👤 Tom J Forsen

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Also published as: T Forsen,
articles
A Albrechtsen, N Grarup, Y Li +105 more · 2013 · Diabetologia · Springer · added 2026-04-24
Human complex metabolic traits are in part regulated by genetic determinants. Here we applied exome sequencing to identify novel associations of coding polymorphisms at minor allele frequencies (MAFs) Show more
Human complex metabolic traits are in part regulated by genetic determinants. Here we applied exome sequencing to identify novel associations of coding polymorphisms at minor allele frequencies (MAFs) >1% with common metabolic phenotypes. The study comprised three stages. We performed medium-depth (8×) whole exome sequencing in 1,000 cases with type 2 diabetes, BMI >27.5 kg/m(2) and hypertension and in 1,000 controls (stage 1). We selected 16,192 polymorphisms nominally associated (p < 0.05) with case-control status, from four selected annotation categories or from loci reported to associate with metabolic traits. These variants were genotyped in 15,989 Danes to search for association with 12 metabolic phenotypes (stage 2). In stage 3, polymorphisms showing potential associations were genotyped in a further 63,896 Europeans. Exome sequencing identified 70,182 polymorphisms with MAF >1%. In stage 2 we identified 51 potential associations with one or more of eight metabolic phenotypes covered by 45 unique polymorphisms. In meta-analyses of stage 2 and stage 3 results, we demonstrated robust associations for coding polymorphisms in CD300LG (fasting HDL-cholesterol: MAF 3.5%, p = 8.5 × 10(-14)), COBLL1 (type 2 diabetes: MAF 12.5%, OR 0.88, p = 1.2 × 10(-11)) and MACF1 (type 2 diabetes: MAF 23.4%, OR 1.10, p = 8.2 × 10(-10)). We applied exome sequencing as a basis for finding genetic determinants of metabolic traits and show the existence of low-frequency and common coding polymorphisms with impact on common metabolic traits. Based on our study, coding polymorphisms with MAF above 1% do not seem to have particularly high effect sizes on the measured metabolic traits. Show less
📄 PDF DOI: 10.1007/s00125-012-2756-1
MACF1
Rona J Strawbridge, Josée Dupuis, Inga Prokopenko +105 more · 2011 · Diabetes · added 2026-04-24
Rona J Strawbridge, Josée Dupuis, Inga Prokopenko, Adam Barker, Emma Ahlqvist, Denis Rybin, John R Petrie, Mary E Travers, Nabila Bouatia-Naji, Antigone S Dimas, Alexandra Nica, Eleanor Wheeler, Han Chen, Benjamin F Voight, Jalal Taneera, Stavroula Kanoni, John F Peden, Fabiola Turrini, Stefan Gustafsson, Carina Zabena, Peter Almgren, David J P Barker, Daniel Barnes, Elaine M Dennison, Johan G Eriksson, Per Eriksson, Elodie Eury, Lasse Folkersen, Caroline S Fox, Timothy M Frayling, Anuj Goel, Harvest F Gu, Momoko Horikoshi, Bo Isomaa, Anne U Jackson, Karen A Jameson, Eero Kajantie, Julie Kerr-Conte, Teemu Kuulasmaa, Johanna Kuusisto, Ruth J F Loos, Jian'an Luan, Konstantinos Makrilakis, Alisa K Manning, María Teresa Martínez-Larrad, Narisu Narisu, Maria Nastase Mannila, John Ohrvik, Clive Osmond, Laura Pascoe, Felicity Payne, Avan A Sayer, Bengt Sennblad, Angela Silveira, Alena Stancáková, Kathy Stirrups, Amy J Swift, Ann-Christine Syvänen, Tiinamaija Tuomi, Ferdinand M van 't Hooft, Mark Walker, Michael N Weedon, Weijia Xie, Björn Zethelius, DIAGRAM Consortium, GIANT Consortium, MuTHER Consortium, CARDIoGRAM Consortium, C4D Consortium, Halit Ongen, Anders Mälarstig, Jemma C Hopewell, Danish Saleheen, John Chambers, Sarah Parish, John Danesh, Jaspal Kooner, Claes-Göran Ostenson, Lars Lind, Cyrus C Cooper, Manuel Serrano-Ríos, Ele Ferrannini, Tom J Forsen, Robert Clarke, Maria Grazia Franzosi, Udo Seedorf, Hugh Watkins, Philippe Froguel, Paul Johnson, Panos Deloukas, Francis S Collins, Markku Laakso, Emmanouil T Dermitzakis, Michael Boehnke, Mark I McCarthy, Nicholas J Wareham, Leif Groop, François Pattou, Anna L Gloyn, George V Dedoussis, Valeriya Lyssenko, James B Meigs, Inês Barroso, Richard M Watanabe, Erik Ingelsson, Claudia Langenberg, Anders Hamsten, Jose C Florez Show less
Proinsulin is a precursor of mature insulin and C-peptide. Higher circulating proinsulin levels are associated with impaired β-cell function, raised glucose levels, insulin resistance, and type 2 diab Show more
Proinsulin is a precursor of mature insulin and C-peptide. Higher circulating proinsulin levels are associated with impaired β-cell function, raised glucose levels, insulin resistance, and type 2 diabetes (T2D). Studies of the insulin processing pathway could provide new insights about T2D pathophysiology. We have conducted a meta-analysis of genome-wide association tests of ∼2.5 million genotyped or imputed single nucleotide polymorphisms (SNPs) and fasting proinsulin levels in 10,701 nondiabetic adults of European ancestry, with follow-up of 23 loci in up to 16,378 individuals, using additive genetic models adjusted for age, sex, fasting insulin, and study-specific covariates. Nine SNPs at eight loci were associated with proinsulin levels (P < 5 × 10(-8)). Two loci (LARP6 and SGSM2) have not been previously related to metabolic traits, one (MADD) has been associated with fasting glucose, one (PCSK1) has been implicated in obesity, and four (TCF7L2, SLC30A8, VPS13C/C2CD4A/B, and ARAP1, formerly CENTD2) increase T2D risk. The proinsulin-raising allele of ARAP1 was associated with a lower fasting glucose (P = 1.7 × 10(-4)), improved β-cell function (P = 1.1 × 10(-5)), and lower risk of T2D (odds ratio 0.88; P = 7.8 × 10(-6)). Notably, PCSK1 encodes the protein prohormone convertase 1/3, the first enzyme in the insulin processing pathway. A genotype score composed of the nine proinsulin-raising alleles was not associated with coronary disease in two large case-control datasets. We have identified nine genetic variants associated with fasting proinsulin. Our findings illuminate the biology underlying glucose homeostasis and T2D development in humans and argue against a direct role of proinsulin in coronary artery disease pathogenesis. Show less
no PDF DOI: 10.2337/db11-0415
VPS13C