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1دورية أكاديمية
المؤلفون: Stephens, SH, Hartz, SM, Hoft, NR, Saccone, NL, Corley, RC, Hewitt, JK, Hopfer, CJ, Breslau, N, Coon, H, Chen, XN, Ducci, F, Dueker, N, Franceschini, N, Frank, J, Han, YH, Hansel, NN, Jiang, CH, Korhonen, T, Lind, PA, Liu, J, Lyytikainen, LP, Michel, M, Shaffer, JR, Short, SE, Sun, JZ, Teumer, A, Thompson, JR, Vogelzangs, N, Vink, JM, Wenzlaff, A, Wheeler, W, Yang, BZ, Aggen, SH, Balmforth, AJ, Baumeister, SE, Beaty, TH, Benjamin, DJ, Bergen, AW, Broms, U, Cesarini, D, Chatterjee, N, Chen, JC, Cheng, YC, Cichon, S, Couper, D, Cucca, F, Dick, D, Foroud, T, Furberg, H, Giegling, I, Gillespie, NA, Gu, FY, Hall, AS, Haellfors, J, Han, S, Hartmann, AM, Heikkilae, K, Hickie, IB, Hottenga, JJ, Jousilahti, P, Kaakinen, M, Kaehoenen, M, Koellinger, PD, Kittner, S, Konte, B, Landi, MT, Laatikainen, T, Leppert, M, Levy, SM, Mathias, RA, McNeil, DW, Medland, SE, Montgomery, GW, Murray, T, Nauck, M, North, KE, Pare, PD, Pergadia, M, Ruczinski, I, Salomaa, V, Viikari, J, Willemsen, G, Barnes, KC, Boerwinkle, E, Boomsma, DI, Caporaso, N, Edenberg, HJ, Francks, C, Gelernter, J, Grabe, HJ, Hops, H, Jarvelin, MR, Johannesson, M, Kendler, KS, Lehtimaeki, T, Magnusson, PKE, Marazita, ML, Marchini, J, Mitchell, BD, Noethen, MM, Penninx, BW, Raitakari, O, Rietschel, M, Rujescu, D, Samani, NJ, Schwartz, AG, Shete, S, Spitz, M, Swan, GE, Volzke, H, Veijola, J, Wei, QY, Amos, C, Cannon, DS, Grucza, R, Hatsukami, D, Heath, A, Johnson, EO, Kaprio, J, Madden, P, Martin, NG, Stevens, VL, Weiss, RB, Kraft, P, Bierut, LJ, Ehringer, MA
المصدر: Genetic epidemiology. 37(8):846-859
مصطلحات موضوعية: Medicin och hälsovetenskap
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2دورية أكاديمية
المؤلفون: Liu C. -T., Merino J., Rybin D., DiCorpo D., Benke K. S., Bragg-Gresham J. L., Canouil M., Corre T., Grallert H., Isaacs A., Kutalik Z., Lahti J., Marullo L., Marzi C., Rasmussen-Torvik L. J., Rocheleau G., Rueedi R., Scapoli C., Verweij N., Vogelzangs N., Willems S. M., Yengo L., Bakker S. J. L., Beilby J., Hui J., Kajantie E., Muller-Nurasyid M., Rathmann W., Balkau B., Bergmann S., Eriksson J. G., Florez J. C., Froguel P., Harris T., Hung J., James A. L., Kavousi M., Miljkovic I., Musk A. W., Palmer L. J., Peters A., Roussel R., van der harst P., van Duijn C. M., Vollenweider P., Barroso I., Prokopenko I., Dupuis J., Meigs J. B., Bouatia-Naji N.
المساهمون: Liu, C. -T., Merino, J., Rybin, D., Dicorpo, D., Benke, K. S., Bragg-Gresham, J. L., Canouil, M., Corre, T., Grallert, H., Isaacs, A., Kutalik, Z., Lahti, J., Marullo, L., Marzi, C., Rasmussen-Torvik, L. J., Rocheleau, G., Rueedi, R., Scapoli, C., Verweij, N., Vogelzangs, N., Willems, S. M., Yengo, L., Bakker, S. J. L., Beilby, J., Hui, J., Kajantie, E., Muller-Nurasyid, M., Rathmann, W., Balkau, B., Bergmann, S., Eriksson, J. G., Florez, J. C., Froguel, P., Harris, T., Hung, J., James, A. L., Kavousi, M., Miljkovic, I., Musk, A. W., Palmer, L. J., Peters, A., Roussel, R., van der harst, P., van Duijn, C. M., Vollenweider, P., Barroso, I., Prokopenko, I., Dupuis, J., Meigs, J. B., Bouatia-Naji, N.
مصطلحات موضوعية: Medical genetics, Type 2 diabetes
الوصف: Type 2 diabetes (T2D) affects the health of millions of people worldwide. The identification of genetic determinants associated with changes in glycemia over time might illuminate biological features that precede the development of T2D. Here we conducted a genome-wide association study of longitudinal fasting glucose changes in up to 13,807 non-diabetic individuals of European descent from nine cohorts. Fasting glucose change over time was defined as the slope of the line defined by multiple fasting glucose measurements obtained over up to 14 years of observation. We tested for associations of genetic variants with inverse-normal transformed fasting glucose change over time adjusting for age at baseline, sex, and principal components of genetic variation. We found no genome-wide significant association (P < 5 × 10−8) with fasting glucose change over time. Seven loci previously associated with T2D, fasting glucose or HbA1c were nominally (P < 0.05) associated with fasting glucose change over time. Limited power influences unambiguous interpretation, but these data suggest that genetic effects on fasting glucose change over time are likely to be small. A public version of the data provides a genomic resource to combine with future studies to evaluate shared genetic links with T2D and other metabolic risk traits.
