Lack of evidence for the 1484insG variant at the 3'-UTR of the protein tyrosine phosphatase 1B (PTP1B) gene as a genetic determinant of diabetic nephropathy development in type 1 diabetic patients

Insulin resistance (IR) is likely to precede and to play a role in diabetic nephropathy (DN) in both type 1 (T1D) [1] and type 2 diabetes [2]. IR and DN may also share common genetic determinants [3–6]. The gene encoding PTP1B, a tyrosine phosphatase which inhibits insulin signalling, is an excellent candidate for IR and related disorders. We recently have identified a 1484insG variation in the 3′-untranslated region (UTR) of the gene which stabilizes PTP1B mRNA and associates with IR in the general population [7]. Our aim was to verify whether the PTP1B 1484insG variant [as evaluated by polymerase chain reaction (PCR) and SacII enzyme digestion] plays a role in the development of DN in patients with T1D. In a case–control study, 288 European patients with T1D were enrolled. There were 170 patients with microalbuminuria [albumin excretion rate (AER) = 30–300 mg/24 h or albumin/creatinine ratio (ACR) = 2.5 males/3.5 females, 30 mg/mmol on two or more consecutive occasions] or persistent proteinuria (AER >300 mg/24 h or ACR >30 mg/mmol or a urine sample dipstick positive for protein on two or more consecutive occasions)