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5. Disentangling the genetics of lean mass.

Author

Karasik, David, Zillikens, M Carola, Hsu, Yi-Hsiang, Aghdassi, Ali, Akesson, Kristina, Amin, Najaf, Barroso, Inês, Bennett, David A, Bertram, Lars, Bochud, Murielle, Borecki, Ingrid B, Broer, Linda, Buchman, Aron S, Byberg, Liisa, Campbell, Harry, Campos-Obando, Natalia, Cauley, Jane A, Cawthon, Peggy M, Chambers, John C, Chen, Zhao, Cho, Nam H, Choi, Hyung Jin, Chou, Wen-Chi, Cummings, Steven R, de Groot, Lisette CPGM, De Jager, Phillip L, Demuth, Ilja, Diatchenko, Luda, Econs, Michael J, Eiriksdottir, Gudny, Enneman, Anke W, Eriksson, Joel, Eriksson, Johan G, Estrada, Karol, Evans, Daniel S, Feitosa, Mary F, Fu, Mao, Gieger, Christian, Grallert, Harald, Gudnason, Vilmundur, Lenore, Launer J, Hayward, Caroline, Hofman, Albert, Homuth, Georg, Huffman, Kim M, Husted, Lise B, Illig, Thomas, Ingelsson, Erik, Ittermann, Till, Jansson, John-Olov, Johnson, Toby, Biffar, Reiner, Jordan, Joanne M, Jula, Antti, Karlsson, Magnus, Khaw, Kay-Tee, Kilpeläinen, Tuomas O, Klopp, Norman, Kloth, Jacqueline SL, Koller, Daniel L, Kooner, Jaspal S, Kraus, William E, Kritchevsky, Stephen, Kutalik, Zoltán, Kuulasmaa, Teemu, Kuusisto, Johanna, Laakso, Markku, Lahti, Jari, Lang, Thomas, Langdahl, Bente L, Lerch, Markus M, Lewis, Joshua R, Lill, Christina, Lind, Lars, Lindgren, Cecilia, Liu, Yongmei, Livshits, Gregory, Ljunggren, Östen, Loos, Ruth JF, Lorentzon, Mattias, Luan, Jian'an, Luben, Robert N, Malkin, Ida, McGuigan, Fiona E, Medina-Gomez, Carolina, Meitinger, Thomas, Melhus, Håkan, Mellström, Dan, Michaëlsson, Karl, Mitchell, Braxton D, Morris, Andrew P, Mosekilde, Leif, Nethander, Maria, Newman, Anne B, O'Connell, Jeffery R, Oostra, Ben A, Orwoll, Eric S, Palotie, Aarno, Peacock, Munro, and Perola, Markus

Subjects
Muscle, Skeletal, Adipose Tissue, Body Fluid Compartments, Humans, RNA-Binding Proteins, Receptor, Melanocortin, Type 4, Extracellular Matrix Proteins, Absorptiometry, Photon, Body Composition, Electric Impedance, Phenotype, Polymorphism, Single Nucleotide, Adolescent, Adult, Aged, Aged, 80 and over, Middle Aged, European Continental Ancestry Group, Female, Male, Versicans, Genome-Wide Association Study, Young Adult, ADAMTS Proteins, Alpha-Ketoglutarate-Dependent Dioxygenase FTO, body composition, skeletal muscle, body fat, meta-analysis of genome-wide association studies, metabolic profile, Prevention, Genetics, Human Genome, 2.1 Biological and endogenous factors, Nutrition & Dietetics, Engineering, Medical and Health Sciences
Abstract

BackgroundLean body mass (LM) plays an important role in mobility and metabolic function. We previously identified five loci associated with LM adjusted for fat mass in kilograms. Such an adjustment may reduce the power to identify genetic signals having an association with both lean mass and fat mass.ObjectivesTo determine the impact of different fat mass adjustments on genetic architecture of LM and identify additional LM loci.MethodsWe performed genome-wide association analyses for whole-body LM (20 cohorts of European ancestry with n = 38,292) measured using dual-energy X-ray absorptiometry) or bioelectrical impedance analysis, adjusted for sex, age, age2, and height with or without fat mass adjustments (Model 1 no fat adjustment; Model 2 adjustment for fat mass as a percentage of body mass; Model 3 adjustment for fat mass in kilograms).ResultsSeven single-nucleotide polymorphisms (SNPs) in separate loci, including one novel LM locus (TNRC6B), were successfully replicated in an additional 47,227 individuals from 29 cohorts. Based on the strengths of the associations in Model 1 vs Model 3, we divided the LM loci into those with an effect on both lean mass and fat mass in the same direction and refer to those as "sumo wrestler" loci (FTO and MC4R). In contrast, loci with an impact specifically on LM were termed "body builder" loci (VCAN and ADAMTSL3). Using existing available genome-wide association study databases, LM increasing alleles of SNPs in sumo wrestler loci were associated with an adverse metabolic profile, whereas LM increasing alleles of SNPs in "body builder" loci were associated with metabolic protection.ConclusionsIn conclusion, we identified one novel LM locus (TNRC6B). Our results suggest that a genetically determined increase in lean mass might exert either harmful or protective effects on metabolic traits, depending on its relation to fat mass.

