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1. Multiethnic Genome-wide Association Study of Diabetic Retinopathy using Liability Threshold Modeling of Duration of Diabetes and Glycemic Control

Author

Pollack, Samuela, Igo, Robert P, Jensen, Richard A, Christiansen, Mark, Li, Xiaohui, Cheng, Ching-Yu, Ng, Maggie CY, Smith, Albert V, Rossin, Elizabeth J, Segrè, Ayellet V, Davoudi, Samaneh, Tan, Gavin S, Chen, Yii-Der Ida, Kuo, Jane Z, Dimitrov, Latchezar M, Stanwyck, Lynn K, Meng, Weihua, Hosseini, S Mohsen, Imamura, Minako, Nousome, Darryl, Kim, Jihye, Hai, Yang, Jia, Yucheng, Ahn, Jeeyun, Leong, Aaron, Shah, Kaanan, Park, Kyu Hyung, Guo, Xiuqing, Ipp, Eli, Taylor, Kent D, Adler, Sharon G, Sedor, John R, Freedman, Barry I, Group, DCCT EDIC Research Group Family Investigation of Nephropathy and Diabetes-Eye Research, Lee, I-Te, Sheu, Wayne H-H, Kubo, Michiaki, Takahashi, Atsushi, Hadjadj, Samy, Marre, Michel, Tregouet, David-Alexandre, Mckean-Cowdin, Roberta, Varma, Rohit, McCarthy, Mark I, Groop, Leif, Ahlqvist, Emma, Lyssenko, Valeriya, Agardh, Elisabet, Morris, Andrew, Doney, Alex SF, Colhoun, Helen M, Toppila, Iiro, Sandholm, Niina, Groop, Per-Henrik, Maeda, Shiro, Hanis, Craig L, Penman, Alan, Chen, Ching J, Hancock, Heather, Mitchell, Paul, Craig, Jamie E, Chew, Emily Y, Paterson, Andrew D, Grassi, Michael A, Palmer, Colin, Bowden, Donald W, Yaspan, Brian L, Siscovick, David, Cotch, Mary Frances, Wang, Jie Jin, Burdon, Kathryn P, Wong, Tien Y, Klein, Barbara EK, Klein, Ronald, Rotter, Jerome I, Iyengar, Sudha K, Price, Alkes, and Sobrin, Lucia

Subjects
Biomedical and Clinical Sciences, Genetics, Eye Disease and Disorders of Vision, Diabetes, Human Genome, Prevention, 2.1 Biological and endogenous factors, Aetiology, Metabolic and endocrine, Good Health and Well Being, Blood Glucose, Diabetes Mellitus, Type 2, Diabetic Retinopathy, Genetic Predisposition to Disease, Genome-Wide Association Study, Genotype, Glycated Hemoglobin, Humans, Meta-Analysis as Topic, Polymorphism, Single Nucleotide, Protein Binding, Family Investigation of Nephropathy and Diabetes-Eye Research Group, DCCT/EDIC Research Group, Medical and Health Sciences, Endocrinology & Metabolism, Biomedical and clinical sciences
Abstract

To identify genetic variants associated with diabetic retinopathy (DR), we performed a large multiethnic genome-wide association study. Discovery included eight European cohorts (n = 3,246) and seven African American cohorts (n = 2,611). We meta-analyzed across cohorts using inverse-variance weighting, with and without liability threshold modeling of glycemic control and duration of diabetes. Variants with a P value

Published
2019

2. A Genome-Wide Association Study of Diabetic Kidney Disease in Subjects With Type 2 Diabetes

Author

van Zuydam, Natalie R, Ahlqvist, Emma, Sandholm, Niina, Deshmukh, Harshal, Rayner, N William, Abdalla, Moustafa, Ladenvall, Claes, Ziemek, Daniel, Fauman, Eric, Robertson, Neil R, McKeigue, Paul M, Valo, Erkka, Forsblom, Carol, Harjutsalo, Valma, Perna, Annalisa, Rurali, Erica, Marcovecchio, M Loredana, Igo, Robert P, Salem, Rany M, Perico, Norberto, Lajer, Maria, Käräjämäki, Annemari, Imamura, Minako, Kubo, Michiaki, Takahashi, Atsushi, Sim, Xueling, Liu, Jianjun, van Dam, Rob M, Jiang, Guozhi, Tam, Claudia HT, Luk, Andrea OY, Lee, Heung Man, Lim, Cadmon KP, Szeto, Cheuk Chun, So, Wing Yee, Chan, Juliana CN, Ang, Su Fen, Dorajoo, Rajkumar, Wang, Ling, Clara, Tan Si Hua, McKnight, Amy-Jayne, Duffy, Seamus, Pezzolesi, Marcus G, Marre, Michel, Gyorgy, Beata, Hadjadj, Samy, Hiraki, Linda T, Ahluwalia, Tarunveer S, Almgren, Peter, Schulz, Christina-Alexandra, Orho-Melander, Marju, Linneberg, Allan, Christensen, Cramer, Witte, Daniel R, Grarup, Niels, Brandslund, Ivan, Melander, Olle, Paterson, Andrew D, Tregouet, David, Maxwell, Alexander P, Lim, Su Chi, Ma, Ronald CW, Tai, E Shyong, Maeda, Shiro, Lyssenko, Valeriya, Tuomi, Tiinamaija, Krolewski, Andrzej S, Rich, Stephen S, Hirschhorn, Joel N, Florez, Jose C, Dunger, David, Pedersen, Oluf, Hansen, Torben, Rossing, Peter, Remuzzi, Giuseppe, Brosnan, Mary Julia, Palmer, Colin NA, Groop, Per-Henrik, Colhoun, Helen M, Groop, Leif C, McCarthy, Mark I, Koivula, S, Uggeldahl, T, Forslund, T, Halonen, A, Koistinen, A, Koskiaho, P, Laukkanen, M, Saltevo, J, Tiihonen, M, Forsen, M, Granlund, H, Jonsson, A-C, Nyroos, B, Kinnunen, P, Orvola, A, Salonen, T, Vähänen, A, Paldanius, Kotka R, and Riihelä, M