وصف الملف: STAMPA
العلاقة: info:eu-repo/semantics/altIdentifier/pmid/31263163; info:eu-repo/semantics/altIdentifier/wos/WOS:000473294100026; volume:9; issue:1; firstpage:9439-1; lastpage:9439-8; numberofpages:8; journal:SCIENTIFIC REPORTS; info:eu-repo/grantAgreement/EC/H2020/703787; http://hdl.handle.net/11392/2417434Test; info:eu-repo/semantics/altIdentifier/scopus/2-s2.0-85068203036; https://www.nature.com/articles/s41598-019-45823-7Test
الإتاحة: https://doi.org/10.1038/s41598-019-45823-7Test
http://hdl.handle.net/11392/2417434Test
https://www.nature.com/articles/s41598-019-45823-7Test -
3دورية أكاديمية
المؤلفون: Tofte, N. (Nete), Vogelzangs, N. (Nicole), Mook-Kanamori, D. (Dennis), Brahimaj, A. (Adela), Nano, J. (Jana), Ahmadizar, F. (Fariba), van Dijk, K.W. (Ko Willems), Frimodt-Møller, M. (Marie), Arts, I. (Ilja), Beulens, J.W.J. (Joline W J), Rutters, F. (Femke), Heijden, A.A.W.A. (Amber A. W.) van der, Kavousi, M. (Maryam), Stehouwer, C.D. (Coen), Nijpels, M.G.A.A.M. (Giel), van Greevenbroek, M.M.J. (Marleen M J), Kallen, C.J. van der, Rossing, K., Ahluwalia, T.S. (Tarunveer Singh), Hart, L.M. (Leen) 't
المصدر: Journal of Clinical Endocrinology and Metabolism vol. 105 no. 7
مصطلحات موضوعية: albuminuria, meta-analysis, metabolomics, NMR, renal function
الوصف: CONTEXT: There is a need for novel biomarkers and better understanding of the pathophysiology of diabetic kidney disease. OBJECTIVE: To investigate associations between plasma metabolites and kidney function in people with type 2 diabetes (T2D). DESIGN: 3089 samples from individuals with T2D, collected between 1999 and 2015, from 5 independent Dutch cohort studies were included. Up to 7 years follow-up was available in 1100 individuals from 2 of the cohorts. MAIN OUTCOME MEASURES: Plasma metabolites (n = 149) were measured by nuclear magnetic resonance spectroscopy. Associations between metabolites and estimated glomerular filtration rate (eGFR), urinary albumin-to-creatinine ratio (UACR), and eGFR slopes were investigated in each study followed by random effect meta-analysis. Adjustments included traditional cardiovascular risk factors and correction for multiple testing. RESULTS: In total, 125 metabolites were significantly associated (PFDR = 1.5×10-32 - 0.046; β = -11.98-2.17) with eGFR. Inverse associations with eGFR were demonstrated for branched-chain and aromatic amino acids (AAAs), glycoprotein acetyls, triglycerides (TGs), lipids in very low-density lipoproteins (VLDL) subclasses, and fatty acids (PFDR < 0.03). We observed positive associations with cholesterol and phospholipids in high-density lipoproteins (HDL) and apolipoprotein A1 (PFDR < 0.05). Albeit some metabolites were associated with UACR levels (P < 0.05), significance was lost after correction for multiple testing. Tyrosine and HDL-related metabolites were positively associated with eGFR slopes before adjustment for multiple testing (PTyr = 0.003; PHDLrelated < 0.05), but not after. CONCLUSIONS: This study identified metabolites associated with impaired kidney function in T2D, implying involvement of lipid and amino acid metabolism in the pathogenesis. Whether these processes precede or are consequences of renal impairment needs further investigation.
وصف الملف: application/pdf
العلاقة: http://repub.eur.nl/pub/127471Test; urn:hdl:1765/127471
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4دورية أكاديمية
المؤلفون: Bot, M, Milaneschi, Y, Al-Shehri, T, Amin, N, Garmaeva, S, Onderwater, GLJ, Pool, R, Thesing, CS, Vijfhuizen, LS, Vogelzangs, N, Arts, ICW, Demirkan, A, Van Duijn, C, Van Greevenbroek, M, Van der Kallen, CJH, Köhler, S, Ligthart, L, Van den Maagdenberg, AMJM, Mook-Kanamori, DO, De Mutsert, R, Tiemeier, H, Schram, MT, Stehouwer, CDA, Terwindt, GM, Willems van Dijk, K, Fu, J, Zhernakova, A, Beekman, M, Slagboom, PE, Boomsma, DI, Penninx, BWJH, BBMRI-NL Metabolomics Consortium
المصدر: Biological Psychiatry , 87 (5) pp. 409-418. (2020)
مصطلحات موضوعية: Biomarkers, Cardiovascular, Depression, Metabolites, Metabolomics, Pooled analysis
الوصف: BACKGROUND: Depression has been associated with metabolic alterations, which adversely impact cardiometabolic health. Here, a comprehensive set of metabolic markers, predominantly lipids, was compared between depressed and nondepressed persons. METHODS: Nine Dutch cohorts were included, comprising 10,145 control subjects and 5283 persons with depression, established with diagnostic interviews or questionnaires. A proton nuclear magnetic resonance metabolomics platform provided 230 metabolite measures: 51 lipids, fatty acids, and low-molecular-weight metabolites; 98 lipid composition and particle concentration measures of lipoprotein subclasses; and 81 lipid and fatty acids ratios. For each metabolite measure, logistic regression analyses adjusted for gender, age, smoking, fasting status, and lipid-modifying medication were performed within cohort, followed by random-effects meta-analyses. RESULTS: Of the 51 lipids, fatty acids, and low-molecular-weight metabolites, 21 were significantly related to depression (false discovery rate q < .05). Higher levels of apolipoprotein B, very-low-density lipoprotein cholesterol, triglycerides, diglycerides, total and monounsaturated fatty acids, fatty acid chain length, glycoprotein acetyls, tyrosine, and isoleucine and lower levels of high-density lipoprotein cholesterol, acetate, and apolipoprotein A1 were associated with increased odds of depression. Analyses of lipid composition indicators confirmed a shift toward less high-density lipoprotein and more very-low-density lipoprotein and triglyceride particles in depression. Associations appeared generally consistent across gender, age, and body mass index strata and across cohorts with depressive diagnoses versus symptoms. CONCLUSIONS: This large-scale meta-analysis indicates a clear distinctive profile of circulating lipid metabolites associated with depression, potentially opening new prevention or treatment avenues for depression and its associated cardiometabolic comorbidity.
وصف الملف: text
العلاقة: https://discovery.ucl.ac.uk/id/eprint/10106134/3/Asselbergs_Manuscript_BBMRImetab_dep_R4_v_clean.pdfTest; https://discovery.ucl.ac.uk/id/eprint/10106134Test/
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5دورية أكاديمية
المؤلفون: Generaal, E., Vogelzangs, N., Macfarlane, G.J., Geenen, R., Smit, J.H., de Geus, E.J.C.N., Dekker, J., Penninx, B.W.J.H.
المساهمون: Leerstoel Geenen, Stress and self-regulation
مصطلحات موضوعية: Chronic pain, cortisol, inflammation, autonomic nervous system, life change events, Taverne
الوصف: Dysfunction of biological stress systems and adverse life events, independently and in interaction, have been hypothesized to predict chronic pain persistence. Conversely, these factors may hamper the improvement of chronic pain. Longitudinal evidence is currently lacking. We examined whether: 1) function of biological stress systems, 2) adverse life events, and 3) their combination predict the improvement of chronic multisite musculoskeletal pain. Subjects of the Netherlands Study of Depression and Anxiety (NESDA) with chronic multisite musculoskeletal pain at baseline (N = 665) were followed-up 2, 4, and 6 years later. The Chronic Pain Grade Questionnaire was used to determine improvement (not meeting the criteria) of chronic multisite musculoskeletal pain at follow-up. Baseline assessment of biological stress systems included function of hypothalamic-pituitary-adrenal axis (1-hour cortisol awakening response, evening level, and post dexamethasone level), the immune system (basal and lipopolysaccharide-stimulated inflammatory markers), the autonomic nervous system (heart rate, pre-ejection period, SD of the normal-to-normal interval, and respiratory sinus arrhythmia). The number of adverse life events were assessed at baseline and 2-year follow-up using the List of Threatening Events Questionnaire. We showed that hypothalamic-pituitary-adrenal axis, immune system, and autonomic nervous system functioning and adverse life events were not associated with the improvement of chronic multisite musculoskeletal pain, either as a main effect or in interaction. This longitudinal study could not confirm that biological stress system dysfunction and adverse life events affect the course of chronic multisite musculoskeletal pain.
وصف الملف: application/pdf
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6دورية أكاديمية
المؤلفون: Dupuis, J, Langenberg, C, Prokopenko, I, Saxena, R, Soranzo, N, Jackson, AU, Wheeler, E, Glazer, NL, Bouatia-Naji, N, Gloyn, AL, Lindgren, CM, Magi, R, Morris, AP, Randall, J, Johnson, T, Elliott, P, Rybin, D, Thorleifsson, G, Steinthorsdottir, V, Henneman, P, Grallert, H, Dehghan, A, Hottenga, JJ, Franklin, CS, Navarro, P, Song, K, Goel, A, Perry, JRB, Egan, JM, Lajunen, T, Grarup, N, Sparso, T, Doney, A, Voight, BF, Stringham, HM, Li, M, Kanoni, S, Shrader, P, Cavalcanti-Proenca, C, Kumari, M, Qi, L, Timpson, NJ, Gieger, C, Zabena, C, Rocheleau, G, Ingelsson, E, An, P, O'Connell, J, Luan, J, Elliott, A, McCarroll, SA, Payne, F, Roccasecca, RM, Pattou, F, Sethupathy, P, Ardlie, K, Ariyurek, Y, Balkau, B, Barter, P, Beilby, JP, Ben-Shlomo, Y, Benediktsson, R, Bennett, AJ, Bergmann, S, Bochud, M, Boerwinkle, E, Bonnefond, A, Bonnycastle, LL, Borch-Johnsen, K, Bottcher, Y, Brunner, E, Bumpstead, SJ, Charpentier, G, Chen, YDI, Chines, P, Clarke, R, Coin, LJM, Cooper, MN, Cornelis, M, Crawford, G, Crisponi, L, Day, INM, de Geus, EJC, Delplanque, J, Dina, C, Erdos, MR, Fedson, AC, Fischer-Rosinsky, A, Forouhi, NG, Fox, CS, Frants, R, Franzosi, MG, Galan, P, Goodarzi, MO, Graessler, J, Groves, CJ, Grundy, S, Gwilliam, R, Gyllensten, U, Hadjadj, S, Hallmans, G, Hammond, N, Han, XJ, Hartikainen, AL, Hassanali, N, Hayward, C, Heath, SC, Hercberg, S, Herder, C, Hicks, AA, Hillman, DR, Hingorani, AD, Hofman, A, Hui, J, Hung, J, Isomaa, B, Johnson, PRV, Jorgensen, T, Jula, A, Kaakinen, M, Kaprio, J, Kesaniemi, YA, Kivimaki, M, Knight, B, Koskinen, S, Kovacs, P, Kyvik, KO, Lathrop, GM, Lawlor, DA, Le