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dc.contributor.authorStefan, Norberten_US
dc.contributor.authorSun, Qien_US
dc.contributor.authorFritsche, Andreasen_US
dc.contributor.authorMachann, Jürgenen_US
dc.contributor.authorSchick, Fritzen_US
dc.contributor.authorGerst, Feliciaen_US
dc.contributor.authorJeppesen, Charlotteen_US
dc.contributor.authorJoost, Hans-Georgen_US
dc.contributor.authorHu, Frank B.en_US
dc.contributor.authorBoeing, Heineren_US
dc.contributor.authorUllrich, Susanneen_US
dc.contributor.authorHäring, Hans-Ulrichen_US
dc.contributor.authorSchulze, Matthias B.en_US
dc.date.accessioned2014-04-11T14:11:03Z
dc.date.issued2014en_US
dc.identifier.citationStefan, N., Q. Sun, A. Fritsche, J. Machann, F. Schick, F. Gerst, C. Jeppesen, et al. 2014. “Impact of the Adipokine Adiponectin and the Hepatokine Fetuin-A on the Development of Type 2 Diabetes: Prospective Cohort- and Cross-Sectional Phenotyping Studies.” PLoS ONE 9 (3): e92238. doi:10.1371/journal.pone.0092238. http://dx.doi.org/10.1371/journal.pone.0092238.en
dc.identifier.issn1932-6203en
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:12064378
dc.description.abstractBackground: Among adipokines and hepatokines, adiponectin and fetuin-A were consistently found to predict the incidence of type 2 diabetes, both by regulating insulin sensitivity. Objective: To determine to what extent circulating adiponectin and fetuin-A are independently associated with incident type 2 diabetes in humans, and the major mechanisms involved. Methods: Relationships with incident diabetes were tested in two cohort studies: within the European Prospective Investigation into Cancer and Nutrition (EPIC)-Potsdam study (628 cases) and the Nurses' Health Study (NHS; 470 cases). Relationships with body fat compartments, insulin sensitivity and insulin secretion were studied in the Tübingen Lifestyle Intervention Program (TULIP; N = 358). Results: Circulating adiponectin and fetuin-A, independently of several confounders and of each other, associated with risk of diabetes in EPIC-Potsdam (RR for 1 SD: adiponectin: 0.45 [95% CI 0.37–0.54], fetuin-A: 1.18 [1.05–1.32]) and the NHS (0.51 [0.42–0.62], 1.35 [1.16–1.58]). