ProfessorPaulElliott

Sovio U, Bennett AJ, Millwood IY, Molitor J, O'Reilly PF, Timpson NJ, Kaakinen M, Laitinen J, Haukka J, Pillas D, Tzoulaki I, Molitor J, Hoggart C, Coin LJM, Whittaker J, Pouta A, Hartikainen A-L, Freimer NB, Widen E, Peltonen L, Elliott P, McCarthy MI, Jarvelin M-Ret al., 2009, Genetic Determinants of Height Growth Assessed Longitudinally from Infancy to Adulthood in the Northern Finland Birth Cohort 1966, PLOS Genetics, Vol: 5, ISSN: 1553-7390

Recent genome-wide association (GWA) studies have identified dozens of common variants associated with adult height. However, it is unknown how these variants influence height growth during childhood. We derived peak height velocity in infancy (PHV1) and puberty (PHV2) and timing of pubertal height growth spurt from parametric growth curves fitted to longitudinal height growth data to test their association with known height variants. The study consisted of N = 3,538 singletons from the prospective Northern Finland Birth Cohort 1966 with genotype data and frequent height measurements (on average 20 measurements per person) from 0–20 years. Twenty-six of the 48 variants tested associated with adult height (p<0.05, adjusted for sex and principal components) in this sample, all in the same direction as in previous GWA scans. Seven SNPs in or near the genes HHIP, DLEU7, UQCC, SF3B4/SV2A, LCORL, and HIST1H1D associated with PHV1 and five SNPs in or near SOCS2, SF3B4/SV2A, C17orf67, CABLES1, and DOT1L with PHV2 (p<0.05). We formally tested variants for interaction with age (infancy versus puberty) and found biologically meaningful evidence for an age-dependent effect for the SNP in SOCS2 (p = 0.0030) and for the SNP in HHIP (p = 0.045). We did not have similar prior evidence for the association between height variants and timing of pubertal height growth spurt as we had for PHVs, and none of the associations were statistically significant after correction for multiple testing. The fact that in this sample, less than half of the variants associated with adult height had a measurable effect on PHV1 or PHV2 is likely to reflect limited power to detect these associations in this dataset. Our study is the first genetic association analysis on longitudinal height growth in a prospective cohort from birth to adulthood and gives grounding for future research on the genetic regulation of human height during different periods of growth.

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Vineis P, Elliott P, 2009, Why is epidemiology necessary to policy-making?, JOURNAL OF EPIDEMIOLOGY AND COMMUNITY HEALTH, Vol: 63, Pages: 186-187, ISSN: 0143-005X

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• Citations: 2

Stutzmann F, Cauchi S, Durand E, Calvacanti-Proenca C, Pigeyre M, Hartikainen A-L, Sovio U, Tichet J, Marre M, Weill J, Balkau B, Potoczna N, Laitinen J, Elliott P, Jarvelin M-R, Horber F, Meyre D, Froguel Pet al., 2009, Common genetic variation near <i>MC4R</i> is associated with eating behaviour patterns in European populations, INTERNATIONAL JOURNAL OF OBESITY, Vol: 33, Pages: 373-378, ISSN: 0307-0565

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• Citations: 78

Elliott P, Richardson S, Abellan JJ, Thomson A, de Hoogh C, Jarup L, Briggs DJet al., 2009, Geographic density of landfill sites and risk of congenital anomalies in England: authors' response, OCCUPATIONAL AND ENVIRONMENTAL MEDICINE, Vol: 66, Pages: 140-140, ISSN: 1351-0711

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• Citations: 2

Brown IJ, Elliott P, Robertson CE, Chan Q, Daviglus ML, Dyer AR, Huang C-C, Rodriguez BL, Sakata K, Ueshima H, Van Horn L, Zhao L, Stamler Jet al., 2009, Dietary starch intake of individuals and their blood pressure: the international study of macronutrients and micronutrients and blood pressure, JOURNAL OF HYPERTENSION, Vol: 27, Pages: 231-236, ISSN: 0263-6352

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• Citations: 22

Elliott P, Richardson S, Abellan JJ, Thomson A, de Hoogh C, Jarup L, Briggs DJet al., 2009, Geographic density of landfill sites and risk of congenital anomalies in England, OCCUPATIONAL AND ENVIRONMENTAL MEDICINE, Vol: 66, Pages: 81-89, ISSN: 1351-0711