Bacquer, O, Lecoeur, C, Li, Y, Lyssenko, V, Mahley, R, Mangino, M, Manning, AK, Martinez-Larrad, MT, McAteer, JB, McCulloch, LJ, McPherson, R, Meisinger, C, Melzer, D, Meyre, D, Mitchell, BD, Morken, MA, Mukherjee, S, Naitza, S, Narisu, N, Neville, MJ, Oostra, BA, Orru, M, Pakyz, R, Palmer, CNA, Paolisso, G, Pattaro, C, Pearson, D, Peden, JF, Pedersen, NL, Perola, M, Pfeiffer, AFH, Pichler, I, Polasek, O, Posthuma, D, Potter, SC, Pouta, A, Province, MA, Psaty, BM, Rathmann, W, Rayner, NW, Rice, K, Ripatti, S, Rivadeneira, F, Roden, M, Rolandsson, O, Sandbaek, A, Sandhu, M, Sanna, S, Sayer, AA, Scheet, P, Scott, LJ, Seedorf, U, Sharp, SJ, Shields, B, Sigurosson, G, Sijbrands, EJG, Silveira, A, Simpson, L, Singleton, A, Smith, NL, Sovio, U, Swift, A, Syddall, H, Syvanen, AC, Tanaka, T, Thorand, B, Tichet, J, Tonjes, A, Tuomi, T, Uitterlinden, AG, van Dijk, KW, van Hoek, M, Varma, D, Visvikis-Siest, S, Vitart, V, Vogelzangs, N, Waeber, G, Wagner, PJ, Walley, A, Walters, GB, Ward, KL, Watkins, H, Weedon, MN, Wild, SH, Willemsen, G, Witteman, JCM, Yarnell, JWG, Zeggini, E, Zelenika, D, Zethelius, B, Zhai, GJ, Zhao, JH, Zillikens, MC, Borecki, IB, Loos, RJF, Meneton, P, Magnusson, PKE, Nathan, DM, Williams, GH, Hattersley, AT, Silander, K, Salomaa, V, Smith, GD, Bornstein, SR, Schwarz, P, Spranger, J, Karpe, F, Shuldiner, AR, Cooper, C, Dedoussis, GV, Serrano-Rios, M, Morris, AD, Lind, L, Palmer, LJ, Hu, FB, Franks, PW, Ebrahim, S, Marmot, M, Kao, WHL, Pankow, JS, Sampson, MJ, Kuusisto, J, Laakso, M, Hansen, T, Pedersen, O, Pramstaller, PP, Wichmann, HE, Illig, T, Rudan, I, Wright, AF, Stumvoll, M, Campbell, H, Wilson, JF, Bergman, RN, Buchanan, TA, Collins, FS, Mohlke, KL, Tuomilehto, J, Valle, TT, Altshuler, D, Rotter, JI, Siscovick, DS, Penninx, BWJH, Boomsma, DI, Deloukas, P, Spector, TD, Frayling, TM, Ferrucci, L, Kong, A, Thorsteinsdottir, U, Stefansson, K, van Duijn, CM, Aulchenko, YS, Cao, A, Scuteri, A, Schlessinger, D, Uda, M, Ruokonen, A, Jarvelin, MR, Waterworth, DM, Vollenweider, P, Peltonen, L, Mooser, V, Abecasis, GR, Wareham, NJ, Sladek, R, Froguel, P, Watanabe, RM, Meigs, JB, Groop, L, Boehnke, M, McCarthy, MI, Florez, JC, Barroso, I
المصدر: Nature genetics. 42(2):105-U32
مصطلحات موضوعية: Medicin och hälsovetenskap
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7دورية أكاديمية
المؤلفون: Generaal, E., Vogelzangs, N., MacFarlane, G.J., Geenen, R., Smit, J.H., de Geus, E.J.C.N., Penninx, B.W.J.H., Dekker, J.
المساهمون: Stress and self-regulation, Leerstoel Geenen
مصطلحات موضوعية: Taverne
الوصف: Objectives Dysregulated biological stress systems and adverse life events, independently and in interaction, have been hypothesised to initiate chronic pain. We examine whether (1) function of biological stress systems, (2) adverse life events, and (3) their combination predict the onset of chronic multisite musculoskeletal pain. Methods Subjects (n=2039) of the Netherlands Study of Depression and Anxiety, free from chronic multisite musculoskeletal pain at baseline, were identified using the Chronic Pain Grade Questionnaire and followed up for the onset of chronic multisite musculoskeletal pain over 6 years. Baseline assessment of biological stress systems comprised function of the hypothalamic-pituitary-adrenal axis (1-h cortisol awakening response, evening levels, postdexamethasone levels), the immune system (basal and lipopolysaccharide-stimulated inflammation) and the autonomic nervous system (heart rate, pre-ejection period, SD of the normal-to-normal interval, respiratory sinus arrhythmia). The number of recent adverse life events was assessed at baseline using the List of Threatening Events Questionnaire. Results Hypothalamic-pituitary-adrenal axis, immune system and autonomic nervous system functioning was not associated with onset of chronic multisite musculoskeletal pain, either by itself or in interaction with adverse life events. Adverse life events did predict onset of chronic multisite musculoskeletal pain (HR per event=1.14, 95% CI 1.04 to 1.24, p=0.005). Conclusions This longitudinal study could not confirm that dysregulated biological stress systems increase the risk of developing chronic multisite musculoskeletal pain. Adverse life events were a risk factor for the onset of chronic multisite musculoskeletal pain, suggesting that psychosocial factors play a role in triggering the development of this condition.
