BACKGROUND: Inositol polyphosphate phosphatase-like 1 (INPPL1, SHIP2) is a negative regulator of insulin signalling and has previously been found to be associated with hypertension, obesity and type 2 diabetes in a cohort of families with diabetes in the UK presenting features of metabolic syndrome. In particular, a haplotype of three genetic polymorphisms (rs2276047, rs9886 and an insertion/deletion polymorphism in intron 1) was found to be strongly associated with increased susceptibility to hypertension. OBJECTIVE AND METHODS: To assess if INPPL1 variants play a direct role in the development of essential hypertension, we genotyped the three previously associated INPPL1 polymorphisms in a cohort of 712 families with severe hypertension from the BRIGHT study transmission disequilibrium test cohort. RESULTS: We found no evidence of significant association between hypertension and any of the three INPPL1 polymorphisms or haplotypes (p>0.1). CONCLUSION: These results suggest that INPPL1 variants may be involved in mechanisms causing hypertension in metabolic syndrome patients specifically.
BACKGROUND: Inositol polyphosphate phosphatase-like 1 (INPPL1, SHIP2) is a negative regulator of insulin signalling and has previously been found to be associated with hypertension, obesity and type 2 diabetes in a cohort of families with diabetes in the UK presenting features of metabolic syndrome. In particular, a haplotype of three genetic polymorphisms (rs2276047, rs9886 and an insertion/deletion polymorphism in intron 1) was found to be strongly associated with increased susceptibility to hypertension. OBJECTIVE AND METHODS: To assess if INPPL1 variants play a direct role in the development of essential hypertension, we genotyped the three previously associated INPPL1 polymorphisms in a cohort of 712 families with severe hypertension from the BRIGHT study transmission disequilibrium test cohort. RESULTS: We found no evidence of significant association between hypertension and any of the three INPPL1 polymorphisms or haplotypes (p>0.1). CONCLUSION: These results suggest that INPPL1 variants may be involved in mechanisms causing hypertension in metabolic syndrome patients specifically.
Authors: Mark W Sleeman; Katherine E Wortley; Ka-Man V Lai; Lori C Gowen; Jennifer Kintner; William O Kline; Karen Garcia; Trevor N Stitt; George D Yancopoulos; Stanley J Wiegand; David J Glass Journal: Nat Med Date: 2005-01-16 Impact factor: 53.440
Authors: X Xu; J J Rogus; H A Terwedow; J Yang; Z Wang; C Chen; T Niu; B Wang; H Xu; S Weiss; N J Schork; Z Fang Journal: Am J Hum Genet Date: 1999-06 Impact factor: 11.025
Authors: D Gauguier; P Froguel; V Parent; C Bernard; M T Bihoreau; B Portha; M R James; L Penicaud; M Lathrop; A Ktorza Journal: Nat Genet Date: 1996-01 Impact factor: 38.330
Authors: Pamela J Kaisaki; Marc Delépine; Peng Y Woon; Liam Sebag-Montefiore; Steven P Wilder; Stephan Menzel; Nathalie Vionnet; Evelyne Marion; Jean-Pierre Riveline; Guillaume Charpentier; Stéphane Schurmans; Jonathan C Levy; Mark Lathrop; Martin Farrall; Dominique Gauguier Journal: Diabetes Date: 2004-07 Impact factor: 9.461
Authors: Stephen J Newhouse; Chris Wallace; Richard Dobson; Charles Mein; Janine Pembroke; Martin Farrall; David Clayton; Morris Brown; Nilesh Samani; Anna Dominiczak; John M Connell; John Webster; G Mark Lathrop; Mark Caulfield; Patricia B Munroe Journal: Hum Mol Genet Date: 2005-05-11 Impact factor: 6.150
Authors: Melissa Hunter; Yijie Wang; Tim Eubank; Christopher Baran; Patrick Nana-Sinkam; Clay Marsh Journal: Front Biosci (Landmark Ed) Date: 2009-01-01