Subjects
Diabetes, Genetics, Human Genome, Aetiology, 2.1 Biological and endogenous factors, Metabolic and endocrine, Good Health and Well Being, Adult, Aged, Aged, 80 and over, Case-Control Studies, Diabetes Mellitus, Type 2, Diabetic Nephropathies, Female, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Kidney Failure, Chronic, Male, Middle Aged, Polymorphism, Single Nucleotide, Renal Insufficiency, Chronic, Finnish Diabetic Nephropathy Study, Hong Kong Diabetes Registry Theme-based Research Scheme Project Group, Warren 3 and Genetics of Kidneys in Diabetes (GoKinD) Study Group, GENIE (GEnetics of Nephropathy an International Effort) Consortium, Diabetes Control and Complications Trial (DCCT)/Epidemiology of Diabetes Interventions and Complications (EDIC) Research Group, SUrrogate markers for Micro- and Macrovascular hard endpoints for Innovative diabetes Tools (SUMMIT) Consortium, Medical and Health Sciences, Endocrinology & Metabolism
Abstract

Identification of sequence variants robustly associated with predisposition to diabetic kidney disease (DKD) has the potential to provide insights into the pathophysiological mechanisms responsible. We conducted a genome-wide association study (GWAS) of DKD in type 2 diabetes (T2D) using eight complementary dichotomous and quantitative DKD phenotypes: the principal dichotomous analysis involved 5,717 T2D subjects, 3,345 with DKD. Promising association signals were evaluated in up to 26,827 subjects with T2D (12,710 with DKD). A combined T1D+T2D GWAS was performed using complementary data available for subjects with T1D, which, with replication samples, involved up to 40,340 subjects with diabetes (18,582 with DKD). Analysis of specific DKD phenotypes identified a novel signal near GABRR1 (rs9942471, P = 4.5 × 10-8) associated with microalbuminuria in European T2D case subjects. However, no replication of this signal was observed in Asian subjects with T2D or in the equivalent T1D analysis. There was only limited support, in this substantially enlarged analysis, for association at previously reported DKD signals, except for those at UMOD and PRKAG2, both associated with estimated glomerular filtration rate. We conclude that, despite challenges in addressing phenotypic heterogeneity, access to increased sample sizes will continue to provide more robust inference regarding risk variant discovery for DKD.

Published
2018

3. Impact of Type 2 Diabetes Susceptibility Variants on Quantitative Glycemic Traits Reveals Mechanistic Heterogeneity

Author

Dimas, Antigone S, Lagou, Vasiliki, Barker, Adam, Knowles, Joshua W, Mägi, Reedik, Hivert, Marie-France, Benazzo, Andrea, Rybin, Denis, Jackson, Anne U, Stringham, Heather M, Song, Ci, Fischer-Rosinsky, Antje, Boesgaard, Trine Welløv, Grarup, Niels, Abbasi, Fahim A, Assimes, Themistocles L, Hao, Ke, Yang, Xia, Lecoeur, Cécile, Barroso, Inês, Bonnycastle, Lori L, Böttcher, Yvonne, Bumpstead, Suzannah, Chines, Peter S, Erdos, Michael R, Graessler, Jurgen, Kovacs, Peter, Morken, Mario A, Narisu, Narisu, Payne, Felicity, Stancakova, Alena, Swift, Amy J, Tönjes, Anke, Bornstein, Stefan R, Cauchi, Stéphane, Froguel, Philippe, Meyre, David, Schwarz, Peter EH, Häring, Hans-Ulrich, Smith, Ulf, Boehnke, Michael, Bergman, Richard N, Collins, Francis S, Mohlke, Karen L, Tuomilehto, Jaakko, Quertemous, Thomas, Lind, Lars, Hansen, Torben, Pedersen, Oluf, Walker, Mark, Pfeiffer, Andreas FH, Spranger, Joachim, Stumvoll, Michael, Meigs, James B, Wareham, Nicholas J, Kuusisto, Johanna, Laakso, Markku, Langenberg, Claudia, Dupuis, Josée, Watanabe, Richard M, Florez, Jose C, Ingelsson, Erik, McCarthy, Mark I, Prokopenko, Inga, and Investigators, on behalf of the MAGIC

Subjects
Biomedical and Clinical Sciences, Genetics, Diabetes, Autoimmune Disease, Clinical Research, Prevention, Aetiology, 2.1 Biological and endogenous factors, Metabolic and endocrine, Alleles, Cluster Analysis, Diabetes Mellitus, Type 2, Female, Gene Frequency, Genetic Predisposition to Disease, Genetic Variation, Genome-Wide Association Study, Humans, Insulin, Insulin Resistance, Insulin Secretion, Insulin-Secreting Cells, Male, Polymorphism, Single Nucleotide, Quantitative Trait Loci, Risk Factors, Transcription Factors, MAGIC Investigators, Medical and Health Sciences, Endocrinology & Metabolism, Biomedical and clinical sciences
Abstract

Patients with established type 2 diabetes display both β-cell dysfunction and insulin resistance. To define fundamental processes leading to the diabetic state, we examined the relationship between type 2 diabetes risk variants at 37 established susceptibility loci, and indices of proinsulin processing, insulin secretion, and insulin sensitivity. We included data from up to 58,614 nondiabetic subjects with basal measures and 17,327 with dynamic measures. We used additive genetic models with adjustment for sex, age, and BMI, followed by fixed-effects, inverse-variance meta-analyses. Cluster analyses grouped risk loci into five major categories based on their relationship to these continuous glycemic phenotypes. The first cluster (PPARG, KLF14, IRS1, GCKR) was characterized by primary effects on insulin sensitivity. The second cluster (MTNR1B, GCK) featured risk alleles associated with reduced insulin secretion and fasting hyperglycemia. ARAP1 constituted a third cluster characterized by defects in insulin processing. A fourth cluster (TCF7L2, SLC30A8, HHEX/IDE, CDKAL1, CDKN2A/2B) was defined by loci influencing insulin processing and secretion without a detectable change in fasting glucose levels. The final group contained 20 risk loci with no clear-cut associations to continuous glycemic traits. By assembling extensive data on continuous glycemic traits, we have exposed the diverse mechanisms whereby type 2 diabetes risk variants impact disease predisposition.

Published
2014

4. Genome-wide association identifies nine common variants associated with fasting proinsulin levels and provides new insights into the pathophysiology of type 2 diabetes.