Published
2019

6. Genome-wide association study in 79,366 European-ancestry individuals informs the genetic architecture of 25-hydroxyvitamin D levels

Author

Jiang, Xia, O’Reilly, Paul F, Aschard, Hugues, Hsu, Yi-Hsiang, Richards, J Brent, Dupuis, Josée, Ingelsson, Erik, Karasik, David, Pilz, Stefan, Berry, Diane, Kestenbaum, Bryan, Zheng, Jusheng, Luan, Jianan, Sofianopoulou, Eleni, Streeten, Elizabeth A, Albanes, Demetrius, Lutsey, Pamela L, Yao, Lu, Tang, Weihong, Econs, Michael J, Wallaschofski, Henri, Völzke, Henry, Zhou, Ang, Power, Chris, McCarthy, Mark I, Michos, Erin D, Boerwinkle, Eric, Weinstein, Stephanie J, Freedman, Neal D, Huang, Wen-Yi, Van Schoor, Natasja M, van der Velde, Nathalie, Groot, Lisette CPGM de, Enneman, Anke, Cupples, L Adrienne, Booth, Sarah L, Vasan, Ramachandran S, Liu, Ching-Ti, Zhou, Yanhua, Ripatti, Samuli, Ohlsson, Claes, Vandenput, Liesbeth, Lorentzon, Mattias, Eriksson, Johan G, Shea, M Kyla, Houston, Denise K, Kritchevsky, Stephen B, Liu, Yongmei, Lohman, Kurt K, Ferrucci, Luigi, Peacock, Munro, Gieger, Christian, Beekman, Marian, Slagboom, Eline, Deelen, Joris, Heemst, Diana van, Kleber, Marcus E, März, Winfried, de Boer, Ian H, Wood, Alexis C, Rotter, Jerome I, Rich, Stephen S, Robinson-Cohen, Cassianne, den Heijer, Martin, Jarvelin, Marjo-Riitta, Cavadino, Alana, Joshi, Peter K, Wilson, James F, Hayward, Caroline, Lind, Lars, Michaëlsson, Karl, Trompet, Stella, Zillikens, M Carola, Uitterlinden, Andre G, Rivadeneira, Fernando, Broer, Linda, Zgaga, Lina, Campbell, Harry, Theodoratou, Evropi, Farrington, Susan M, Timofeeva, Maria, Dunlop, Malcolm G, Valdes, Ana M, Tikkanen, Emmi, Lehtimäki, Terho, Lyytikäinen, Leo-Pekka, Kähönen, Mika, Raitakari, Olli T, Mikkilä, Vera, Ikram, M Arfan, Sattar, Naveed, Jukema, J Wouter, Wareham, Nicholas J, Langenberg, Claudia, Forouhi, Nita G, Gundersen, Thomas E, Khaw, Kay-Tee, Butterworth, Adam S, Danesh, John, and Spector, Timothy

Subjects
Epidemiology, Biological Sciences, Health Sciences, Genetics, Human Genome, Clinical Research, 2.1 Biological and endogenous factors, Aetiology, Inflammatory and immune system, Amidohydrolases, Autoimmune Diseases, Cohort Studies, Female, Genome-Wide Association Study, Humans, Male, Polymorphism, Single Nucleotide, Vesicular Transport Proteins, Vitamin D, White People
Abstract

Vitamin D is a steroid hormone precursor that is associated with a range of human traits and diseases. Previous GWAS of serum 25-hydroxyvitamin D concentrations have identified four genome-wide significant loci (GC, NADSYN1/DHCR7, CYP2R1, CYP24A1). In this study, we expand the previous SUNLIGHT Consortium GWAS discovery sample size from 16,125 to 79,366 (all European descent). This larger GWAS yields two additional loci harboring genome-wide significant variants (P = 4.7×10-9 at rs8018720 in SEC23A, and P = 1.9×10-14 at rs10745742 in AMDHD1). The overall estimate of heritability of 25-hydroxyvitamin D serum concentrations attributable to GWAS common SNPs is 7.5%, with statistically significant loci explaining 38% of this total. Further investigation identifies signal enrichment in immune and hematopoietic tissues, and clustering with autoimmune diseases in cell-type-specific analysis. Larger studies are required to identify additional common SNPs, and to explore the role of rare or structural variants and gene-gene interactions in the heritability of circulating 25-hydroxyvitamin D levels.

Published
2018

8. Genetic Variants Associated with Circulating Parathyroid Hormone

Author

Robinson-Cohen, Cassianne, Lutsey, Pamela L, Kleber, Marcus E, Nielson, Carrie M, Mitchell, Braxton D, Bis, Joshua C, Eny, Karen M, Portas, Laura, Eriksson, Joel, Lorentzon, Mattias, Koller, Daniel L, Milaneschi, Yuri, Teumer, Alexander, Pilz, Stefan, Nethander, Maria, Selvin, Elizabeth, Tang, Weihong, Weng, Lu-Chen, Wong, Hoi Suen, Lai, Dongbing, Peacock, Munro, Hannemann, Anke, Völker, Uwe, Homuth, Georg, Nauk, Matthias, Murgia, Federico, Pattee, Jack W, Orwoll, Eric, Zmuda, Joseph M, Riancho, Jose Antonio, Wolf, Myles, Williams, Frances, Penninx, Brenda, Econs, Michael J, Ryan, Kathleen A, Ohlsson, Claes, Paterson, Andrew D, Psaty, Bruce M, Siscovick, David S, Rotter, Jerome I, Pirastu, Mario, Streeten, Elizabeth, März, Winfried, Fox, Caroline, Coresh, Josef, Wallaschofski, Henri, Pankow, James S, de Boer, Ian H, and Kestenbaum, Bryan

Subjects
Biomedical and Clinical Sciences, Clinical Sciences, Human Genome, Genetics, Prevention, Clinical Research, 2.1 Biological and endogenous factors, Aetiology, Good Health and Well Being, Adult, Aged, Europe, Female, Genetic Variation, Genome-Wide Association Study, Humans, Male, Middle Aged, Parathyroid Hormone, Polymorphism, Single Nucleotide, genome-wide association study, human genetics, mineral metabolism, parathyroid hormone, Urology & Nephrology, Clinical sciences
Abstract

Parathyroid hormone (PTH) is a primary calcium regulatory hormone. Elevated serum PTH concentrations in primary and secondary hyperparathyroidism have been associated with bone disease, hypertension, and in some studies, cardiovascular mortality. Genetic causes of variation in circulating PTH concentrations are incompletely understood. We performed a genome-wide association study of serum PTH concentrations among 29,155 participants of European ancestry from 13 cohort studies (n=22,653 and n=6502 in discovery and replication analyses, respectively). We evaluated the association of single nucleotide polymorphisms (SNPs) with natural log-transformed PTH concentration adjusted for age, sex, season, study site, and principal components of ancestry. We discovered associations of SNPs from five independent regions with serum PTH concentration, including the strongest association with rs6127099 upstream of CYP24A1 (P=4.2 × 10-53), a gene that encodes the primary catabolic enzyme for 1,25-dihydroxyvitamin D and 25-dihydroxyvitamin D. Each additional copy of the minor allele at this SNP associated with 7% higher serum PTH concentration. The other SNPs associated with serum PTH concentration included rs4074995 within RGS14 (P=6.6 × 10-17), rs219779 adjacent to CLDN14 (P=3.5 × 10-16), rs4443100 near RTDR1 (P=8.7 × 10-9), and rs73186030 near CASR (P=4.8 × 10-8). Of these five SNPs, rs6127099, rs4074995, and rs219779 replicated. Thus, common genetic variants located near genes involved in vitamin D metabolism and calcium and renal phosphate transport associated with differences in circulating PTH concentrations. Future studies could identify the causal variants at these loci, and the clinical and functional relevance of these variants should be pursued.

Published
2017

10. Effect of Allele-Specific Clcn7G213R siRNA Delivered Via a Novel Nanocarrier on Bone Phenotypes in ADO2 Mice on 129S Background.

Author

Saffie-Siebert, Suzanne, Alam, Imranul, Sutera, Flavia Maria, Dehsorkhi, Ashkan, Torabi-Pour, Nissim, Baran-Rachwalska, Paulina, Iamartino, Luca, Teti, Anna, Maurizi, Antonio, Gerard-O'Riley, Rita L., Acton, Dena, and Econs, Michael J.

Subjects
PHENOTYPES, BONE density, SMALL interfering RNA, BONE diseases, OSTEOGENESIS imperfecta, FEMUR, TERIPARATIDE, DYSPLASIA
Abstract

Autosomal dominant osteopetrosis type 2 (ADO2) is a rare inherited bone disorder characterised by dense but brittle bones. It displays striking phenotypic variability, with the most severe symptoms, including blindness and bone marrow failure. Disease management largely relies on symptomatic treatment since there is no safe and effective treatment. Most ADO2 cases are caused by heterozygous loss-of-function mutations in the CLCN7 gene, which encodes an essential Cl−/H+ antiporter for proper bone resorption by osteoclasts. Thus, siRNA-mediated silencing of the mutant allele is a promising therapeutic approach, but targeting bone for first-in-human translation remains challenging. Here, we demonstrate the utility of silicon-stabilised hybrid lipid nanoparticles (sshLNPs) as a next-generation nucleic acid nanocarrier capable of delivering allele-specific siRNA to bone. Using a Clcn7G213R knock-in mouse model recapitulating one of the most common human ADO2 mutations and based on the 129S genetic background (which produces the most severe disease phenotype amongst current models), we show substantial knockdown of the mutant allele in femur when siRNA targeting the pathogenic variant is delivered by sshLNPs. We observed lower areal bone mineral density in femur and reduced trabecular thickness in femur and tibia, when siRNA-loaded sshLNPs were administered subcutaneously (representing the most relevant administration route for clinical adoption and patient adherence). Importantly, sshLNPs have improved stability over conventional LNPs and enable 'post hoc loading' for point-of-care formulation. The treatment was well tolerated, suggesting that sshLNP-enabled gene therapy might allow successful clinical translation of essential new treatments for ADO2 and potentially other rare genetic bone diseases. [ABSTRACT FROM AUTHOR]

Published
2024
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11. Autosomal Dominant Osteopetrosis (ADO) Caused by a Missense Variant in the TCIRG1 Gene.

Author

Jodeh, Wade, Katz, Amy J, Hart, Marian, Warden, Stuart J, Niziolek, Paul, Alam, Imranul, Ing, Steven, Polgreen, Lynda E, Imel, Erik A, and Econs, Michael J

Subjects
MISSENSE mutation, OSTEOPETROSIS, GENETIC variation, RECESSIVE genes, PHENOTYPIC plasticity, CHLORIDE channels, FRACTURE healing, T cells
Abstract

Context Autosomal dominant osteopetrosis (ADO) is a rare genetic disorder resulting from impaired osteoclastic bone resorption. Clinical manifestations frequently include fractures, osteonecrosis (particularly of the jaw or maxilla), osteomyelitis, blindness, and/or bone marrow failure. ADO usually results from heterozygous missense variants in the Chloride Channel 7 gene (CLCN7) that cause disease by a dominant negative mechanism. Variants in the T-cell immune regulator 1 gene (TCIRG1) are commonly identified in autosomal recessive osteopetrosis but have only been reported in 1 patient with ADO. Case Description Here, we report 3 family members with a single heterozygous missense variant (p.Gly579Arg) in TCIRG1 who have a phenotype consistent with ADO. Three of 5 protein prediction programs suggest this variant likely inhibits the function of TCIRG1. Conclusion This is the first description of adult presentation of ADO caused by a TCIRG1 variant. Similar to families with ADO from CLCN7 mutations, this variant in TCIRG1 results in marked phenotype variability, with 2 subjects having severe disease and the third having very mild disease. This family report implicates TCIRG1 missense mutations as a cause of ADO and demonstrates that the marked phenotypic variability in ADO may extend to disease caused by TCIRG1 missense mutations. [ABSTRACT FROM AUTHOR]

Published
2024
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12. Contributors

Author

Al Sabie, Farah, primary, Bacchetta, Justine, additional, Brandenburg, Vincent, additional, Chang Hu, Ming, additional, Chen, Chang Huei, additional, Chen, Lingfeng, additional, Clinkenbeard, Erica L., additional, Econs, Michael J., additional, Egli-Spichtig, Daniela, additional, Erben, Reinhold G., additional, Erem, Sarah, additional, Faraco, Carlos C., additional, Fukumoto, Seiji, additional, Goetz, Regina, additional, Grabner, Alexander, additional, Haffner, Dieter, additional, Hanudel, Mark R., additional, He, Ping, additional, Heine, Gunnar H., additional, Hewison, Martin, additional, Hillebrands, Jan-Luuk, additional, Hruska, Keith A., additional, Huang, Chou-Long, additional, Imel, Erik A., additional, Jovanovich, Anna, additional, Krick, Stefanie, additional, Kuro-o, Makoto, additional, Lee, Seong Min, additional, Leifheit-Nestler, Maren, additional, Mencke, Rik, additional, Moe, Orson W., additional, Mohammadi, Moosa, additional, Musgrove, John, additional, Neyra, Javier A., additional, Olauson, Hannes, additional, Perry, Katherine Wesseling, additional, Perwad, Farzana, additional, Pike, J. Wesley, additional, Razzaque, Mohammed S., additional, Richter, Beatrice, additional, Salusky, Isidro B., additional, Section, Renal, additional, Seiler-Mußler, Sarah, additional, Struemph, Taylor, additional, Vervloet, Marc G., additional, Vrabec, Curtis, additional, Williams, Matthew J., additional, Wright, Clinton B., additional, and Zinkle, Allen, additional

Published
2021
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14. Autoimmune hyperphosphatemic tumoral calcinosis in a patient with FGF23 autoantibodies

Author

Roberts, Mary Scott, Burbelo, Peter D., Egli-Spichtig, Daniela, Perwad, Farzana, Romero, Christopher J., Ichikawa, Shoji, Farrow, Emily, Econs, Michael J., Guthrie, Lori C., Collins, Michael T., and Gafni, Rachel I.

Subjects
Calcinosis -- Care and treatment, Fibroblast growth factors -- Research, Gene expression -- Research, Autoantibodies, Type 1 diabetes, Diabetes mellitus, Hyperostosis, Luciferase, Autoimmunity, Calcification (Physiology), Phosphorus imbalance, B cells, Antibodies, Biochemistry, Health care industry
Abstract

Hyperphosphatemic familial tumoral calcinosis (HFTC)/hyperostosis-hyperphosphatemia syndrome (HHS) is an autosomal recessive disorder of ectopic calcification due to deficiency of or resistance to intact fibroblast growth factor 23 (iFGF23). Inactivating mutations in FGF23, N-acetylgalactosaminyltransferase 3 (GALNT3), or KLOTHO (KL) have been reported as causing HFTC/HHS. We present what we believe is the first identified case of autoimmune hyperphosphatemic tumoral calcinosis in an 8-year-old boy. In addition to the classical clinical and biochemical features of hyperphosphatemic tumoral calcinosis, the patient exhibited markedly elevated intact and C-terminal FGF23 levels, suggestive of FGF23 resistance. However, no mutations in FGF23, KL, or FGF receptor 1 (FGFR1) were identified. He subsequently developed type 1 diabetes mellitus, which raised the possibility of an autoimmune cause for hyperphosphatemic tumoral calcinosis. Luciferase immunoprecipitation systems revealed markedly elevated FGF23 autoantibodies without detectable FGFR1 or Klotho autoantibodies. Using an in vitro FGF23 functional assay, we found that the FGF23 autoantibodies in the patient's plasma blocked downstream signaling via the MAPK/ERK signaling pathway in a dose-dependent manner. Thus, this report describes the first case, to our knowledge, of autoimmune hyperphosphatemic tumoral calcinosis with pathogenic autoantibodies targeting FGF23. Identification of this pathophysiology extends the etiologic spectrum of hyperphosphatemic tumoral calcinosis and suggests that immunomodulatory therapy may be an effective treatment., IntroductionFibroblast growth fact 23 (FGF23) is a phosphate- and 1,25[(OH).sub.2] vitamin D-regulating (1,25D-regulating) hormone produced by osteoblasts and osteocytes (1). FGF23 acts via FGF receptor 1 (FGFR1) coupled with the [...]