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• Citations: 40

Ormond G, Nieuwenhuijsen MJ, Nelson P, Toledano MB, Iszatt N, Geneletti S, Elliott Pet al., 2009, Endocrine Disruptors in the Workplace, Hair Spray, Folate Supplementation, and Risk of Hypospadias: Case-Control Study, ENVIRONMENTAL HEALTH PERSPECTIVES, Vol: 117, Pages: 303-307, ISSN: 0091-6765

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• Citations: 123

Willer CJ, Speliotes EK, Loos RJF, Li S, Lindgren CM, Heid IM, Berndt SI, Elliott AL, Jackson AU, Lamina C, Lettre G, Lim N, Lyon HN, McCarroll SA, Papadakis K, Qi L, Randall JC, Roccasecca RM, Sanna S, Scheet P, Weedon MN, Wheeler E, Zhao JH, Jacobs LC, Prokopenko I, Soranzo N, Tanaka T, Timpson NJ, Almgren P, Bennett A, Bergman RN, Bingham SA, Bonnycastle LL, Brown M, Burtt NLP, Chines P, Coin L, Collins FS, Connell JM, Cooper C, Smith GD, Dennison EM, Deodhar P, Elliott P, Erdos MR, Estrada K, Evans DM, Gianniny L, Gieger C, Gillson CJ, Guiducci C, Hackett R, Hadley D, Hall AS, Havulinna AS, Hebebrand J, Hofman A, Isomaa B, Jacobs KB, Johnson T, Jousilahti P, Jovanovic Z, Khaw K-T, Kraft P, Kuokkanen M, Kuusisto J, Laitinen J, Lakatta EG, Luan J, Luben RN, Mangino M, McArdle WL, Meitinger T, Mulas A, Munroe PB, Narisu N, Ness AR, Northstone K, O'Rahilly S, Purmann C, Rees MG, Ridderstrale M, Ring SM, Rivadeneira F, Ruokonen A, Sandhu MS, Saramies J, Scott LJ, Scuteri A, Silander K, Sims MA, Song K, Stephens J, Stevens S, Stringham HM, Tung YCL, Valle TT, Van Duijn CM, Vimaleswaran KS, Vollenweider P, Waeber G, Wallace C, Watanabe RM, Waterworth DM, Watkins N, Witteman JCM, Zeggini E, Zhai G, Zillikens MC, Altshuler D, Caulfield MJ, Chanock SJ, Farooqi IS, Ferrucci L, Guralnik JM, Hattersley AT, Hu FB, Jarvelin M-R, Laakso M, Mooser V, Ong KK, Ouwehand WH, Salomaa V, Samani NJ, Spector TD, Tuomi T, Tuomilehto J, Uda M, Uitterlinden AG, Wareham NJ, Deloukas P, Frayling TM, Groop LC, Hayes RB, Hunter DJ, Mohlke KL, Peltonen L, Schlessinger D, Strachan DP, Wichmann H-E, McCarthy MI, Boehnke M, Barroso I, Abecasis GR, Hirschhorn JNet al., 2009, Six new loci associated with body mass index highlight a neuronal influence on body weight regulation, NATURE GENETICS, Vol: 41, Pages: 25-34, ISSN: 1061-4036