وصف الملف: application/pdf
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8دورية أكاديمية
المؤلفون: Vogelzangs, N, de Jonge, P, Smit, J H, Bahn, S, Penninx, B W
المصدر: Vogelzangs , N , de Jonge , P , Smit , J H , Bahn , S & Penninx , B W 2016 , ' Cytokine production capacity in depression and anxiety ' , Translational Psychiatry , vol. 6 , no. 5 , 825 , pp. e825 . https://doi.org/10.1038/tp.2016.92Test
مصطلحات موضوعية: CORONARY-HEART-DISEASE, COMORBIDITY SURVEY REPLICATION, C-REACTIVE PROTEIN, DSM-IV DISORDERS, PSYCHOMETRIC PROPERTIES, DIFFERENTIAL ASSOCIATION, GENERAL-POPULATION, BIPOLAR DISORDER, MAJOR DEPRESSION, INFLAMMATION
الوصف: Recent studies have suggested that immune function may be dysregulated in persons with depressive and anxiety disorders. Few studies examined the expression of cytokines in response to ex vivo stimulation of blood by lipopolysaccharide (LPS) to study the innate production capacity of cytokines in depression and anxiety. To investigate this, baseline data from the Netherlands Study of Depression and Anxiety (NESDA) were used, including persons (18-65 years; 66% women) with current (that is, past month; N=591) or remitted (N=354) DSM-IV depressive or anxiety disorders and healthy controls (N=297). Depressive and anxiety symptoms were measured by means of the Inventory of Depressive Symptomatology (IDS) and the Beck Anxiety Inventory (BAI). Using Multi-Analyte Profiling technology, plasma levels of 13 cytokines were assayed after whole blood stimulation by addition of LPS. Basal plasma levels of C-reactive protein, interleukin-6 and tumor necrosis factor-α were also available. A basal and a LPS summary index were created. Results show that LPS-stimulated inflammation was associated with increased odds of current depressive/anxiety disorders (odds ratio (OR)=1.28, P=0.009), as was the case for basal inflammation (OR=1.28, P=0.001). These associations were no longer significant after adjustment for lifestyle and health (OR=1.13, P=0.21; OR=1.07, P=0.45, respectively). After adjustment for lifestyle and health, interleukin-8 was associated with both remitted (OR=1.25, P=0.02) and current (OR=1.28, P=0.005) disorders. In addition, LPS-stimulated inflammation was associated with more severe depressive (β=0.129, P<0.001) and anxiety (β=0.165, P<0.001) symptoms, as was basal inflammation. Unlike basal inflammation, LPS-stimulated inflammation was still associated with (anxiety) symptom severity after adjustment for lifestyle and health (IDS: interleukin (IL)-8, MCP-1, MMP2; BAI: LPS index, IL-6, IL-8, IL-10, IL-18, MCP-1, MMP2, TNF-β). To conclude, lifestyle and health factors may partly explain higher levels of ...
الإتاحة: https://doi.org/10.1038/tp.2016.92Test
https://cris.maastrichtuniversity.nl/en/publications/5d52faab-4c57-4af2-a44f-6f1c6aa17857Test -
9دورية أكاديمية
المؤلفون: Palmer, N, McDonough, C, Hicks, P, Roh, B, Wing, MR, An, S, Hester, J, Cooke, J, Bostrom, M, Rudock, M, Talbert, M, Lewis, J, Ferrara, A, Lu, L, Ziegler, J, Sale, M, Divers, J, Shriner, D, Adeyemo, A, Rotimi, C, Ng, M, Langefeld, C, Freedman, B, Bowden, D, Voight, B, Scott, L, Steinthorsdottir, V, Morris, A, Dina, C, Welch, R, Zeggini, E, Huth, C, Aulchenko, Y, Thorleifsson, G, McCulloch, L, Ferreira, T, Grallert, H, Amin, N, Wu, G, Willer, C, Raychaudhuri, S, McCarroll, SA, Langenberg, C, Hofmann, O, Dupuis, J, Qi, L, Segre, A, van Hoek, M, Navarro, P, Ardlie, K, Balkau, B, Benediktsson, R, Bennett, A, Blagieva, R, Boerwinkle, E, Bonnycastle, L, Bostrom, K, Bravenboer, B, Bumpstead, S, Burtt, N, Charpentier, G, Chines, P, Cornelis, M, Couper, D, Crawford, G, Doney, A, Elliott, K, Elliott, A, Erdos, MR, Fox, C, Franklin, C, Ganser, M, Gieger, C, Grarup, N, Green, T, Griffin, S, Groves, C, Guiducci, C, Hadjadj, S, Hassanali, N, Herder, C, Isomaa, B, Jackson, A, Johnson, P, Jorgensen, T, Kao, W, Klopp, N, Kong, A, Kraft, P, Kuusisto, J, Lauritzen, T, Li, M, Lieverse, A, Lindgren, C, Lyssenko, V, Marre, M, Meitinger, T, Midthjell, K, Morken, M, Narisu, N, Nilsson, P, Owen, K, Payne, F, Perry, JR, Petersen, A, Platou, C, Proenca, C, Prokopenko, I, Rathmann, W, Rayner, N, Robertson, N, Rocheleau, G, Roden, M, Sampson, M, Saxena, R, Shields, B, Shrader, P, Sigurdsson, G, Sparso, T, Strassburger, K, Stringham, H, Sun, Q, Swift, A, Thorand, B, Tichet, J, Tuomi, T, van Dam, R, van Haeften, T, van Herpt, T, van