Poster Presentation Australian Diabetes Society and the Australian Diabetes Educators Association Annual Scientific Meeting 2014


Maria A Matuszek 1 , Sobana Thillainathan 1 , Arsha Anton 1 , Nicola J Armstrong 2
  1. School of Medical Sciences, University of New South Wales, Sydney, NSW, Australia
  2. School of Mathematics and Statistics, University of Sydney, Sydney, NSW, Australia

Introduction: Type 2 diabetes (T2D) is prevalent in non-Caucasians, especially South Asians (SA)1 and appears to have a genetic contribution2. We have reported that young (19-23 years) SA and South-East/East Asian (SEA) males and females (BMI<24 kg/m2) without T2D, already present with an elevated post-meal insulin3,4.The current study examined this population for single nucleotide polymorphism (SNP) frequencies in genes associated with T2D risk2. Method: Glucose and insulin were measured in fasting blood and for up to 2 hours following a 75 g glucose challenge, in 22 Caucasians (C), 19 SA and 15 SEA. DNA was extracted from fasting blood at the Australian Genome Research Facility. The genes (and SNPs) studied were PPARG2 (rs1801282, rs3892175); TCF7L2 (rs4918789, rs10885409, rs7903146, rs12255372, rs11196205, rs290487); KCNJ11 (rs5219); FTO (rs9939609); CDKAL1 (rs7756992); HHEX (rs1111875); KCNJ15 (rs3746876); KCNQ1 (rs2237892); RAPGEF1 (rs11243444); ADIPOQ (rs182052, rs7649121); MTNR1B (rs2166706, rs10830963); GCK (rs4607517), G6PC2 (rs560887), and PCK1 (rs2071023). Results: There was no difference in fasting glucose, glucose AUC, BMI or % body fat. Insulin (fasting, non-fasting and AUC) was higher in SA compared with C (P≤0.05). Ignoring ethnicity, an association was found between rs7903146 and insulin AUC (P=0.0392), however this was not significant when ethnicity was included potentially due to small sample sizes. Differences in allele frequencies between C and SA were identified in both SNPs of MTNR1B examined; rs10830963 (with CC:(68%), GC:(32%), GG:(0%); and CC:(26%), GC:(63%), GC:(11%); for C and SA respectively (P=.009)); and rs2166706 (with CC:(0%), TC:(45%), TT:(55%) and CC:(16%), TC:(63%), TT:(21%); for C and SA respectively (P=.02)). Conclusion: Studies of MTNR1B in SA are limited. However, it has been suggested that variation at MTNR1B contributes to raised plasma glucose and increased T2D risk in Asian Indians5. The current study’s results suggest that MTNR1B warrants further research in SA with elevated post-meal insulin.

  1. Mohan et al 2007 Indian J Med Res 125:217-230
  2. Elbein (2009) J Diabetes Science Technology 3:685-689
  3. Matuszek, Thillainathan (2009) (abstract) Heart Foundation Conference
  4. Matuszek et al (2009) (abstract) Australian Diabetes Society Conference
  5. Chambers et al (2009) Diabetes 58:2703-2708