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• Citations: 1344

Prokopenko I, Langenberg C, Florez JC, Saxena R, Soranzo N, Thorleifsson G, Loos RJF, Manning AK, Jackson AU, Aulchenko Y, Potter SC, Erdos MR, Sanna S, Hottenga J-J, Wheeler E, Kaakinen M, Lyssenko V, Chen W-M, Ahmadi K, Beckmann JS, Bergman RN, Bochud M, Bonnycastle LL, Buchanan TA, Cao A, Cervino A, Coin L, Collins FS, Crisponi L, De Geus EJC, Dehghan A, Deloukas P, Doney ASF, Elliott P, Freimer N, Gateva V, Herder C, Hofman A, Hughes TE, Hunt S, Illig T, Inouye M, Isomaa B, Johnson T, Kong A, Krestyaninova M, Kuusisto J, Laakso M, Lim N, Lindblad U, Lindgren CM, McCann OT, Mohlke KL, Morris AD, Naitza S, Orru M, Palmer CNA, Pouta A, Randall J, Rathmann W, Saramies J, Scheet P, Scott LJ, Scuteri A, Sharp S, Sijbrands E, Smit JH, Song K, Steinthorsdottir V, Stringham HM, Tuomi T, Tuomilehto J, Uitterlinden AG, Voight BF, Waterworth D, Wichmann H-E, Willemsen G, Witteman JCM, Yuan X, Zhao JH, Zeggini E, Schlessinger D, Sandhu M, Boomsma DI, Uda M, Spector TD, Penninx BWJH, Altshuler D, Vollenweider P, Jarvelin MR, Lakatta E, Waeber G, Fox CS, Peltonen L, Groop LC, Mooser V, Cupples LA, Thorsteinsdottir U, Boehnke M, Barroso I, Van Duijn C, Dupuis J, Watanabe RM, Stefansson K, McCarthy MI, Wareham NJ, Meigs JB, Abecasis GRet al., 2009, Variants in <i>MTNR1B</i> influence fasting glucose levels, NATURE GENETICS, Vol: 41, Pages: 77-81, ISSN: 1061-4036

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• Citations: 573

Sabatti C, Service SK, Hartikainen A-L, Pouta A, Ripatti S, Brodsky J, Jones CG, Zaitlen NA, Varilo T, Kaakinen M, Sovio U, Ruokonen A, Laitinen J, Jakkula E, Coin L, Hoggart C, Collins A, Turunen H, Gabriel S, Elliot P, McCarthy MI, Daly MJ, Jarvelin M-R, Freimer NB, Peltonen Let al., 2009, Genome-wide association analysis of metabolic traits in a birth cohort from a founder population, NATURE GENETICS, Vol: 41, Pages: 35-46, ISSN: 1061-4036

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• Citations: 575

Aulchenko YS, Ripatti S, Lindqvist I, Boomsma D, Heid IM, Pramstaller PP, Penninx BWJH, Janssens ACJW, Wilson JF, Spector T, Martin NG, Pedersen NL, Kyvik KO, Kaprio J, Hofman A, Freimer NB, Jarvelin M-R, Gyllensten U, Campbell H, Rudan I, Johansson A, Marroni F, Hayward C, Vitart V, Jonasson I, Pattaro C, Wright A, Hastie N, Pichler I, Hicks AA, Falchi M, Willemsen G, Hottenga J-J, de Geus EJC, Montgomery GW, Whitfield J, Magnusson P, Saharinen J, Perola M, Silander K, Isaacs A, Sijbrands EJG, Uitterlinden AG, Witteman JCM, Oostra BA, Elliott P, Ruokonen A, Sabatti C, Gieger C, Meitinger T, Kronenberg F, Doering A, Wichmann H-E, Smit JH, McCarthy MI, van Duijn CM, Peltonen Let al., 2009, Loci influencing lipid levels and coronary heart disease risk in 16 European population cohorts, NATURE GENETICS, Vol: 41, Pages: 47-55, ISSN: 1061-4036

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• Citations: 702

Bouatia-Naji N, Bonnefond A, Cavalcanti-Proenca C, Sparso T, Holmkvist J, Marchand M, Delplanque J, Lobbens S, Rocheleau G, Durand E, De Graeve F, Chevre JC, Borch-Johnsen K, Hartikainen AL, Ruokonen A, Tichet J, Marre M, Weill J, Heude B, Tauber M, Lemaire K, Schuit F, Elliott P, Jorgensen T, Charpentier G, Hadjadj S, Cauchi S, Vaxillaire M, Sladek R, Visvikis-Siest S, Balkau B, Levy-Marchal C, Pattou F, Meyre D, Blakemore AI, Jarvelin MR, Walley AJ, Hansen T, Dina C, Pedersen O, Froguel Pet al., 2009, A variant near MTNR1B is associated with increased fasting plasma glucose levels and type 2 diabetes risk, Nat Genet, Vol: 41, Pages: 89-94, ISSN: 1546-1718