Author

Strawbridge, Rona J, Dupuis, Josée, Prokopenko, Inga, Barker, Adam, Ahlqvist, Emma, Rybin, Denis, Petrie, John R, Travers, Mary E, Bouatia-Naji, Nabila, Dimas, Antigone S, Nica, Alexandra, Wheeler, Eleanor, Chen, Han, Voight, Benjamin F, Taneera, Jalal, Kanoni, Stavroula, Peden, John F, Turrini, Fabiola, Gustafsson, Stefan, Zabena, Carina, Almgren, Peter, Barker, David JP, Barnes, Daniel, Dennison, Elaine M, Eriksson, Johan G, Eriksson, Per, Eury, Elodie, Folkersen, Lasse, Fox, Caroline S, Frayling, Timothy M, Goel, Anuj, Gu, Harvest F, Horikoshi, Momoko, Isomaa, Bo, Jackson, Anne U, Jameson, Karen A, Kajantie, Eero, Kerr-Conte, Julie, Kuulasmaa, Teemu, Kuusisto, Johanna, Loos, Ruth JF, Luan, Jian'an, Makrilakis, Konstantinos, Manning, Alisa K, Martínez-Larrad, María Teresa, Narisu, Narisu, Nastase Mannila, Maria, Ohrvik, John, Osmond, Clive, Pascoe, Laura, Payne, Felicity, Sayer, Avan A, Sennblad, Bengt, Silveira, Angela, Stancáková, Alena, Stirrups, Kathy, Swift, Amy J, Syvänen, Ann-Christine, Tuomi, Tiinamaija, van 't Hooft, Ferdinand M, Walker, Mark, Weedon, Michael N, Xie, Weijia, Zethelius, Björn, DIAGRAM Consortium, GIANT Consortium, MuTHER Consortium, CARDIoGRAM Consortium, C4D Consortium, Ongen, Halit, Mälarstig, Anders, Hopewell, Jemma C, Saleheen, Danish, Chambers, John, Parish, Sarah, Danesh, John, Kooner, Jaspal, Ostenson, Claes-Göran, Lind, Lars, Cooper, Cyrus C, Serrano-Ríos, Manuel, Ferrannini, Ele, Forsen, Tom J, Clarke, Robert, Franzosi, Maria Grazia, Seedorf, Udo, Watkins, Hugh, Froguel, Philippe, Johnson, Paul, Deloukas, Panos, Collins, Francis S, Laakso, Markku, Dermitzakis, Emmanouil T, Boehnke, Michael, McCarthy, Mark I, Wareham, Nicholas J, Groop, Leif, Pattou, François, Gloyn, Anna L, and Dedoussis, George V

Subjects
DIAGRAM Consortium, GIANT Consortium, MuTHER Consortium, CARDIoGRAM Consortium, C4D Consortium, Humans, Diabetes Mellitus, Type 2, Insulin, Proinsulin, Fasting, Genotype, Polymorphism, Single Nucleotide, Genome, Human, Adult, Female, Male, Genetic Variation, Diabetes Mellitus, Type 2, Polymorphism, Single Nucleotide, Genome, Human, Endocrinology & Metabolism, Medical and Health Sciences
Abstract

ObjectiveProinsulin 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.Research design and methodsWe 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.ResultsNine 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.ConclusionsWe 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.

Published
2011

5. A Bivariate Genome-Wide Approach to Metabolic Syndrome STAMPEED Consortium

Author

Kraja, Aldi T, Vaidya, Dhananjay, Pankow, James S, Goodarzi, Mark O, Assimes, Themistocles L, Kullo, Iftikhar J, Sovio, Ulla, Mathias, Rasika A, Sun, Yan V, Franceschini, Nora, Absher, Devin, Li, Guo, Zhang, Qunyuan, Feitosa, Mary F, Glazer, Nicole L, Haritunians, Talin, Hartikainen, Anna-Liisa, Knowles, Joshua W, North, Kari E, Iribarren, Carlos, Kral, Brian, Yanek, Lisa, O’Reilly, Paul F, McCarthy, Mark I, Jaquish, Cashell, Couper, David J, Chakravarti, Aravinda, Psaty, Bruce M, Becker, Lewis C, Province, Michael A, Boerwinkle, Eric, Quertermous, Thomas, Palotie, Leena, Jarvelin, Marjo-Riitta, Becker, Diane M, Kardia, Sharon LR, Rotter, Jerome I, Chen, Yii-Der Ida, and Borecki, Ingrid B

Subjects
Biomedical and Clinical Sciences, Nutrition, Human Genome, Clinical Research, Cardiovascular, Diabetes, Obesity, Genetics, 2.1 Biological and endogenous factors, Aetiology, Metabolic and endocrine, Adult, Aged, Female, Genetic Predisposition to Disease, Genome-Wide Association Study, Genotype, Humans, Male, Meta-Analysis as Topic, Metabolic Syndrome, Middle Aged, Phenotype, Polymorphism, Single Nucleotide, Medical and Health Sciences, Endocrinology & Metabolism, Biomedical and clinical sciences
Abstract

OBJECTIVE The metabolic syndrome (MetS) is defined as concomitant disorders of lipid and glucose metabolism, central obesity, and high blood pressure, with an increased risk of type 2 diabetes and cardiovascular disease. This study tests whether common genetic variants with pleiotropic effects account for some of the correlated architecture among five metabolic phenotypes that define MetS. RESEARCH DESIGN AND METHODS Seven studies of the STAMPEED consortium, comprising 22,161 participants of European ancestry, underwent genome-wide association analyses of metabolic traits using a panel of ∼2.5 million imputed single nucleotide polymorphisms (SNPs). Phenotypes were defined by the National Cholesterol Education Program (NCEP) criteria for MetS in pairwise combinations. Individuals exceeding the NCEP thresholds for both traits of a pair were considered affected. RESULTS Twenty-nine common variants were associated with MetS or a pair of traits. Variants in the genes LPL, CETP, APOA5 (and its cluster), GCKR (and its cluster), LIPC, TRIB1, LOC100128354/MTNR1B, ABCB11, and LOC100129150 were further tested for their association with individual qualitative and quantitative traits. None of the 16 top SNPs (one per gene) associated simultaneously with more than two individual traits. Of them 11 variants showed nominal associations with MetS per se. The effects of 16 top SNPs on the quantitative traits were relatively small, together explaining from ∼9% of the variance in triglycerides, 5.8% of high-density lipoprotein cholesterol, 3.6% of fasting glucose, and 1.4% of systolic blood pressure. CONCLUSIONS Qualitative and quantitative pleiotropic tests on pairs of traits indicate that a small portion of the covariation in these traits can be explained by the reported common genetic variants.

