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LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00003841naa a2200733 4500
001oai:prod.swepub.kib.ki.se:124979532
003SwePub
008240701s2012 | |||||||||||000 ||eng|
024a http://kipublications.ki.se/Default.aspx?queryparsed=id:1249795322 URI
024a https://doi.org/10.2337/db11-15152 DOI
040 a (SwePub)ki
041 a engb eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
100a Billings, LK4 aut
2451 0a Impact of common variation in bone-related genes on type 2 diabetes and related traits
264 c 2012-07-17
264 1b American Diabetes Association,c 2012
520 a Exploring genetic pleiotropy can provide clues to a mechanism underlying the observed epidemiological association between type 2 diabetes and heightened fracture risk. We examined genetic variants associated with bone mineral density (BMD) for association with type 2 diabetes and glycemic traits in large well-phenotyped and -genotyped consortia. We undertook follow-up analysis in ∼19,000 individuals and assessed gene expression. We queried single nucleotide polymorphisms (SNPs) associated with BMD at levels of genome-wide significance, variants in linkage disequilibrium (r2 > 0.5), and BMD candidate genes. SNP rs6867040, at the ITGA1 locus, was associated with a 0.0166 mmol/L (0.004) increase in fasting glucose per C allele in the combined analysis. Genetic variants in the ITGA1 locus were associated with its expression in the liver but not in adipose tissue. ITGA1 variants appeared among the top loci associated with type 2 diabetes, fasting insulin, β-cell function by homeostasis model assessment, and 2-h post–oral glucose tolerance test glucose and insulin levels. ITGA1 has demonstrated genetic pleiotropy in prior studies, and its suggested role in liver fibrosis, insulin secretion, and bone healing lends credence to its contribution to both osteoporosis and type 2 diabetes. These findings further underscore the link between skeletal and glucose metabolism and highlight a locus to direct future investigations.
700a Hsu, YH4 aut
700a Ackerman, RJ4 aut
700a Dupuis, J4 aut
700a Voight, BF4 aut
700a Rasmussen-Torvik, LJ4 aut
700a Hercberg, S4 aut
700a Lathrop, M4 aut
700a Barnes, D4 aut
700a Langenberg, C4 aut
700a Hui, JN4 aut
700a Fu, M4 aut
700a Bouatia-Naji, N4 aut
700a Lecoeur, C4 aut
700a An, P4 aut
700a Magnusson, PKu Karolinska Institutet4 aut
700a Surakka, I4 aut
700a Ripatti, S4 aut
700a Christiansen, L4 aut
700a Dalgard, C4 aut
700a Folkersen, L4 aut
700a Grundberg, E4 aut
700a Eriksson, Pu Karolinska Institutet4 aut
700a Kaprio, J4 aut
700a Kyvik, KO4 aut
700a Pedersen, NLu Karolinska Institutet4 aut
700a Borecki, IB4 aut
700a Province, MA4 aut
700a Balkau, B4 aut
700a Froguel, P4 aut
700a Shuldiner, AR4 aut
700a Palmer, LJ4 aut
700a Wareham, N4 aut
700a Meneton, P4 aut
700a Johnson, T4 aut
700a Pankow, JS4 aut
700a Karasik, D4 aut
700a Meigs, JB4 aut
700a Kiel, DP4 aut
700a Florez, JC4 aut
710a Karolinska Institutet4 org
773t Diabetesd : American Diabetes Associationg 61:8, s. 2176-2186q 61:8<2176-2186x 1939-327Xx 0012-1797
856u https://diabetes.diabetesjournals.org/content/diabetes/61/8/2176.full.pdf
8564 8u http://kipublications.ki.se/Default.aspx?queryparsed=id:124979532
8564 8u https://doi.org/10.2337/db11-1515

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