In genome-wide association (GWA) data from 2,151 nondiabetic French subjects, we identified rs1387153, near MTNR1B (which encodes the melatonin receptor 2 (MT2)), as a modulator of fasting plasma glucose (FPG; P = 1.3 x 10(-7)). In European populations, the rs1387153 T allele is associated with increased FPG (beta = 0.06 mmol/l, P = 7.6 x 10(-29), N = 16,094), type 2 diabetes (T2D) risk (odds ratio (OR) = 1.15, 95% CI = 1.08-1.22, P = 6.3 x 10(-5), cases N = 6,332) and risk of developing hyperglycemia or diabetes over a 9-year period (hazard ratio (HR) = 1.20, 95% CI = 1.06-1.36, P = 0.005, incident cases N = 515). RT-PCR analyses confirm the presence of MT2 transcripts in neural tissues and show MT2 expression in human pancreatic islets and beta cells. Our data suggest a possible link between circadian rhythm regulation and glucose homeostasis through the melatonin signaling pathway.

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Cauchi S, Stutzmann F, Cavalcanti-Proenca C, Durand E, Pouta A, Hartikainen AL, Marre M, Vol S, Tammelin T, Laitinen J, Gonzalez-Izquierdo A, Blakemore AI, Elliott P, Meyre D, Balkau B, Jarvelin MR, Froguel Pet al., 2009, Combined effects of MC4R and FTO common genetic variants on obesity in European general populations, J Mol Med, Vol: 87, Pages: 537-546, ISSN: 1432-1440

Genome-wide association scans recently identified common polymorphisms, in intron 1 of FTO and 188 kb downstream MC4R, that modulate body mass index (BMI) and associate with increased risk of obesity. Although their individual contribution to obesity phenotype is modest, their combined effects and their interactions with environmental factors remained to be evaluated in large general populations from birth to adulthood. In the present study, we analyzed independent and combined effects of the FTO rs1421085 and MC4R rs17782313 risk alleles on BMI, fat mass, prevalence and incidence of obesity and subsequent type 2 diabetes (T2D) as well as their interactions with physical activity levels and gender in two European prospective population-based cohorts of 4,762 Finnish adolescents (NFBC 1986) and 3,167 French adults (D.E.S.I.R.). Compared to participants carrying neither FTO nor MC4R risk allele (20-24% of the populations), subjects with three or four risk alleles (7-10% of the populations) had a 3-fold increased susceptibility of developing obesity during childhood. In adults, their combined effects were more modest (approximately 1.8-fold increased risk) and associated with a 1.27% increase in fat mass (P = 0.001). Prospectively, we demonstrated that each FTO and MC4R risk allele increased obesity and T2D incidences by 24% (P = 0.02) and 21% (P = 0.02), respectively. However, the effect on T2D disappeared after adjustment for BMI. The Z-BMI and ponderal index of newborns homozygous for the rs1421085 C allele were 0.1 units (P = 0.02) and 0.27 g/cm(3) (P = 0.005) higher, respectively, than in those without FTO risk allele. The MC4R rs17782313 C allele was more associated with obesity and fat mass deposition in males than in females (P = 0.003 and P = 0.03, respectively) and low physical activity accentuated the effect of the FTO polymorphism on BMI increase and obesity prevalence (P = 0.008 and P = 0.01, respectively). In European general populations, the combined eff

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Meyre D, Delplanque J, Chevre JC, Lecoeur C, Lobbens S, Gallina S, Durand E, Vatin V, Degraeve F, Proenca C, Gaget S, Korner A, Kovacs P, Kiess W, Tichet J, Marre M, Hartikainen AL, Horber F, Potoczna N, Hercberg S, Levy-Marchal C, Pattou F, Heude B, Tauber M, McCarthy MI, Blakemore AI, Montpetit A, Polychronakos C, Weill J, Coin LJ, Asher J, Elliott P, Jarvelin MR, Visvikis-Siest S, Balkau B, Sladek R, Balding D, Walley A, Dina C, Froguel Pet al., 2009, Genome-wide association study for early-onset and morbid adult obesity identifies three new risk loci in European populations, Nat Genet, Vol: 41, Pages: 157-159, ISSN: 1546-1718

We analyzed genome-wide association data from 1,380 Europeans with early-onset and morbid adult obesity and 1,416 age-matched normal-weight controls. Thirty-eight markers showing strong association were further evaluated in 14,186 European subjects. In addition to FTO and MC4R, we detected significant association of obesity with three new risk loci in NPC1 (endosomal/lysosomal Niemann-Pick C1 gene, P = 2.9 x 10(-7)), near MAF (encoding the transcription factor c-MAF, P = 3.8 x 10(-13)) and near PTER (phosphotriesterase-related gene, P = 2.1 x 10(-7)).

