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51.07.02.db02-0209v1
51/7/2012    most recent
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Diabetes 51:2012-2017, 2002
© 2002 by the American Diabetes Association, Inc.

Rapid Publication

The Gene INPPL1, Encoding the Lipid Phosphatase SHIP2, Is a Candidate for Type 2 Diabetes In Rat and Man

Evelyne Marion1, Pamela Jane Kaisaki2, Valérie Pouillon1, Cyril Gueydan3, Jonathan C. Levy4, André Bodson5, Georges Krzentowski5, Jean-Claude Daubresse6, Jean Mockel7, Jens Behrends8, Geneviève Servais9, Claude Szpirer10, Véronique Kruys3, Dominique Gauguier2, and Stéphane Schurmans1

1 IRIBHM (Institut de Recherches en Biologie Humaine et Moléculaire), IBMM (Institut de Biologie et de Médecine Moléculaires), ULB (Université Libre de Bruxelles), Gosselies, Belgium
2 Wellcome Trust Centre for Human Genetics, University of Oxford, Headington, U.K.
3 Laboratoire de Chimie Biologique, IBMM, ULB, Gosselies, Belgium
4 Diabetes Research Laboratories, University of Oxford, Headington, U.K.
5 Department of Internal Medicine, Endocrinology-Diabetology, C.H.U. (Centre Hospitalier Universitaire) de Charleroi, site de Jumet, Jumet, Belgium
6 Department of Internal Medicine, Endocrinology-Diabetology, C.H.U. de Charleroi, Charleroi, Belgium
7 Department of Endocrinology, Hopital Erasme, ULB, Brussels, Belgium
8 Department of Clinical Endocrinology, Medical School Hannover, Germany
9 Department of Immunology, C.H.U. Brugmann-Huderf, ULB, Brussels, Belgium
10 Laboratoire de Biologie du Développement, IBMM, ULB, Gosselies, Belgium

Genetic susceptibility to type 2 diabetes involves many genes, most of which are still unknown. The lipid phosphatase SHIP2 is a potent negative regulator of insulin signaling and sensitivity in vivo and is thus a good candidate gene. Here we report the presence of SHIP2 gene mutations associated with type 2 diabetes in rats and humans. The R1142C mutation specifically identified in Goto-Kakizaki (GK) and spontaneously hypertensive rat strains disrupts a potential class II ligand for Src homology (SH)-3 domain and slightly impairs insulin signaling in cell culture. In humans, a deletion identified in the SHIP2 3' untranslated region (UTR) of type 2 diabetic subjects includes a motif implicated in the control of protein synthesis. In cell culture, the deletion results in reporter messenger RNA and protein overexpression. Finally, genotyping of a cohort of type 2 diabetic and control subjects showed a significant association between the deletion and type 2 diabetes. Altogether, our results show that mutations in the SHIP2 gene contribute to the genetic susceptibility to type 2 diabetes in rats and humans.


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