Vliet-Ostaptchouk, J, Walters, G, Weedon, M, Wijmenga, C, Witteman, J, Bergman, R, Cauchi, S, Collins, F, Gloyn, A, Gyllensten, U, Hansen, T, Hide, W, Hitman, G, Hofman, A, Hunter, D, Hveem, K, Laakso, M, Mohlke, K, Palmer, C, Pramstaller, P, Rudan, I, Sijbrands, E, Stein, L, Tuomilehto, J, Uitterlinden, A, Walker, M, Wareham, N, Watanabe, R, Abecasis, G, Boehm, B, Campbell, H, Daly, M, Hattersley, A, Hu, F, Meigs, J, Pankow, J, Pedersen, O, Wichmann, H, Barroso, I, Florez, J, Frayling, T, Groop, L, Sladek, R, Thorsteinsdottir, U, Wilson, J, Illig, T, Froguel, P, van Duijn, C, Stefansson, K, Altshuler, D, Boehnke, M, McCarthy, M, Soranzo, N, Wheeler, E, Glazer, N, Bouatia-Naji, N, Magi, R, Randall, J, Johnson, T, Elliott, P, Rybin, D, Henneman, P, Dehghan, A, Hottenga, J, Song, K, Goel, A, Egan, J, Lajunen, T, Kanoni, S, Cavalcanti-Proenca, C, Kumari, M, Timpson, N, Zabena, C, Ingelsson, E, An, P, O'Connell, J, Luan, J, Roccasecca, R, Pattou, F, Sethupathy, P, Ariyurek, Y, Barter, P, Beilby, J, Ben-Shlomo, Y, Bergmann, S, Bochud, M, Bonnefond, A, Borch-Johnsen, K, Bottcher, Y, Brunner, E, Chen, Y, Clarke, R, Coin, L, Cooper, M, Crisponi, L, Day, I, de Geus, E, Delplanque, J, Fedson, A, Fischer-Rosinsky, A, Forouhi, N, Frants, R, Franzosi, MG, Galan, P, Goodarzi, M, Graessler, J, Grundy, S, Gwilliam, R, Hallmans, G, Hammond, N, Han, X, Hartikainen, A, Hayward, C, Heath, S, Hercberg, S, Hicks, A, Hillman, DR, Hingorani, A, Hui, J, Hung, J, Jula, A, Kaakinen, M, Kaprio, J, Kesaniemi, Y, Kivimaki, M, Knight, B, Koskinen, S, Kovacs, P, Kyvik, K, Lathrop, G, Lawlor, D, Le Bacquer, O, Lecoeur, C, Li, Y, Mahley, R, Mangino, M, Manning, A, Martinez-Larrad, M, McAteer, J, McPherson, R, Meisinger, C, Melzer, D, Meyre, D, Mitchell, B, Mukherjee, S, Naitza, S, Neville, M, Oostra, B, Orru, M, Pakyz, R, Paolisso, G, Pattaro, C, Pearson, D, Peden, J, Pedersen, N, Perola, M, Pfeiffer, A, Pichler, I, Polasek, O, Posthuma, D, Potter, S, Pouta, A, Province, M, Psaty, B, Rice, K, Ripatti, S, Rivadeneira, F, Rolandsson, O, Sandbaek, A, Sandhu, M, Sanna, S, Sayer, A, Scheet, P, Seedorf, U, Sharp, S, Silveira, A, Simpson, L, Singleton, A, Smith, N, Sovio, U, Syddall, H, Syvanen, A, Tanaka, T, Tonjes, A, van Dijk, K, Varma, D, Visvikis-Siest, S, Vitart, V, Vogelzangs, N, Waeber, G, Wagner, P, Walley, A, Ward, K, Watkins, H, Wild, S, Willemsen, G, Yarnell, J, Zelenika, D, Zethelius, B, Zhai, G, Zhao, J, Zillikens, M, Borecki, I, Loos, R, Meneton, P, Magnusson, P, Nathan, D, Williams, G, Silander, K, Salomaa, V, Smith, G, Bornstein, SR, Schwarz, P, Spranger, J, Karpe, F, Shuldiner, A, Cooper, C, Dedoussis, G, Serrano-Rios, M, Lind, L, Palmer, L, Franks, P, Ebrahim, S, Marmot, M, Wright, A, Stumvoll, M, Hamsten, A, Buchanan, T, Valle, T, Rotter, J, Siscovick, D, Penninx, B, Boomsma, D, Deloukas, P, Spector, T, Ferrucci, L, Cao, A, Scuteri, A, Schlessinger, D, Uda, M, Ruokonen, A, Jarvelin, MR, Waterworth, D, Vollenweider, P, Peltonen, L, Mooser, V
الوصف: African Americans are disproportionately affected by type 2 diabetes (T2DM) yet few studies have examined T2DM using genome-wide association approaches in this ethnicity. The aim of this study was to identify genes associated with T2DM in the African American population. We performed a Genome Wide Association Study (GWAS) using the Affymetrix 6.0 array in 965 African-American cases with T2DM and end-stage renal disease (T2DM-ESRD) and 1029 population-based controls. The most significant SNPs (n=550 independent loci) were genotyped in a replication cohort and 122 SNPs (n=98 independent loci) were further tested through genotyping three additional validation cohorts followed by meta-analysis in all five cohorts totaling 3,132 cases and 3,317 controls. Twelve SNPs had evidence of association in the GWAS (P<0.0071), were directionally consistent in the Replication cohort and were associated with T2DM in subjects without nephropathy (P<0.05). Meta-analysis in all cases and controls revealed a single SNP reaching genome-wide significance (P<2.5x10(-8)). SNP rs7560163 (P=7.0x10(-9), OR (95% CI)=0.75 (0.67-0.84)) is located intergenically between RND3 and RBM43. Four additional loci (rs7542900, rs4659485, rs2722769 and rs7107217) were associated with T2DM (P<0.05) and reached more nominal levels of significance (P<2.5x10(-5)) in the overall analysis and may represent novel loci that contribute to T2DM. We have identified novel T2DM-susceptibility variants in the African-American population. Notably, T2DM risk was associated with the major allele and implies an interesting genetic architecture in this population. These results suggest that multiple loci underlie T2DM susceptibility in the African-American population and that these loci are distinct from those identified in other ethnic populations.