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Yuan X, Waterworth D, Perry JRB, Lim N, Song K, Chambers JC, Zhang W, Vollenweider P, Stirnadel H, Johnson T, Bergmann S, Beckmann ND, Li Y, Ferrucci L, Melzer D, Hernandez D, Singleton A, Scott J, Elliott P, Waeber G, Cardon L, Frayling TM, Kooner JS, Mooser Vet al., 2008, Population-Based Genome-wide Association Studies Reveal Six Loci Influencing Plasma Levels of Liver Enzymes, AMERICAN JOURNAL OF HUMAN GENETICS, Vol: 83, Pages: 520-528, ISSN: 0002-9297

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• Citations: 336

Caulfield MJ, Munroe PB, O'Neill D, Witkowska K, Charchar FJ, Doblado M, Evans S, Eyheramendy S, Onipinla A, Howard P, Shaw-Hawkins S, Dobson RJ, Wallace C, Newhouse SJ, Brown M, Connell JM, Dominiczak A, Farrall M, Lathrop GM, Samani NJ, Kumari M, Marmot M, Brunner E, Chambers J, Elliott P, Kooner J, Laan M, Org E, Veldre G, Viigimaa M, Cappuccio FP, Ji C, Iacone R, Strazzullo P, Moley KH, Cheeseman Cet al., 2008, SLC2A9 is a high-capacity urate transporter in humans, PLoS Medicine, Vol: 5, Pages: 1509-1523, ISSN: 1549-1277

BackgroundSerum uric acid levels in humans are influenced by diet, cellular breakdown, and renal elimination, and correlate with blood pressure, metabolic syndrome, diabetes, gout, and cardiovascular disease. Recent genome-wide association scans have found common genetic variants of SLC2A9 to be associated with increased serum urate level and gout. The SLC2A9 gene encodes a facilitative glucose transporter, and it has two splice variants that are highly expressed in the proximal nephron, a key site for urate handling in the kidney. We investigated whether SLC2A9 is a functional urate transporter that contributes to the longstanding association between urate and blood pressure in man.Methods and FindingsWe expressed both SLC2A9 splice variants in Xenopus laevis oocytes and found both isoforms mediate rapid urate fluxes at concentration ranges similar to physiological serum levels (200–500 μM). Because SLC2A9 is a known facilitative glucose transporter, we also tested whether glucose or fructose influenced urate transport. We found that urate is transported by SLC2A9 at rates 45- to 60-fold faster than glucose, and demonstrated that SLC2A9-mediated urate transport is facilitated by glucose and, to a lesser extent, fructose. In addition, transport is inhibited by the uricosuric benzbromarone in a dose-dependent manner (Ki = 27 μM). Furthermore, we found urate uptake was at least 2-fold greater in human embryonic kidney (HEK) cells overexpressing SLC2A9 splice variants than nontransfected kidney cells. To confirm that our findings were due to SLC2A9, and not another urate transporter, we showed that urate transport was diminished by SLC2A9-targeted siRNA in a second mammalian cell line. In a cohort of men we showed that genetic variants of SLC2A9 are associated with reduced urinary urate clearance, which fits with common variation at SLC2A9 leading to increased serum urate. We found no evidence of association with hypertension (odds ratio 0.98, 95% confidenc

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Nicholson JK, Holmes E, Elliott P, 2008, The metabolome-wide association study: A new look at human disease risk factors, JOURNAL OF PROTEOME RESEARCH, Vol: 7, Pages: 3637-3638, ISSN: 1535-3893

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• Citations: 65

Holmes E, Loo RL, Cloarec O, Coen M, Yang H, Malbaum E, Bruce S, Chan Q, Elliott P, Stamler J, Wilson ID, Lindon JC, Nicholson JKet al., 2008, Detection of urinary drug metabolite (xenometabolome) signatures in molecular epidemiology studies via statistical total correlation (NMR) spectroscopy (vol 79, pg 2629, 2007), ANALYTICAL CHEMISTRY, Vol: 80, Pages: 6142-6143, ISSN: 0003-2700