Published
2018
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20. Fine mapping of bone structure and strength QTLs in heterogeneous stock rat

Author

Alam, Imranul, Koller, Daniel L., Cañete, Toni, Blázquez, Gloria, Mont-Cardona, Carme, López-Aumatell, Regina, Martínez-Membrives, Esther, Díaz-Morán, Sira, Tobeña, Adolf, Fernández-Teruel, Alberto, Stridh, Pernilla, Diez, Margarita, Olsson, Tomas, Johannesson, Martina, Baud, Amelie, Econs, Michael J., and Foroud, Tatiana

Published
2015
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34. Contributors

Author

Aiello, Lloyd Paul, primary, Alatzoglou, Kyriaki S., additional, Alexander, Erik K., additional, Allan, Carolyn A., additional, Allolio, Bruno, additional, Amino, Nobuyuki, additional, Anawalt, Bradley D., additional, Angelos, Peter, additional, Arboleda, Valerie A., additional, Auchus, Richard J., additional, Axelrod, Lloyd, additional, Bahn, Rebecca S., additional, Baker, MD, PhD, FRACP, H.W. Gordon, additional, Barak, Shlomi, additional, Barnes, Randall B., additional, Barthel, Andreas, additional, Bastepe, Murat, additional, Beardsley, Emma K., additional, Beck-Peccoz, Paolo, additional, Bell, Graeme I., additional, Bi, Wenya Linda, additional, Bilezikian, John P., additional, Blum, Manfred, additional, Bonnema, Steen J., additional, Bornstein, Stefan R., additional, Bouillon, Roger, additional, Boulton, Andrew J.M., additional, Braunstein, Glenn D., additional, Bringhurst, F. Richard, additional, Broekmans, Frank J., additional, Bronstein, Marcello D., additional, Brown, Edward M., additional, Brown, Wendy A., additional, Bulun, Serdar E., additional, Burch, Henry B., additional, Burger, Henry G., additional, Burney, Richard O., additional, Burt, Morton G., additional, Cagliero, Enrico, additional, Callender, Glenda G., additional, Avancini Caramori, Maria Luiza, additional, Carey, Robert M., additional, Carling, Tobias, additional, Cavagnini, Francesco, additional, Cavallerano, Jerry D., additional, Challet, Etienne, additional, Chan, Shu Jin, additional, Chang, R. Jeffrey, additional, Chapurlat, Roland D., additional, Chatterjee, V. Krishna, additional, Chiofalo, Francesco, additional, Chiovato, Luca, additional, Cho, Kyung J., additional, Christison-Lagay, Emily, additional, Christophe, Daniel, additional, Chrousos, George P., additional, Cidlowski, John A., additional, Clemmons, David R., additional, Considine, Robert V., additional, Conti, Marco, additional, Copinschi, Georges, additional, Copps, Kyle D., additional, Cowley, Michael A., additional, Cuttler, Leona, additional, Dattani, Mehul T., additional, Davis, Stephen N., additional, De Felice, Mario, additional, De Groot, Leslie J., additional, de Kretser, David M., additional, DeFronzo, Ralph A., additional, Delli, Ahmed J., additional, Demay, Marie B., additional, Dennedy, Michael C., additional, Di Lauro, Roberto, additional, Dineen, Rosemary, additional, Ding, Su Ann, additional, Dinneen, Sean F., additional, Drucker, Daniel J., additional, Dumont, Jacques E., additional, Dungan, Kathleen M., additional, Dunn, Ian F., additional, Econs, Michael J., additional, Ehrmann, David A., additional, Eisenhofer, Graeme, additional, Ergun-Longmire, Berrin, additional, Eugster, Erica A., additional, Farooqi, Sadaf I., additional, Fassnacht, Martin, additional, Fauser, Bart C.J.M., additional, Fenzi, Gianfranco, additional, Ferrannini, Ele, additional, Findlay, David M., additional, Finlayson, Courtney Anne, additional, Fisher, Delbert A., additional, Francis, Isaac R., additional, Freeman, Mason W., additional, Frohman, Lawrence A., additional, Frydenberg, Mark, additional, Fuller, Peter J., additional, Gaglia, Jason L., additional, Galizia, Gianluigi, additional, Gardella, Thomas J., additional, Garvey, Katharine C., additional, Genant, Harry K., additional, German, Michael S., additional, Gevers, Evelien F., additional, Giraldi, Francesca Pecori, additional, Giudice, Linda C., additional, Giustina, Andrea, additional, Glasier, Anna, additional, Glorieux, Francis H., additional, Goldfine, Allison B., additional, Gooren, Louis J., additional, Gordon, David F., additional, Gregerson, Karen A., additional, Grogan, Raymon H., additional, Gross, Milton D., additional, Grossman, Ashley B., additional, Gruber, Matthias, additional, Guimarães, Valeria C., additional, Gurnell, Mark, additional, Haddad, Nadine G., additional, Haisenleder, Daniel J., additional, Handelsman, David J., additional, Hanks, John B., additional, Hannon, Mark J., additional, Harno, Erika, additional, Hebrok, Matthias, additional, Hedger, Mark P., additional, Hegedüs, Laszlo, additional, Heindel, Jerrold J., additional, Hernandez, Arturo, additional, Herndon, Maria K., additional, Ho, Ken K.Y., additional, Horseman, Nelson D., additional, Hughes, Ieuan A., additional, Hupfeld, Christopher J., additional, Hussain, Hero K., additional, Iodice, Valeria, additional, James, Benjamin C., additional, Jameson, J. Larry, additional, Jones, Glenville, additional, Josso, Nathalie, additional, Jüppner, Harald, additional, Juszczak, Agata, additional, Kalish, Jeffrey, additional, Kaplan, Edwin