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@ARTICLE{Krger:141710,
      author       = {J. Kröger and K. Meidtner and N. Stefan and M. Guevara and
                      N. D. Kerrison and E. Ardanaz and D. Aune and H. Boeing and
                      M. Dorronsoro and C. Dow and G. Fagherazzi and P. W. Franks
                      and H. Freisling and M. J. Gunter and J. M. Huerta and R.
                      Kaaks$^*$ and T. J. Key and K. T. Khaw and V. Krogh and T.
                      Kühn$^*$ and F. R. Mancini and A. Mattiello and P. M.
                      Nilsson and A. Olsen and K. Overvad and D. Palli and J. R.
                      Quirós and O. Rolandsson and C. Sacerdote and N. Sala and
                      E. Salamanca-Fernández and I. Sluijs and A. M. W.
                      Spijkerman and A. Tjonneland and K. K. Tsilidis and R.
                      Tumino and Y. T. van der Schouw and N. G. Forouhi and S. J.
                      Sharp and C. Langenberg and E. Riboli and M. B. Schulze and
                      N. J. Wareham},
      title        = {{C}irculating {F}etuin-{A} and {R}isk of {T}ype 2
                      {D}iabetes: {A} {M}endelian {R}andomization {A}nalysis.},
      journal      = {Diabetes},
      volume       = {67},
      number       = {6},
      issn         = {1939-327X},
      address      = {Alexandria, Va},
      publisher    = {Assoc.},
      reportid     = {DKFZ-2018-01981},
      pages        = {1200 - 1205},
      year         = {2018},
      abstract     = {Fetuin-A, a hepatic-origin protein, is strongly positively
                      associated with risk of type 2 diabetes in human
                      observational studies, but it is unknown whether this
                      association is causal. We aimed to study the potential
                      causal relation of circulating fetuin-A to risk of type 2
                      diabetes in a Mendelian randomization study with single
                      nucleotide polymorphisms located in the fetuin-A-encoding
                      AHSG gene. We used data from eight European countries of the
                      European Prospective Investigation into Cancer and Nutrition
                      (EPIC)-InterAct case-cohort study including 10,020 incident
                      cases. Plasma fetuin-A concentration was measured in a
                      subset of 965 subcohort participants and 654 case subjects.
                      A genetic score of the AHSG single nucleotide polymorphisms
                      was strongly associated with fetuin-A $(28\%$ explained
                      variation). Using the genetic score as instrumental variable
                      of fetuin-A, we observed no significant association of a 50
                      µg/mL higher fetuin-A concentration with diabetes risk
                      (hazard ratio 1.02 $[95\%$ CI 0.97, 1.07]). Combining our
                      results with those from the DIAbetes Genetics Replication
                      And Meta-analysis (DIAGRAM) consortium (12,171 case
                      subjects) also did not suggest a clear significant relation
                      of fetuin-A with diabetes risk. In conclusion, although
                      there is mechanistic evidence for an effect of fetuin-A on
                      insulin sensitivity and secretion, this study does not
                      support a strong, relevant relationship between circulating
                      fetuin-A and diabetes risk in the general population.},
      keywords     = {AHSG protein, human (NLM Chemicals) / Biomarkers (NLM
                      Chemicals) / alpha-2-HS-Glycoprotein (NLM Chemicals)},
      cin          = {C020},
      ddc          = {610},
      cid          = {I:(DE-He78)C020-20160331},
      pnm          = {323 - Metabolic Dysfunction as Risk Factor (POF3-323)},
      pid          = {G:(DE-HGF)POF3-323},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:29523632},
      doi          = {10.2337/db17-1268},
      url          = {https://inrepo02.dkfz.de/record/141710},
}