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Burton PR, Hansell AL, Fortier I, Manolio TA, Khoury MJ, Little J, Elliott Pet al., 2008, Size matters: just how big is BIG? Quantifying realistic sample size requirements for human genome epidemiology, International Journal of Epidemiology, Vol: 38, Pages: 263-273, ISSN: 1464-3685

Background Despite earlier doubts, a string of recent successes indicates that if sample sizes are large enough, it is possible—both in theory and in practice—to identify and replicate genetic associations with common complex diseases. But human genome epidemiology is expensive and, from a strategic perspective, it is still unclear what ‘large enough’ really means. This question has critical implications for governments, funding agencies, bioscientists and the tax-paying public. Difficult strategic decisions with imposing price tags and important opportunity costs must be taken.Methods Conventional power calculations for case–control studies disregard many basic elements of analytic complexity—e.g. errors in clinical assessment, and the impact of unmeasured aetiological determinants—and can seriously underestimate true sample size requirements. This article describes, and applies, a rigorous simulation-based approach to power calculation that deals more comprehensively with analytic complexity and has been implemented on the web as ESPRESSO: (www.p3gobservatory.org/powercalculator.htm).Results Using this approach, the article explores the realistic power profile of stand-alone and nested case–control studies in a variety of settings and provides a robust quantitative foundation for determining the required sample size both of individual biobanks and of large disease-based consortia. Despite universal acknowledgment of the importance of large sample sizes, our results suggest that contemporary initiatives are still, at best, at the lower end of the range of desirable sample size. Insufficient power remains particularly problematic for studies exploring gene–gene or gene–environment interactions.Discussion Sample size calculation must be both accurate and realistic, and we must continue to strengthen national and international cooperation in the design, conduct, harmonization and integration of studies in hum

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Elliott P, Savitz DA, 2008, Design issues in small-area studies of environment and health, ENVIRONMENTAL HEALTH PERSPECTIVES, Vol: 116, Pages: 1098-1104, ISSN: 0091-6765

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• Citations: 38

Miura K, Stamler J, Nakagawa H, Elliott P, Ueshima H, Chan Q, Brown IJ, Tzoulaki I, Saitoh S, Dyer AR, Daviglus ML, Kesteloot H, Okayama A, Curb JD, Rodriguez BL, Elmer PJ, Steffen LM, Robertson C, Zhao Let al., 2008, Relationship of dietary linoleic acid to blood pressure - The International Study of Macro-Micronutrients and Blood Pressure study, HYPERTENSION, Vol: 52, Pages: 408-414, ISSN: 0194-911X

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• Citations: 62

Tzoulaki I, Brown IJ, Chan Q, Van Horn L, Ueshima H, Zhao L, Stamler J, Elliott Pet al., 2008, Relation of iron and red meat intake to blood pressure: cross sectional epidemiological study, BRITISH MEDICAL JOURNAL, Vol: 337, ISSN: 0959-535X

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• Citations: 72

Zhang W, Zabaneh D, Balding D, McCarthy MI, Elliott P, Scott J, Kooner JS, Chambers JCet al., 2008, Are Indian Asians genetically homogeneous? Implications for genetic association studies, Annual Scientific Conference of the British-Cardiovascular-Society/British-Society-for-Cardiovascular-Research, Publisher: B M J PUBLISHING GROUP, Pages: A65-A65, ISSN: 1355-6037

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Barber TM, Bennett AJ, Groves CJ, Sovio U, Ruokonen A, Martikainen H, Pouta, Pouta A, Hartikainen AL, Elliott P, Lindgren CM, Freathy RM, Koch K, Ouwehand WH, Karpe F, Conway GS, Wass JA, Järvelin MR, Franks S, McCarthy MIet al., 2008, Association of variants in the fat mass and obesity associated (FTO) gene with polycystic ovary syndrome, Diabetalogia, Vol: 51, Pages: 1153-1158

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Chambers JC, Zhang W, Zabaneh D, Balding D, McCarthy MI, Scott J, Elliott P, Kooner JSet al., 2008, Does genetic variation in FTO account for the increased risk of obesity and type 2 diabetes in UK Indian Asians?, Annual Scientific Conference of the British-Cardiovascular-Society/British-Society-for-Cardiovascular-Research, Publisher: B M J PUBLISHING GROUP, Pages: A58-A59, ISSN: 1355-6037