Published
2011

7. Association Analysis of 29,956 Individuals Confirms That a Low-Frequency Variant at CCND2 Halves the Risk of Type 2 Diabetes by Enhancing Insulin Secretion

Author

Yaghootkar, Hanieh, Stancáková, Alena, Freathy, Rachel M., Vangipurapu, Jagadish, Weedon, Michael N., Xie, Weijia, Wood, Andrew R., Ferrannini, Ele, Mari, Andrea, Ring, Susan M., Lawlor, Debbie A., Davey Smith, George, Jørgensen, Torben, Hansen, Torben, Pedersen, Oluf, Steinthorsdottir, Valgerdur, Gubjartsson, Daniel F., Thorleifsson, Gudmar, Thorsteinsdottir, Unnur, Stefansson, Kari, Hattersley, Andrew T., Walker, Mark, Morris, Andrew D., McCarthy, Mark I., Palmer, Colin N.A., Laakso, Markku, and Frayling, Timothy M.

Published
2015
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8. Age- and Sex-Specific Causal Effects of Adiposity on Cardiovascular Risk Factors

Author

Fall, Tove, Hägg, Sara, Ploner, Alexander, Mägi, Reedik, Fischer, Krista, Draisma, Harmen H.M., Sarin, Antti-Pekka, Benyamin, Beben, Ladenvall, Claes, Åkerlund, Mikael, Kals, Mart, Esko, Tõnu, Nelson, Christopher P., Kaakinen, Marika, Huikari, Ville, Mangino, Massimo, Meirhaeghe, Aline, Kristiansson, Kati, Nuotio, Marja-Liisa, Kobl, Michael, Grallert, Harald, Dehghan, Abbas, Kuningas, Maris, de Vries, Paul S., de Bruijn, Renée F.A.G., Willems, Sara M., Heikkilä, Kauko, Silventoinen, Karri, Pietiläinen, Kirsi H., Legry, Vanessa, Giedraitis, Vilmantas, Goumidi, Louisa, Syvänen, Ann-Christine, Strauch, Konstantin, Koenig, Wolfgang, Lichtner, Peter, Herder, Christian, Palotie, Aarno, Menni, Cristina, Uitterlinden, André G., Kuulasmaa, Kari, Havulinna, Aki S., Moreno, Luis A., Gonzalez-Gross, Marcela, Evans, Alun, Tregouet, David-Alexandre, Yarnell, John W.G., Virtamo, Jarmo, Ferrières, Jean, Veronesi, Giovanni, Perola, Markus, Arveiler, Dominique, Brambilla, Paolo, Lind, Lars, Kaprio, Jaakko, Hofman, Albert, Stricker, Bruno H., van Duijn, Cornelia M., Ikram, M. Arfan, Franco, Oscar H., Cottel, Dominique, Dallongeville, Jean, Hall, Alistair S., Jula, Antti, Tobin, Martin D., Penninx, Brenda W., Peters, Annette, Gieger, Christian, Samani, Nilesh J., Montgomery, Grant W., Whitfield, John B., Martin, Nicholas G., Groop, Leif, Spector, Tim D., Magnusson, Patrik K., Amouyel, Philippe, Boomsma, Dorret I., Nilsson, Peter M., Järvelin, Marjo-Riitta, Lyssenko, Valeriya, Metspalu, Andres, Strachan, David P., Salomaa, Veikko, Ripatti, Samuli, Pedersen, Nancy L., Prokopenko, Inga, McCarthy, Mark I., and Ingelsson, Erik

Published
2015
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9. Common Genetic Variants Highlight the Role of Insulin Resistance and Body Fat Distribution in Type 2 Diabetes, Independent of Obesity

Author

Scott, Robert A., Fall, Tove, Pasko, Dorota, Barker, Adam, Sharp, Stephen J., Arriola, Larraitz, Balkau, Beverley, Barricarte, Aurelio, Barroso, Inês, Boeing, Heiner, Clavel-Chapelon, Françoise, Crowe, Francesca L., Dekker, Jacqueline M., Fagherazzi, Guy, Ferrannini, Ele, Forouhi, Nita G., Franks, Paul W., Gavrila, Diana, Giedraitis, Vilmantas, Grioni, Sara, Groop, Leif C., Kaaks, Rudolf, Key, Timothy J., Kühn, Tilman, Lotta, Luca A., Nilsson, Peter M., Overvad, Kim, Palli, Domenico, Panico, Salvatore, Quirós, J. Ramón, Rolandsson, Olov, Roswall, Nina, Sacerdote, Carlotta, Sala, Núria, Sánchez, María-José, Schulze, Matthias B., Siddiq, Afshan, Slimani, Nadia, Sluijs, Ivonne, Spijkerman, Annemieke M.W., Tjonneland, Anne, Tumino, Rosario, van der A, Daphne L., Yaghootkar, Hanieh, McCarthy, Mark I., Semple, Robert K., Riboli, Elio, Walker, Mark, Ingelsson, Erik, Frayling, Tim M., Savage, David B., Langenberg, Claudia, and Wareham, Nicholas J.

Published
2014
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11. Expression of phosphofructokinase in skeletal muscle is influenced by genetic variation and associated with insulin sensitivity

Author

Keildson, Sarah, Fadista, Joao, Ladenvall, Claes, Hedman, Asa K., Elgzyri, Targ, Small, Kerrin S., Grundberg, Elin, Nica, Alexandra C., Glass, Daniel, Richards, J. Brent, Barrett, Amy, Nisbet, James, Zheng, Hou-Feng, Ronn, Tina, Strom, Kristoffer, Eriksson, Karl-Fredrik, Prokopenko, Inga, Spector, Timothy D., Dermitzakis, Emmanouil T., Deloukas, Panos, McCarthy, Mark I., Rung, Johan, Groop, Leif, Franks, Paul W., Lindgren, Cecilia M., and Hansson, Ola

Subjects
Genetic research, Musculoskeletal system -- Physiological aspects, Genetic variation -- Research, Phosphotransferases -- Identification and classification, Health
Abstract

Using an integrative approach in which genetic variation, gene expression, and clinical phenotypes are assessed in relevant tissues may help functionally characterize the contribution of genetics to disease susceptibility. We sought to identify genetic variation influencing skeletal muscle gene expression (expression quantitative trait loci [eQTLs]) as well as expression associated with measures of insulin sensitivity. We investigated associations of 3,799,401 genetic variants in expression of >7,000 genes from three cohorts (n = 104). We identified 287 genes with cis-acting eQTLs (false discovery rate [FDR] DOI: 10.2337/db13-1301, Although genome-wide association studies (GWASs) have identified thousands of single nucleotide polymorphisms (SNPs) associated with traits and diseases, the molecular mechanisms underlying these associations remain largely unknown. Changes in gene [...]

