The lipid phosphatase SHIP2 controls insulin sensitivity

Serge Clément, Ulrike Krause, Florence Desmedt, Jean-François Tanti, Jens Behrends, Xavier Pesesse, Takehiko Sasaki, Joseph Penninger, Margaret Doherty, Willy Malaisse, Jacques E. Dumont, Yannick Le Marchand-Brustel, Christophe Erneux, Louis Hue and Stéphane Schurmans ()
Additional contact information
Serge Clément: IRIBHN, IBMM
Ulrike Krause: ICP, Hormone and Metabolic Research Unit
Florence Desmedt: IRIBHN, Campus Erasme
Jean-François Tanti: INSERM E9911, Faculté de Médecine
Jens Behrends: IRIBHN, IBMM
Xavier Pesesse: IRIBHN, Campus Erasme
Takehiko Sasaki: University of Toronto
Joseph Penninger: University of Toronto
Margaret Doherty: Laboratoire de Médecine Expérimentale, Campus Erasme
Willy Malaisse: Laboratoire de Médecine Expérimentale, Campus Erasme
Jacques E. Dumont: IRIBHN, IBMM
Yannick Le Marchand-Brustel: INSERM E9911, Faculté de Médecine
Christophe Erneux: IRIBHN, Campus Erasme
Louis Hue: ICP, Hormone and Metabolic Research Unit
Stéphane Schurmans: IRIBHN, IBMM

Nature, 2001, vol. 409, issue 6816, 92-97

Abstract: Abstract Insulin is the primary hormone involved in glucose homeostasis, and impairment of insulin action and/or secretion has a critical role in the pathogenesis of diabetes mellitus. Type-II SH2-domain-containing inositol 5-phosphatase, or ‘SHIP2’, is a member of the inositol polyphosphate 5-phosphatase family1. In vitro studies have shown that SHIP2, in response to stimulation by numerous growth factors and insulin, is closely linked to signalling events mediated by both phosphoinositide-3-OH kinase and Ras/mitogen-activated protein kinase2,3,4,5. Here we report the generation of mice lacking the SHIP2 gene. Loss of SHIP2 leads to increased sensitivity to insulin, which is characterized by severe neonatal hypoglycaemia, deregulated expression of the genes involved in gluconeogenesis, and perinatal death. Adult mice that are heterozygous for the SHIP2 mutation have increased glucose tolerance and insulin sensitivity associated with an increased recruitment of the GLUT4 glucose transporter and increased glycogen synthesis in skeletal muscles. Our results show that SHIP2 is a potent negative regulator of insulin signalling and insulin sensitivity in vivo.

Date: 2001
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DOI: 10.1038/35051094

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