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Loos RJF, Lindgren CM, Li S, Wheeler E, Zhao JH, Prokopenko I, Inouye M, Freathy RM, Attwood AP, Beckmann JS, Berndt SI, Bergmann S, Bennett AJ, Bingham SA, Bochud M, Brown M, Cauchi S, Connell JM, Cooper C, Smith GD, Day I, Dina C, De S, Dermitzakis ET, Doney ASF, Elliott KS, Elliott P, Evans DM, Farooqi IS, Froguel P, Ghori J, Groves CJ, Gwilliam R, Hadley D, Hall AS, Hattersley AT, Hebebrand J, Heid IM, Herrera B, Hinney A, Hunt SE, Jarvelin M-R, Johnson T, Jolley JDM, Karpe F, Keniry A, Khaw K-T, Luben RN, Mangino M, Marchini J, McArdle WL, McGinnis R, Meyre D, Munroe PB, Morris AD, Ness AR, Neville MJ, Nica AC, Ong KK, O'Rahilly S, Owen KR, Palmer CNA, Papadakis K, Potter S, Pouta A, Qi L, Randall JC, Rayner NW, Ring SM, Sandhu MS, Scherag A, Sims MA, Song K, Soranzo N, Speliotes EK, Syddall HE, Teichmann SA, Timpson NJ, Tobias JH, Uda M, Vogel CIG, Wallace C, Waterworth DM, Weedon MN, Willer CJ, Wraight VL, Yuan X, Zeggini E, Hirschhorn JN, Strachan DP, Ouwehand WH, Caulfield MJ, Samani NJ, Frayling TM, Vollenweider P, Waeber G, Mooser V, Deloukas P, McCarthy MI, Wareham NJ, Barroso Iet al., 2008, Common variants near <i>MC4R</i> are associated with fat mass, weight and risk of obesity, NATURE GENETICS, Vol: 40, Pages: 768-775, ISSN: 1061-4036

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• Citations: 991

Chambers JC, Elliott P, Zabaneh D, Zhang W, Li Y, Froguel P, Balding D, Scott J, Kooner JSet al., 2008, Common genetic variation near <i>MC4R</i> is associated with waist circumference and insulin resistance, NATURE GENETICS, Vol: 40, Pages: 716-718, ISSN: 1061-4036

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• Citations: 382

Bouatia-Naji N, Rocheleau G, Van Lommel L, Lemaire K, Schuit F, Cavalcanti-Proenca C, Marchand M, Hartikainen A-L, Sovio U, De Graeve F, Rung J, Vaxillaire M, Tichet J, Marre M, Balkau B, Weill J, Elliott P, Jarvelin M-R, Meyre D, Polychronakos C, Dina C, Sladek R, Froguel Pet al., 2008, A polymorphism within the <i>G6PC2</i> gene is associated with fasting plasma glucose levels, SCIENCE, Vol: 320, Pages: 1085-1088, ISSN: 0036-8075

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• Citations: 190

Holmes E, Loo RL, Stamler J, Bictash M, Yap IKS, Chan Q, Ebbels T, De Iorio M, Brown IJ, Veselkov KA, Daviglus ML, Kesteloot H, Ueshima H, Zhao L, Nicholson JK, Elliott Pet al., 2008, Human metabolic phenotype diversity and its association with diet and blood pressure, NATURE, Vol: 453, Pages: 396-U50, ISSN: 0028-0836

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• Citations: 812

Freathy RM, Timpson NJ, Lawlor DA, Pouta A, Ben-Shlomo Y, Ruokonen A, Ebrahim S, Shields B, Zeggini E, Weedon MN, Lindgren CM, Lango H, Melzer D, Ferrucci L, Paolisso G, Neville MJ, Karpe F, Palmer CNA, Morris AD, Elliott P, Jarvelin M-R, Smith GD, McCarthy MI, Hattersley AT, Frayling TMet al., 2008, Common variation in the FTO gene alters diabetes-related metabolic traits to the extent expected given its effect on BMI, DIABETES, Vol: 57, Pages: 1419-1426, ISSN: 0012-1797

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• Citations: 248