Published
2014
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14. Mendelian Randomization Studies Do Not Support a Causal Role for Reduced Circulating Adiponectin Levels in Insulin Resistance and Type 2 Diabetes

Author

Yaghootkar, Hanieh, Lamina, Claudia, Scott, Robert A., Dastani, Zari, Hivert, Marie-France, Warren, Liling L., Stancáková, Alena, Buxbaum, Sarah G., Lyytikäinen, Leo-Pekka, Henneman, Peter, Wu, Ying, Cheung, Chloe Y.Y., Pankow, James S., Jackson, Anne U., Gustafsson, Stefan, Zhao, Jing Hua, Ballantyne, Christie M., Xie, Weijia, Bergman, Richard N., Boehnke, Michael, el Bouazzaoui, Fatiha, Collins, Francis S., Dunn, Sandra H., Dupuis, Josee, Forouhi, Nita G., Gillson, Christopher, Hattersley, Andrew T., Hong, Jaeyoung, Kähönen, Mika, Kuusisto, Johanna, Kedenko, Lyudmyla, Kronenberg, Florian, Doria, Alessandro, Assimes, Themistocles L., Ferrannini, Ele, Hansen, Torben, Hao, Ke, Häring, Hans, Knowles, Joshua W., Lindgren, Cecilia M., Nolan, John J., Paananen, Jussi, Pedersen, Oluf, Quertermous, Thomas, Smith, Ulf, Lehtimäki, Terho, Liu, Ching-Ti, Loos, Ruth J.F., McCarthy, Mark I., Morris, Andrew D., Vasan, Ramachandran S., Spector, Tim D., Teslovich, Tanya M., Tuomilehto, Jaakko, van Dijk, Ko Willems, Viikari, Jorma S., Zhu, Na, Langenberg, Claudia, Ingelsson, Erik, Semple, Robert K., Sinaiko, Alan R., Palmer, Colin N.A., Walker, Mark, Lam, Karen S.L., Paulweber, Bernhard, Mohlke, Karen L., van Duijn, Cornelia, Raitakari, Olli T., Bidulescu, Aurelian, Wareham, Nick J., Laakso, Markku, Waterworth, Dawn M., Lawlor, Debbie A., Meigs, James B., Richards, J. Brent, and Frayling, Timothy M.

Published
2013
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15. Genome-Wide Association Study Identifies a Novel Locus Contributing to Type 2 Diabetes Susceptibility in Sikhs of Punjabi Origin From India

Author

Saxena, Richa, Saleheen, Danish, Been, Latonya F., Garavito, Martha L., Braun, Timothy, Bjonnes, Andrew, Young, Robin, Ho, Weang Kee, Rasheed, Asif, Frossard, Philippe, Sim, Xueling, Hassanali, Neelam, Radha, Venkatesan, Chidambaram, Manickam, Liju, Samuel, Rees, Simon D., Ng, Daniel Peng-Keat, Wong, Tien-Yin, Yamauchi, Toshimasa, Hara, Kazuo, Tanaka, Yasushi, Hirose, Hiroshi, McCarthy, Mark I., Morris, Andrew P., Basit, Abdul, Barnett, Anthony H., Katulanda, Prasad, Matthews, David, Mohan, Viswanathan, Wander, Gurpreet S., Singh, Jai Rup, Mehra, Narinder K., Ralhan, Sarju, Kamboh, M. Ilyas, Mulvihill, John J., Maegawa, Hiroshi, Tobe, Kazuyuki, Maeda, Shiro, Cho, Yoon S., Tai, E. Shyong, Kelly, M. Ann, Chambers, John C., Kooner, Jaspal S., Kadowaki, Takashi, Deloukas, Panos, Rader, Daniel J., Danesh, John, and Sanghera, Dharambir K.

Published
2013
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16. Mutations in HNF1A Result in Marked Alterations of Plasma Glycan Profile

Author

Thanabalasingham, Gaya, Huffman, Jennifer E., Kattla, Jayesh J., Novokmet, Mislav, Rudan, Igor, Gloyn, Anna L., Hayward, Caroline, Adamczyk, Barbara, Reynolds, Rebecca M., Muzinic, Ana, Hassanali, Neelam, Pucic, Maja, Bennett, Amanda J., Essafi, Abdelkader, Polasek, Ozren, Mughal, Saima A., Redzic, Irma, Primorac, Dragan, Zgaga, Lina, Kolcic, Ivana, Hansen, Torben, Gasperikova, Daniela, Tjora, Erling, Strachan, Mark W.J., Nielsen, Trine, Stanik, Juraj, Klimes, Iwar, Pedersen, Oluf B., Njølstad, Pål R., Wild, Sarah H., Gyllensten, Ulf, Gornik, Olga, Wilson, James F., Hastie, Nicholas D., Campbell, Harry, McCarthy, Mark I., Rudd, Pauline M., Owen, Katharine R., Lauc, Gordan, and Wright, Alan F.

Published
2013
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18. Genome-Wide Association Study for Type 2 Diabetes in Indians Identifies a New Susceptibility Locus at 2q21

Author

Tabassum, Rubina, Chauhan, Ganesh, Dwivedi, Om Prakash, Mahajan, Anubha, Jaiswal, Alok, Kaur, Ismeet, Bandesh, Khushdeep, Singh, Tejbir, Mathai, Benan John, Pandey, Yogesh, Chidambaram, Manickam, Sharma, Amitabh, Chavali, Sreenivas, Sengupta, Shantanu, Ramakrishnan, Lakshmi, Venkatesh, Pradeep, Aggarwal, Sanjay K., Ghosh, Saurabh, Prabhakaran, Dorairaj, Srinath, Reddy K., Saxena, Madhukar, Banerjee, Monisha, Mathur, Sandeep, Bhansali, Anil, Shah, Viral N., Madhu, Sri Venkata, Marwaha, Raman K., Basu, Analabha, Scaria, Vinod, McCarthy, Mark I., Venkatesan, Radha, Mohan, Viswanathan, Tandon, Nikhil, and Bharadwaj, Dwaipayan

Published
2013
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19. Insights into the molecular mechanism for type 2 diabetes susceptibility at the KCNQ1 locus from temporal changes m imploring stares in human islets

Author

Travers, Mary E., Mackay, Deborah J.G., Nitert, Marloes Dekker, Morris, Andrew P., Lindgren, Cecilia M., Berry, Andrew, Johnson, Paul R., Hanley, Neil, Groop, Left C., McCarthy, Mark I., and Gloyn, Anna L.