L., additional, Karavitaki, Niki, additional, Karczewska-Kupczewska, Monika, additional, Khattab, Ahmed, additional, Klein, David C., additional, Klein, Ronald, additional, Kleinau, Gunnar, additional, Koontz, Michaela, additional, Kopchick, John J., additional, Kopp, Peter, additional, Kowalska, Irina, additional, Krane, Stephen M., additional, Krohn, Knut, additional, Kronenberg, Henry M., additional, Lamos, Elizabeth M., additional, Lania, Andrea, additional, Lau, Sue Lynn, additional, Laws, Edward R., additional, Lazarus, John H., additional, Learoyd, Diana L., additional, Lebovitz, Harold E., additional, Lenmark, Åke, additional, List, Edward O., additional, Loveland, Kate, additional, Low, David A., additional, Macchia, Paolo E., additional, Maclaren, Noel K., additional, Madeiros-Neto, Geraldo, additional, Maenhaut, Carine, additional, Maes, Christa, additional, Main, Katharina M., additional, Malchoff, Carl D., additional, Malchoff, Diana M., additional, Malik, Rayaz A., additional, Mandel, Susan J., additional, Mantzoros, Christos S., additional, Maratos-Flier, Eleftheria, additional, Marino, Michele, additional, Marshall, John C., additional, Martin, T. John, additional, Martin, Thomas F.J., additional, Mathias, Christopher J., additional, McGee, Elizabeth A., additional, McKenzie, Travis, additional, McLachlan, Robert I., additional, Meier, Juris J., additional, Melmed, Shlomo, additional, Metzger, Boyd E., additional, Meyer-Bahlburg, Heino F.L., additional, Millar, Robert P., additional, Miller, Walter L., additional, Misra, Madhusmita, additional, Molitch, Mark E., additional, Moravek, Molly B., additional, Morris, Damian G., additional, Nagar, Sapna, additional, Nakamoto, Jon, additional, New, Maria I., additional, Nieman, Lynnette K., additional, Nilson, John H., additional, Ntali, Georgia, additional, O’Bryan, Moira, additional, O’Rahilly, Stephen, additional, Öberg, Kjell, additional, Olefsky, Jerrold M., additional, Olson, Matthew T., additional, Pacak, Karel, additional, Pacini, Furio, additional, Padia, Shetal H., additional, Paschke, Ralf, additional, Pasquel, Francisco J., additional, Perry, Katherine Wesseling, additional, Persani, Luca, additional, Philipson, Louis H., additional, Pina, Christian, additional, Pomposelli, Frank B., additional, Potts, John T., additional, Quigley, Charmian A., additional, Quinkler, Marcus O., additional, Quirk, Christine Campion, additional, Rajpert-De Meyts, Ewa, additional, Ravussin, Eric, additional, Ray, David W., additional, Refetoff, Samuel, additional, Retnakaran, Ravi, additional, Rey, Rodolfo A., additional, Rhodes, Christopher J., additional, Ridgway, E. Chester, additional, Risbridger, Gail P., additional, Rizza, Robert A., additional, Robinson, Bruce G., additional, Roger, Pierre P., additional, Rosenfeld, Michael G., additional, Rosenfield, Robert L., additional, Rossing, Peter, additional, Rubin, Robert T., additional, Rubio, Ileana G.S., additional, Ruderman, Neil B., additional, Russo, Jose, additional, Russo, Irma H., additional, Salusky, Isidro B., additional, Santoro, Nanette, additional, Scully, Kathleen M., additional, Sexton, Patrick M., additional, Shulman, Gerald I., additional, Silva, Paolo S., additional, Silverberg, Shonni J., additional, Singer, Frederick R., additional, Skakkebaek, Niels E., additional, Skaznik-Wikiel, Malgorzata E., additional, Skowronska-Krawczyk, Dorota, additional, Smith, Carolyn L., additional, Smith, Philip W., additional, Smith, Roger, additional, Smith, Steven R., additional, Snyder, Peter J., additional, St. Germain, Donald L., additional, St-Arnaud, René, additional, Steiner, Donald F., additional, Stewart, Paul M., additional, Strączkowski, Marek, additional, Strauss, Jerome F., additional, Styne, Dennis M., additional, Swan, Karena L., additional, Swerdloff, Ronald S., additional, Tacon, Lyndal J., additional, Tello, Javier A., additional, Thakker, Rajesh V., additional, Thompson, Christopher J., additional, Timmers, Henri J.L.M., additional, Toppari, Jorma, additional, Traub, Michael L., additional, Tsoukas, Michael A., additional, Udelsman, Robert, additional, Umpierrez, Guillermo E., additional, Van den Berghe, Greet, additional, Vassart, Gilbert, additional, Vernon, Ashley H., additional, Vilain, Eric, additional, Visser, Theo J., additional, Vitti, Paolo, additional, Walford, Geoffrey A., additional, Wang, Christina, additional, Weetman, Anthony P., additional, Weigel, Nancy L., additional, Weir, Gordon C., additional, Weiss, Roy E., additional, White, Anne, additional, White, Kenneth E., additional, White, Morris F., additional, Whyte, Michael P., additional, Wiersinga, Wilmar M., additional, Willenberg, Holger S., additional, Wolfsdorf, Joseph I., additional, Wondisford, Fredric E., additional, Wong, Ka Kit, additional, Wysolmerski, John J., additional, Yau, Mabel, additional, Young, Morag J., additional, Younk, Lisa M., additional, Yu, Run, additional, Yuen, Tony, additional, Zeiger, Martha A., additional, Zinman, Bernard, additional, and Zoeller, R. Thomas, additional