العلاقة: https://ora.ox.ac.uk/objects/uuid:d2ac5e39-ffb6-4d76-b93f-ff4690682998Test; https://doi.org/10.1371/journal.pone.0029202Test
الإتاحة: https://doi.org/10.1371/journal.pone.0029202Test
https://ora.ox.ac.uk/objects/uuid:d2ac5e39-ffb6-4d76-b93f-ff4690682998Test -
10دورية أكاديمية
المؤلفون: Dastani, Z, Hivert, M, Timpson, N, Perry, JR, Yuan, X, Scott, R, Henneman, P, Heid, I, Kizer, JR, Lyytikainen, L, Fuchsberger, C, Tanaka, T, Morris, A, Small, K, Isaacs, A, Beekman, M, Coassin, S, Lohman, K, Qi, L, Kanoni, S, Pankow, J, Uh, H, Wu, Y, Bidulescu, A, Rasmussen-Torvik, L, Greenwood, C, Ladouceur, M, Grimsby, J, Manning, A, Liu, C, Kooner, J, Mooser, V, Vollenweider, P, Kapur, K, Chambers, J, Wareham, N, Langenberg, C, Frants, R, Willems-Vandijk, K, Oostra, B, Willems, S, Lamina, C, Winkler, T, Psaty, B, Tracy, R, Brody, J, Chen, I, Viikari, J, Kahonen, M, Pramstaller, P, Evans, D, St Pourcain, B, Sattar, N, Wood, A, Bandinelli, S, Carlson, O, Egan, J, Bohringer, S, van Heemst, D, Kedenko, L, Kristiansson, K, Nuotio, M, Loo, B, Harris, T, Garcia, M, Kanaya, A, Haun, M, Klopp, N, Wichmann, H, Deloukas, P, Katsareli, E, Couper, D, Duncan, B, Kloppenburg, M, Adair, L, Borja, J, Wilson, J, Musani, S, Guo, X, Johnson, T, Semple, R, Teslovich, T, Allison, M, Redline, S, Buxbaum, S, Mohlke, K, Meulenbelt, I, Ballantyne, C, Dedoussis, G, Hu, F, Liu, Y, Paulweber, B, Spector, T, Slagboom, P, Ferrucci, L, Jula, A, Perola, M, Raitakari, O, Florez, J, Salomaa, V, Eriksson, J, Frayling, T, Hicks, A, Lehtimaki, T, Smith, G, Siscovick, D, Kronenberg, F, van Duijn, C, Loos, R, Waterworth, D, Meigs, J, Dupuis, J, Richards, J, Voight, B, Scott, L, Steinthorsdottir, V, Dina, C, Welch, R, Zeggini, E, Huth, C, Aulchenko, Y, Thorleifsson, G, McCulloch, L, Ferreira, T, Grallert, H, Amin, N, Wu, G, Willer, C, Raychaudhuri, S, McCarroll, SA, Hofmann, O, Segre, A, van Hoek, M, Navarro, P, Ardlie, K, Balkau, B, Benediktsson, R, Bennett, A, Blagieva, R, Boerwinkle, E, Bonnycastle, L, Bostrom, K, Bravenboer, B, Bumpstead, S, Burtt, N, Charpentier, G, Chines, P, Cornelis, M, Crawford, G, Doney, A, Elliott, K, Elliott, A, Erdos, MR, Fox, C, Franklin, C, Ganser, M, Gieger, C, Grarup, N, Green, T, Griffin, S, Groves, C, Guiducci, C, Hadjadj, S, Hassanali, N, Herder, C, Isomaa, B, Jackson, A, Johnson, P, Jorgensen, T, Kao, W, Kong, A, Kraft, P, Kuusisto, J, Lauritzen, T, Li, M, Lieverse, A, Lindgren, C, Lyssenko, V, Marre, M, Meitinger, T, Midthjell, K, Morken, M, Narisu, N, Nilsson, P, Owen, K, Payne, F, Petersen, A, Platou, C, Proenca, C, Prokopenko, I, Rathmann, W, Rayner, N, Robertson, N, Rocheleau, G, Roden, M, Sampson, M, Saxena, R, Shields, B, Shrader, P, Sigurosson, G, Sparso, T, Strassburger, K, Stringham, H, Sun, Q, Swift, A, Thorand, B, Tichet, J, Tuomi, T, van Dam, R, van Haeften, T, van Herpt, T, van Vliet-Ostaptchouk, J, Walters, G, Weedon, M, Wijmenga, C, Witteman, J, Bergman, R, Cauchi, S, Collins, F, Gloyn, A, Gyllensten, U, Hansen, T, Hide, W, Hitman, G, Hofman, A, Hunter, D, Hveem, K, Laakso, M, Palmer, C, Rudan, I, Sijbrands, E, Stein, L, Tuomilehto, J, Uitterlinden, A, Walker, M, Watanabe, R, Abecasis, G, Boehm, B, Campbell, H, Daly, M, Hattersley, A, Pedersen, O, Barroso, I, Groop, L, Sladek, R, Thorsteinsdottir, U, Illig, T, Froguel, P, Stefansson, K, Altshuler, D, Boehnke, M, McCarthy, M, Soranzo, N, Wheeler, E, Glazer, N, Bouatia-Naji, N, Magi, R, Randall, J, Elliott, P, Rybin, D, Dehghan, A, Hottenga, J, Song, K, Goel, A, Lajunen, T, Cavalcanti-Proenca, C, Kumari, M, Zabena, C, Ingelsson, E, An, P, Oandapos, Connell, J, Luan, J, Roccasecca, R, Pattou, F, Sethupathy, P, Ariyurek, Y, Barter, P, Beilby, J, Ben-Shlomo, Y, Bergmann, S, Bochud, M, Bonnefond, A, Borch-Johnsen, K, Bottcher, Y, Brunner, E, Chen, Y, Clarke, R, Coin, L, Cooper, M, Crisponi, L, Day, I, de Geus, E, Delplanque, J, Fedson, A, Fischer-Rosinsky, A, Forouhi, N, Franzosi, MG, Galan, P, Goodarzi, M, Graessler, J, Grundy, S, Gwilliam, R, Hallmans, G, Hammond, N, Han, X, Hartikainen, A, Hayward, C, Heath, S, Hercberg, S, Hillman, DR, Hingorani, A, Hui, J, Hung, J, Kaakinen, M, Kaprio, J, Kesaniemi, Y, Kivimaki, M, Knight, B, Koskinen, S, Kovacs, P, Kyvik, K, Lathrop, G, Lawlor, D, Le