Subjects
Type 2 diabetes -- Research -- Analysis -- Genetic aspects, Health
Abstract

The molecular basis of type 2 diabetes predisposition at most established susceptibility loci remains poorly understood. KCNQ1 maps within the 11p15.5 imprinted domain, a region with an established role in congenital growth phenotypes. Variants intronic to KCNQ1 influence diabetes susceptibility when maternally inherited. By use of quantitative PCR and pyrosequencing of human adult islet and fetal pancreas samples, we investigated the imprinting status of regional transcripts and aimed to determine whether type 2 diabetes risk alleles influence regional DNA methylation and gene expression. The results demonstrate that gene expression patterns differ by developmental stage. CDKNIC showed monoallelic expression in both adult and fetal tissue, whereas PHLDA2, SLC22A18, and SLC22A18AS were biallelically expressed in both tissues. Temporal changes in imprinting were observed for KCNQ1 and KCNQIOT1, with monoallelic expression in fetal tissues and biallelic expression in adult samples. Genotype at the type 2 diabetes risk variant rs2237895 influenced methylation levels of regulatory sequence in fetal pancreas but without demonstrable effects on gene expression. We demonstrate that CDKN1C, KCNQ1, andKCNQIOT1 are most likely to mediate diabetes susceptibility at the KCNQ1 locus and identify temporal differences in imprinting status and methylation effects, suggesting that diabetes risk effects may be mediated in early development., The translation of established type 2 diabetes risk variants into an improved understanding of disease pathology is challenging. Progress has been made primarily at the few loci where causal alleles [...]

Published
2013
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20. Reduced Insulin Exocytosis in Human Pancreatic β-Cells With Gene Variants Linked to Type 2 Diabetes

Author

Rosengren, Anders H., Braun, Matthias, Mahdi, Taman, Andersson, Sofia A., Travers, Mary E., Shigeto, Makoto, Zhang, Enming, Almgren, Peter, Ladenvall, Claes, Axelsson, Annika S., Edlund, Anna, Pedersen, Morten Gram, Jonsson, Anna, Ramracheya, Reshma, Tang, Yunzhao, Walker, Jonathan N., Barrett, Amy, Johnson, Paul R.V., Lyssenko, Valeriya, McCarthy, Mark I., Groop, Leif, Salehi, Albert, Gloyn, Anna L., Renström, Erik, Rorsman, Patrik, and Eliasson, Lena

Published
2012
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21. Total Zinc Intake May Modify the Glucose-Raising Effect of a Zinc Transporter (SLC30A8) Variant: A 14-Cohort Meta-analysis

Author

Kanoni, Stavroula, Nettleton, Jennifer A., Hivert, Marie-France, Ye, Zheng, van Rooij, Frank J.A., Shungin, Dmitry, Sonestedt, Emily, Ngwa, Julius S., Wojczynski, Mary K., Lemaitre, Rozenn N., Gustafsson, Stefan, Anderson, Jennifer S., Tanaka, Toshiko, Hindy, George, Saylor, Georgia, Renstrom, Frida, Bennett, Amanda J., van Duijn, Cornelia M., Florez, Jose C., Fox, Caroline S., Hofman, Albert, Hoogeveen, Ron C., Houston, Denise K., Hu, Frank B., Jacques, Paul F., Johansson, Ingegerd, Lind, Lars, Liu, Yongmei, McKeown, Nicola, Ordovas, Jose, Pankow, James S., Sijbrands, Eric J.G., Syvänen, Ann-Christine, Uitterlinden, André G., Yannakoulia, Mary, Zillikens, M. Carola, Wareham, Nick J., Prokopenko, Inga, Bandinelli, Stefania, Forouhi, Nita G., Cupples, L. Adrienne, Loos, Ruth J., Hallmans, Goran, Dupuis, Josée, Langenberg, Claudia, Ferrucci, Luigi, Kritchevsky, Stephen B., McCarthy, Mark I., Ingelsson, Erik, Borecki, Ingrid B., Witteman, Jacqueline C.M., Orho-Melander, Marju, Siscovick, David S., Meigs, James B., Franks, Paul W., and Dedoussis, George V.

Published
2011
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22. Association of Genetic Loci With Glucose Levels in Childhood and Adolescence: A Meta-Analysis of Over 6,000 Children

Author

Barker, Adam, Sharp, Stephen J., Timpson, Nicholas J., Bouatia-Naji, Nabila, Warrington, Nicole M., Kanoni, Stavroula, Beilin, Lawrence J., Brage, Soren, Deloukas, Panos, Evans, David M., Grontved, Anders, Hassanali, Neelam, Lawlor, Deborah A., Lecoeur, Cecile, Loos, Ruth J.F., Lye, Stephen J., McCarthy, Mark I., Mori, Trevor A., Ndiaye, Ndeye Coumba, Newnham, John P., Ntalla, Ioanna, Pennell, Craig E., St Pourcain, Beate, Prokopenko, Inga, Ring, Susan M., Sattar, Naveed, Visvikis-Siest, Sophie, Dedoussis, George V., Palmer, Lyle J., Froguel, Philippe, Smith, George Davey, Ekelund, Ulf, Wareham, Nicholas J., and Langenberg, Claudia

Published
2011
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23. Mendelian Randomization Studies Do Not Support a Role for Raised Circulating Triglyceride Levels Influencing Type 2 Diabetes, Glucose Levels, or Insulin Resistance

Author

De Silva, N. Maneka G., Freathy, Rachel M., Palmer, Tom M., Donnelly, Louise A., Luan, Jianʼan, Gaunt, Tom, Langenberg, Claudia, Weedon, Michael N., Shields, Beverley, Knight, Beatrice A., Ward, Kirsten J., Sandhu, Manjinder S., Harbord, Roger M., McCarthy, Mark I., Smith, George Davey, Ebrahim, Shah, Hattersley, Andrew T., Wareham, Nicholas, Lawlor, Debbie A., Morris, Andrew D., Palmer, Colin N.A., and Frayling, Timothy M.