Published
2016
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36. Large meta-analysis of genome-wide association studies identifies five loci for lean body mass

Author

Zillikens, M. Carola, Demissie, Serkalem, Hsu, Yi-Hsiang, Yerges-Armstrong, Laura M., Chou, Wen-Chi, Stolk, Lisette, Livshits, Gregory, Broer, Linda, Johnson, Toby, Koller, Daniel L., Kutalik, Zoltán, Luan, Jian’an, Malkin, Ida, Ried, Janina S., Smith, Albert V., Thorleifsson, Gudmar, Vandenput, Liesbeth, Hua Zhao, Jing, Zhang, Weihua, Aghdassi, Ali, Åkesson, Kristina, Amin, Najaf, Baier, Leslie J., Barroso, Inês, Bennett, David A., Bertram, Lars, Biffar, Rainer, Bochud, Murielle, Boehnke, Michael, Borecki, Ingrid B., Buchman, Aron S., Byberg, Liisa, Campbell, Harry, Campos Obanda, Natalia, Cauley, Jane A., Cawthon, Peggy M., Cederberg, Henna, Chen, Zhao, Cho, Nam H., Jin Choi, Hyung, Claussnitzer, Melina, Collins, Francis, Cummings, Steven R., De Jager, Philip L., Demuth, Ilja, Dhonukshe-Rutten, Rosalie A. M., Diatchenko, Luda, Eiriksdottir, Gudny, Enneman, Anke W., Erdos, Mike, Eriksson, Johan G., Eriksson, Joel, Estrada, Karol, Evans, Daniel S., Feitosa, Mary F., Fu, Mao, Garcia, Melissa, Gieger, Christian, Girke, Thomas, Glazer, Nicole L., Grallert, Harald, Grewal, Jagvir, Han, Bok-Ghee, Hanson, Robert L., Hayward, Caroline, Hofman, Albert, Hoffman, Eric P., Homuth, Georg, Hsueh, Wen-Chi, Hubal, Monica J., Hubbard, Alan, Huffman, Kim M., Husted, Lise B., Illig, Thomas, Ingelsson, Erik, Ittermann, Till, Jansson, John-Olov, Jordan, Joanne M., Jula, Antti, Karlsson, Magnus, Khaw, Kay-Tee, Kilpeläinen, Tuomas O., Klopp, Norman, Kloth, Jacqueline S. L., Koistinen, Heikki A., Kraus, William E., Kritchevsky, Stephen, Kuulasmaa, Teemu, Kuusisto, Johanna, Laakso, Markku, Lahti, Jari, Lang, Thomas, Langdahl, Bente L., Launer, Lenore J., Lee, Jong-Young, Lerch, Markus M., Lewis, Joshua R., Lind, Lars, Lindgren, Cecilia, Liu, Yongmei, Liu, Tian, Liu, Youfang, Ljunggren, Östen, Lorentzon, Mattias, Luben, Robert N., Maixner, William, McGuigan, Fiona E., Medina-Gomez, Carolina, Meitinger, Thomas, Melhus, Håkan, Mellström, Dan, Melov, Simon, Michaëlsson, Karl, Mitchell, Braxton D., Morris, Andrew P., Mosekilde, Leif, Newman, Anne, Nielson, Carrie M., O’Connell, Jeffrey R., Oostra, Ben A., Orwoll, Eric S., Palotie, Aarno, Parker, Stephen C. J., Peacock, Munro, Perola, Markus, Peters, Annette, Polasek, Ozren, Prince, Richard L., Räikkönen, Katri, Ralston, Stuart H., Ripatti, Samuli, Robbins, John A., Rotter, Jerome I., Rudan, Igor, Salomaa, Veikko, Satterfield, Suzanne, Schadt, Eric E., Schipf, Sabine, Scott, Laura, Sehmi, Joban, Shen, Jian, Soo Shin, Chan, Sigurdsson, Gunnar, Smith, Shad, Soranzo, Nicole, Stančáková, Alena, Steinhagen-Thiessen, Elisabeth, Streeten, Elizabeth A., Styrkarsdottir, Unnur, Swart, Karin M. A., Tan, Sian-Tsung, Tarnopolsky, Mark A., Thompson, Patricia, Thomson, Cynthia A., Thorsteinsdottir, Unnur, Tikkanen, Emmi, Tranah, Gregory J., Tuomilehto, Jaakko, van Schoor, Natasja M., Verma, Arjun, Vollenweider, Peter, Völzke, Henry, Wactawski-Wende, Jean, Walker, Mark, Weedon, Michael N., Welch, Ryan, Wichmann, H.-Erich, Widen, Elisabeth, Williams, Frances M. K., Wilson, James F., Wright, Nicole C., Xie, Weijia, Yu, Lei, Zhou, Yanhua, Chambers, John C., Döring, Angela, van Duijn, Cornelia M., Econs, Michael J., Gudnason, Vilmundur, Kooner, Jaspal S., Psaty, Bruce M., Spector, Timothy D., Stefansson, Kari, Rivadeneira, Fernando, Uitterlinden, André G., Wareham, Nicholas J., Ossowski, Vicky, Waterworth, Dawn, Loos, Ruth J. F., Karasik, David, Harris, Tamara B., Ohlsson, Claes, and Kiel, Douglas P.