Bacquer, O, Lecoeur, C, Li, Y, Mahley, R, Mangino, M, Martinez-Larrad, M, McAteer, J, McPherson, R, Meisinger, C, Melzer, D, Meyre, D, Mitchell, B, Mukherjee, S, Naitza, S, Neville, M, Orru, M, Pakyz, R, Paolisso, G, Pattaro, C, Pearson, D, Peden, J, Pedersen, N, Pfeiffer, A, Pichler, I, Polasek, O, Posthuma, D, Potter, S, Pouta, A, Province, M, Rice, K, Ripatti, S, Rivadeneira, F, Rolandsson, O, Sandbaek, A, Sandhu, M, Sanna, S, Sayer, A, Scheet, P, Seedorf, U, Sharp, S, Sigurðsson, G, Silveira, A, Simpson, L, Singleton, A, Smith, N, Sovio, U, Syddall, H, Syvanen, A, Tonjes, A, van Dijk, K, Varma, D, Visvikis-Siest, S, Vitart, V, Vogelzangs, N, Waeber, G, Wagner, P, Walley, A, Ward, K, Watkins, H, Wild, S, Willemsen, G, Yarnell, J, Zelenika, D, Zethelius, B, Zhai, G, Zhao, J, Zillikens, M, Borecki, I, Meneton, P, Magnusson, P, Nathan, D, Williams, G, Silander, K, Bornstein, SR, Schwarz, P, Spranger, J, Karpe, F, Shuldiner, A, Cooper, C, Serrano-Rios, M, Lind, L, Palmer, L, Franks, P, Ebrahim, S, Marmot, M, Wright, A, Stumvoll, M, Hamsten, A, Buchanan, T, Valle, T, Rotter, J, Penninx, B, Boomsma, D, Cao, A, Scuteri, A, Schlessinger, D, Uda, M, Ruokonen, A, Jarvelin, MR, Peltonen, L, Musunuru, K, Smith, A, Edmondson, A, Stylianou, I, Koseki, M, Pirruccello, J, Chasman, D, Johansen, C, Fouchier, S, Peloso, G, Barbalic, M, Ricketts, S, Bis, J, Feitosa, M, Orho-Melander, M, Melander, O, Li, X, Cho, Y, Go, M, Kim, Y, Lee, J, Park, T, Kim, K, Sim, X, Ong, RT, Croteau-Chonka, D, Lange, L, Smith, J, Ziegler, A, Zhang, W, Zee, R, Whitfield, J, Thompson, JR, Surakka, I, Smit, J, Sinisalo, J, Scott, J, Saharinen, J, Sabatti, C, Rose, L, Roberts, R, Rieder, M, Parker, A, Pare, G, Donnell, C, Nieminen, MS, Nickerson, D, Montgomery, G, McArdle, W, Masson, D, Martin, N, Marroni, F, Lucas, G, Luben, R, Lokki, M, Lettre, G, Launer, L, Lakatta, E, Laaksonen, R, Konig, I, Khaw, K, Kaplan, L, Johansson, A, Janssens, A, Igl, W, Hovingh, G, Hengstenberg, C, Havulinna, A, Hastie, N, Haritunians, T, Hall, A, Gonzalez, E, Freimer, N, Erdmann, J, Ejebe, K, Doring, A, Dominiczak, A, Demissie, S, de Faire, U, Caulfield, M, Boekholdt, S, Assimes, T, Quertermous, T, Seielstad, M, Wong, T, Tai, E, Feranil, AB, Kuzawa, C, Taylor, H, Gabriel, S, Holm, H, Gudnason, V, Krauss, R, Ordovas, J, Munroe, P, Tall, A, Hegele, R, Kastelein, J, Schadt, E, Strachan, D, Reilly, M, Samani, N, Schunkert, H, Cupples, L, Sandhu, MS, Ridker, P, Rader, D, Kathiresan, S
الوصف: Circulating levels of adiponectin, a hormone produced predominantly by adipocytes, are highly heritable and are inversely associated with type 2 diabetes mellitus (T2D) and other metabolic traits. We conducted a meta-analysis of genome-wide association studies in 39,883 individuals of European ancestry to identify genes associated with metabolic disease. We identified 8 novel loci associated with adiponectin levels and confirmed 2 previously reported loci (P=4.5x10(-8)-1.2x10(-43)). Using a novel method to combine data across ethnicities (N=4,232 African Americans, N=1,776 Asians, and N=29,347 Europeans), we identified two additional novel loci. Expression analyses of 436 human adipocyte samples revealed that mRNA levels of 18 genes at candidate regions were associated with adiponectin concentrations after accounting for multiple testing (pandlt;3x10(-4)). We next developed a multi-SNP genotypic risk score to test the association of adiponectin decreasing risk alleles on metabolic traits and diseases using consortia-level meta-analytic data. This risk score was associated with increased risk of T2D (p=4.3x10(-3), n=22,044), increased triglycerides (p=2.6x10(-14), n=93,440), increased waist-to-hip ratio (p=1.8x10(-5), n=77,167), increased glucose two hours post oral glucose tolerance testing (p=4.4x10(-3), n=15,234), increased fasting insulin (p=0.015, n=48,238), but with lower in HDL-cholesterol concentrations (p=4.5x10(-13), n=96,748) and decreased BMI (p=1.4x10(-4), n=121,335). These findings identify novel genetic determinants of adiponectin levels, which, taken together, influence risk of T2D and markers of insulin resistance.
العلاقة: https://ora.ox.ac.uk/objects/uuid:91016d81-3803-4c00-aa5c-1a3e43c054deTest; https://doi.org/10.1371/journal.pgen.1002607Test
الإتاحة: https://doi.org/10.1371/journal.pgen.1002607Test
https://ora.ox.ac.uk/objects/uuid:91016d81-3803-4c00-aa5c-1a3e43c054deTest
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