Published
2011
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25. 2050-P: A Multiomics Investigation of a Patient-Derived HNF-1A MODY IPSC Disease Model Reveals Insights into Its Role in Pancreatic Islet Development and Function

Author

DUFF, CLAIRE, primary, JENSEN, RIKKE REJNHOLDT, additional, PEREZ-ALCANTARA, MARTA, additional, RASMUSSEN, MIKKEL, additional, GROTZ, ANTJE, additional, JANSEN, MAX, additional, HOLST, BJØRN, additional, CLAUSEN, CHRISTIAN, additional, KRENTZ, NICOLE A.J., additional, HANSSON, MATTIAS, additional, MCCARTHY, MARK I., additional, GLOYN, ANNA L., additional, WESOLOWSKA-ANDERSEN, AGATA, additional, and HONORE, CHRISTIAN, additional

Published
2020
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27. Erratum. Multiethnic Genome-Wide Association Study of Diabetic Retinopathy Using Liability Threshold Modeling of Duration of Diabetes and Glycemic Control. Diabetes 2019;68:441—456

Author

Pollack, Samuela, primary, Igo, Robert P., additional, Jensen, Richard A., additional, Christiansen, Mark, additional, Li, Xiaohui, additional, Cheng, Ching-Yu, additional, Ng, Maggie C.Y., additional, Smith, Albert V., additional, Rossin, Elizabeth J., additional, Segrè, Ayellet V., additional, Davoudi, Samaneh, additional, Tan, Gavin S., additional, Ida Chen, Yii-Der, additional, Kuo, Jane Z., additional, Dimitrov, Latchezar M., additional, Stanwyck, Lynn K., additional, Meng, Weihua, additional, Hosseini, S. Mohsen, additional, Imamura, Minako, additional, Nousome, Darryl, additional, Kim, Jihye, additional, Hai, Yang, additional, Jia, Yucheng, additional, Ahn, Jeeyun, additional, Leong, Aaron, additional, Shah, Kaanan, additional, Park, Kyu Hyung, additional, Guo, Xiuqing, additional, Ipp, Eli, additional, Taylor, Kent D., additional, Adler, Sharon G., additional, Sedor, John R., additional, Freedman, Barry I., additional, Lee, I-Te, additional, Sheu, Wayne H.-H., additional, Kubo, Michiaki, additional, Takahashi, Atsushi, additional, Hadjadj, Samy, additional, Marre, Michel, additional, Tregouet, David-Alexandre, additional, Mckean-Cowdin, Roberta, additional, Varma, Rohit, additional, McCarthy, Mark I., additional, Groop, Leif, additional, Ahlqvist, Emma, additional, Lyssenko, Valeriya, additional, Agardh, Elisabet, additional, Morris, Andrew, additional, Doney, Alex S.F., additional, Colhoun, Helen M., additional, Toppila, Iiro, additional, Sandholm, Niina, additional, Groop, Per-Henrik, additional, Maeda, Shiro, additional, Hanis, Craig L., additional, Penman, Alan, additional, Chen, Ching J., additional, Hancock, Heather, additional, Mitchell, Paul, additional, Craig, Jamie E., additional, Chew, Emily Y., additional, Paterson, Andrew D., additional, Grassi, Michael A., additional, Palmer, Colin, additional, Bowden, Donald W., additional, Yaspan, Brian L., additional, Siscovick, David, additional, Cotch, Mary Frances, additional, Wang, Jie Jin, additional, Burdon, Kathryn P., additional, Wong, Tien Y., additional, Klein, Barbara E.K., additional, Klein, Ronald, additional, Rotter, Jerome I., additional, Iyengar, Sudha K., additional, Price, Alkes L., additional, and Sobrin, Lucia, additional

Published
2020
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28. Detailed Physiologic Characterization Reveals Diverse Mechanisms for Novel Genetic Loci Regulating Glucose and Insulin Metabolism in Humans

Author

Ingelsson, Erik, Langenberg, Claudia, Hivert, Marie-France, Prokopenko, Inga, Lyssenko, Valeriya, Dupuis, Josée, Mägi, Reedik, Sharp, Stephen, Jackson, Anne U., Assimes, Themistocles L., Shrader, Peter, Knowles, Joshua W., Zethelius, Björn, Abbasi, Fahim A., Bergman, Richard N., Bergmann, Antje, Berne, Christian, Boehnke, Michael, Bonnycastle, Lori L., Bornstein, Stefan R., Buchanan, Thomas A., Bumpstead, Suzannah J., Böttcher, Yvonne, Chines, Peter, Collins, Francis S., Cooper, Cyrus C., Dennison, Elaine M., Erdos, Michael R., Ferrannini, Ele, Fox, Caroline S., Graessler, Jürgen, Hao, Ke, Isomaa, Bo, Jameson, Karen A., Kovacs, Peter, Kuusisto, Johanna, Laakso, Markku, Ladenvall, Claes, Mohlke, Karen L., Morken, Mario A., Narisu, Narisu, Nathan, David M., Pascoe, Laura, Payne, Felicity, Petrie, John R., Sayer, Avan A., Schwarz, Peter E., Scott, Laura J., Stringham, Heather M., Stumvoll, Michael, Swift, Amy J., Syvänen, Ann-Christine, Tuomi, Tiinamaija, Tuomilehto, Jaakko, Tönjes, Anke, Valle, Timo T., Williams, Gordon H., Lind, Lars, Barroso, Inês, Quertermous, Thomas, Walker, Mark, Wareham, Nicholas J., Meigs, James B., McCarthy, Mark I., Groop, Leif, Watanabe, Richard M., and Florez, Jose C.

Published
2010
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31. Linkage Disequilibrium Mapping of the Replicated Type 2 Diabetes Linkage Signal on Chromosome 1q

Author

Prokopenko, Inga, Zeggini, Eleftheria, Hanson, Robert L., Mitchell, Braxton D., Rayner, N. William, Akan, Pelin, Baier, Leslie, Das, Swapan K., Elliott, Katherine S., Fu, Mao, Frayling, Timothy M., Groves, Christopher J., Gwilliam, Rhian, Scott, Laura J., Voight, Benjamin F., Hattersley, Andrew T., Hu, Cheng, Morris, Andrew D., Ng, Maggie, Palmer, Colin N.A., Tello-Ruiz, Marcela, Vaxillaire, Martine, Wang, Cong-rong, Stein, Lincoln, Chan, Juliana, Jia, Weiping, Froguel, Philippe, Elbein, Steven C., Deloukas, Panos, Bogardus, Clifton, Shuldiner, Alan R., and McCarthy, Mark I.

