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Association of variation in the interleukin-1 gene family with diabetes and glucose homeostasis.
J. Clin. Endocrinol. Metab. 94, 4575-4583 (2009)
Objective: Proinflammatory cytokine IL-1 beta is capable of decreasing insulin-induced glucose transport. Therefore, we hypothesized that genetic variation in the IL-1 gene family is associated with measures of glucose homeostasis and diabetes. Design and Outcome Measures: Fifteen haplotype-tagging single-nucleotide polymorphisms in the IL-1 alpha, IL-1 beta, and IL-1 receptor antagonist genes were determined in a Finnish population survey (n = 6771). Glucose and insulin concentrations were measured, and indices of insulin resistance and beta-cell function were calculated using the homeostasis model assessment. Two-hour oral glucose tolerance tests were carried out on a subsample of 1390 participants. Associations with prevalent diabetes were tested for replication in a sample of European myocardial infarction survivors (n = 972). Results: The minor allele of the IL-1 beta rs1143634(G -> A) was associated with higher blood glucose than the major allele: 5.37, 5.41, and 5.48 mmol/liter for the GG, AG, and AA genotypes, respectively (multivariate adjusted P for trend < 0.0001; Bonferroni corrected P = 0.00096). The 2-h glucose was also higher (6.45 and 7.20 mmol/liter for the GG vs. AA; P = 0.003, Bonferroni corrected P = 0.045). The haplotype ACG of rs1143634, rs3917356, and rs16944 associated with higher glucose, higher homeostasis model assessment for insulin resistance index, higher 2-h insulin, and prevalent diabetes (adjusted rate ratio = 1.54; 95% confidence interval = 1.03-2.30; P = 0.037). The association with prevalent diabetes was replicated among European myocardial infarction survivors (rate ratio = 2.09; 95% confidence interval = 1.17-3.76; P = 0.013). Conclusions: These results suggest that genetic variation in the IL-1 gene family is associated with measures of glucose homeostasis and prevalent diabetes.
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Publikationstyp
Artikel: Journalartikel
Dokumenttyp
Wissenschaftlicher Artikel
Schlagwörter
insulin-resistance; type-2; mellitus; genome; inflammation; adipocytes; antagonist; mechanisms; calpain-10; variants
ISSN (print) / ISBN
0021-972X
e-ISSN
1945-7197
Quellenangaben
Band: 94,
Heft: 11,
Seiten: 4575-4583
Verlag
Endocrine Society
Verlagsort
Bethesda, Md.
Nichtpatentliteratur
Publikationen
Begutachtungsstatus
Peer reviewed
Institut(e)
Institute of Epidemiology (EPI)