Published
2017
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37. Heterogeneous stock rat: A unique animal model for mapping genes influencing bone fragility

Author

Alam, Imranul, Koller, Daniel L., Sun, Qiwei, Roeder, Ryan K., Cañete, Toni, Blázquez, Gloria, López-Aumatell, Regina, Martínez-Membrives, Esther, Vicens-Costa, Elia, Mont, Carme, Díaz, Sira, Tobeña, Adolf, Fernández-Teruel, Alberto, Whitley, Adam, Strid, Pernilla, Diez, Margarita, Johannesson, Martina, Flint, Jonathan, Econs, Michael J., Turner, Charles H., and Foroud, Tatiana

Published
2011
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38. Cover, Volume 43, Issue 2

Author

Sarafrazi, Soodabeh, primary, Daugherty, Sean C., additional, Miller, Nicole, additional, Boada, Patrick, additional, Carpenter, Thomas O., additional, Chunn, Lauren, additional, Dill, Kariena, additional, Econs, Michael J., additional, Eisenbeis, Scott, additional, Imel, Erik A., additional, Johnson, Britt, additional, Kiel, Mark J., additional, Krolczyk, Stan, additional, Ramesan, Prameela, additional, Truty, Rebecca, additional, and Sabbagh, Yves, additional

Published
2022
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40. Novel PHEX gene locus‐specific database: Comprehensive characterization of vast number of variants associated with X‐linked hypophosphatemia (XLH)

Author

Sarafrazi, Soodabeh, primary, Daugherty, Sean C., additional, Miller, Nicole, additional, Boada, Patrick, additional, Carpenter, Thomas O., additional, Chunn, Lauren, additional, Dill, Kariena, additional, Econs, Michael J., additional, Eisenbeis, Scott, additional, Imel, Erik A., additional, Johnson, Britt, additional, Kiel, Mark J., additional, Krolczyk, Stan, additional, Ramesan, Prameela, additional, Truty, Rebecca, additional, and Sabbagh, Yves, additional

Published
2021
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44. Common genetic determinants of vitamin D insufficiency: a genome-wide association study

Author

Wang, Thomas J, Zhang, Feng, Richards, J Brent, Kestenbaum, Bryan, van Meurs, Joyce B, Berry, Diane, Kiel, Douglas P, Streeten, Elizabeth A, Ohlsson, Claes, Koller, Daniel L, Peltonen, Leena, Cooper, Jason D, O'Reilly, Paul F, Houston, Denise K, Glazer, Nicole L, Vandenput, Liesbeth, Peacock, Munro, Shi, Julia, Rivadeneira, Fernando, McCarthy, Mark I, Anneli, Pouta, de Boer, Ian H, Mangino, Massimo, Kato, Bernet, Smyth, Deborah J, Booth, Sarah L, Jacques, Paul F, Burke, Greg L, Goodarzi, Mark, Cheung, Ching-Lung, Wolf, Myles, Rice, Kenneth, Goltzman, David, Hidiroglou, Nick, Ladouceur, Martin, Wareham, Nicholas J, Hocking, Lynne J, Hart, Deborah, Arden, Nigel K, Cooper, Cyrus, Malik, Suneil, Fraser, William D, Hartikainen, Anna-Liisa, Zhai, Guangju, Macdonald, Helen M, Forouhi, Nita G, Loos, Ruth JF, Reid, David M, Hakim, Alan, Dennison, Elaine, Liu, Yongmei, Power, Chris, Stevens, Helen E, Jaana, Laitinen, Vasan, Ramachandran S, Soranzo, Nicole, Bojunga, Jörg, Psaty, Bruce M, Lorentzon, Mattias, Foroud, Tatiana, Harris, Tamara B, Hofman, Albert, Jansson, John-Olov, Cauley, Jane A, Uitterlinden, Andre G, Gibson, Quince, Järvelin, Marjo-Riitta, Karasik, David, Siscovick, David S, Econs, Michael J, Kritchevsky, Stephen B, Florez, Jose C, Todd, John A, Dupuis, Josee, Hyppönen, Elina, and Spector, Timothy D

Published
2010
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