Published
2009

32. Type 2 Diabetes Risk A l leles A re Associated With Reduced Size at Birth

Author

Freathy, Rachel M., Bennett, Amanda J., Ring, Susan M., Shields, Beverley, Groves, Christopher J., Timpson, Nicholas J., Weedon, Michael N., Zeggini, Eleftheria, Lindgren, Cecilia M., Lango, Hana, Perry, John R.B., Pouta, Anneli, Ruokonen, Aimo, Hyppönen, Elina, Power, Chris, Elliott, Paul, Strachan, David P., Järvelin, Marjo-Riitta, Smith, George Davey, McCarthy, Mark I., Frayling, Timothy M., and Hattersley, Andrew T.

Published
2009

36. Population-Specific Risk of Type 2 Diabetes Conferred by HNF4A P2 Promoter Variants: A Lesson for Replication Studies

Author

Barroso, Inês, Luan, Jianʼan, Wheeler, Eleanor, Whittaker, Pamela, Wasson, Jon, Zeggini, Eleftheria, Weedon, Michael N., Hunt, Sarah, Venkatesh, Ranganath, Frayling, Timothy M., Delgado, Marcos, Neuman, Rosalind J., Zhao, Jinghua, Sherva, Richard, Glaser, Benjamin, Walker, Mark, Hitman, Graham, McCarthy, Mark I., Hattersley, Andrew T., Permutt, M. Alan, Wareham, Nicholas J., and Deloukas, Panagiotis

Published
2008

39. Type 2 diabetes risk alleles are associated with reduced size at birth

Author

Freathy, Rachel M., Bennett, Amanda J., Ring, Susan M., Shields, Beverley, Groves, Christopher J., Timpson, Nicholas J., Weedon, Michael N., Zeggini, Eleftheria, Lindgren, Cecilia M., Lango, Hana, Perry, John R.B., Pouta, Anneli, Ruokonen, Aimo, Hypponen, Elina, Power, Chris, Elliott, Paul, Strachan, David P., Jarvelin, Marjo-Riitta, Smith, George Davey, McCarthy, Mark I., Frayling, Timothy M., and Hattersley, Andrew T.

Subjects
Birth weight -- Health aspects -- Physiological aspects, Birth size -- Health aspects -- Physiological aspects, Allelomorphism -- Physiological aspects -- Health aspects -- Genetic aspects, Type 2 diabetes -- Risk factors -- Genetic aspects, Health
Abstract

OBJECTIVE--Low birth weight is associated with an increased risk of type 2 diabetes. The mechanisms underlying this association are unknown and may represent intrauterine programming or two phenotypes of one genotype. The fetal insulin hypothesis proposes that common genetic variants that reduce insulin secretion or action may predispose to type 2 diabetes and also reduce birth weight, since insulin is a key fetal growth factor. We tested whether common genetic variants that predispose to type 2 diabetes also reduce birth weight. RESEARCH DESIGN AND METHODS--We genotyped single-nucleotide polymorphisms (SNPs) at five recently identified type 2 diabetes loci (CDKAL1, CDKN2A/B, HHEX-IDE, IGF2BP2, and SLC3OA8) in 7,986 mothers and 19,200 offspring from four studies of white Europeans. We tested the association between maternal or fetal genotype at each locus and birth weight of the offspring. RESULTS--We found that type 2 diabetes risk alleles at the CDKAL1 and HHEX-IDE loci were associated with reduced birth weight when inherited by the fetus (21 g [95)A CI 11-31], P = 2 X [10.sup.-5], and 14 g [4-23], P = 0.004, lower birth weight per risk allele, respectively). The 4% of offspring carrying four risk alleles at these two loci were 80 g (95% CI 39-120) lighter at birth than the 8% carrying none ([P.sub.trend] = 5 X 10-7). There were no associations between birth weight and fetal genotypes at the three other loci or maternal genotypes at any locus. CONCLUSIONS--Our results are in keeping with the fetal insulin hypothesis and provide robust evidence that common disease-associated variants can alter size at birth directly through the fetal genotype., Reduced birth weight is associated with late-onset diseases including type 2 diabetes, hypertension, and heart disease (1). The cause of this association is not known. It is often proposed to [...]

Published
2009

40. Common Variation in the FTO Gene Alters Diabetes-Related Metabolic Traits to the Extent Expected Given Its Effect on BMI

Author

Freathy, Rachel M., Timpson, Nicholas J., Lawlor, Debbie A., Pouta, Anneli, Ben-Shlomo, Yoav, Ruokonen, Aimo, Ebrahim, Shah, Shields, Beverley, Zeggini, Eleftheria, Weedon, Michael N., Lindgren, Cecilia M., Lango, Hana, Melzer, David, Ferrucci, Luigi, Paolisso, Giuseppe, Neville, Matthew J., Karpe, Fredrik, Palmer, Colin N.A., Morris, Andrew D., Elliott, Paul, Jarvelin, Marjo-Riitta, Davey Smith, George, McCarthy, Mark I., Hattersley, Andrew T., and Frayling, Timothy M.

Published
2008

45. Evaluation of Common Variants in the Six Known Maturity-Onset Diabetes of the Young (MODY) Genes for Association With Type 2 Diabetes

Author

Winckler, Wendy, Weedon, Michael N., Graham, Robert R., McCarroll, Steven A., Purcell, Shaun, Almgren, Peter, Tuomi, Tiinamaija, Gaudet, Daniel, Boström, Kristina Bengtsson, Walker, Mark, Hitman, Graham, Hattersley, Andrew T., McCarthy, Mark I., Ardlie, Kristin G., Hirschhorn, Joel N., Daly, Mark J., Frayling, Timothy M., Groop, Leif, and Altshuler, David

Published
2007

49. Variation Within the Gene Encoding the Upstream Stimulatory Factor 1 Does Not Influence Susceptibility to Type 2 Diabetes in Samples From Populations With Replicated Evidence of Linkage to Chromosome 1q

Author

Zeggini, Eleftheria, Damcott, Coleen M., Hanson, Robert L., Karim, Mohammad A., Rayner, N. William, Groves, Christopher J., Baier, Leslie J., Hale, Terri C., Hattersley, Andrew T., Hitman, Graham A., Hunt, Sarah E., Knowler, William C., Mitchell, Braxton D., Ng, Maggie C.Y., OʼConnell, Jeffrey R., Pollin, Toni I., Vaxillaire, Martine, Walker, Mark, Wang, Xiaoqin, Whittaker, Pamela, Kunsun, Xiang, Jia, Weiping, Chan, Juliana C. N., Froguel, Philippe, Deloukas, Panos, Shuldiner, Alan R., Elbein, Steven C., and McCarthy, Mark I.

Published
2006

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