyieldanear100%pureC57BL/6J background. Wefound thatfastingplasmaglucoseand insulinlevels were similar in both genotypes. An i.v. glucose tolerance test revealed no differences in glucose clearance and insulin secretion between 12-week-old RIP2-Cre and WT mice. Moreover, insulin secretion in vitro in islets isolated from 28-week-old RIP2-Cre mice and controls was similar. In addition, ß-cell mass was not different between the two genotypes at 28 weeks of age. In our experiments, we observed no differences in glucose tolerance, insulin secretion in vivo and in vitro, or in ß-cell mass between the genotypes. As our RIP2-Cre mice are on a near 100% pure genetic background (C57BL/6J), we suggest that the perturbations in glucose homeostasis previously reported in RIP2-Cre mouse lines can be accounted for by differences in genetic background.







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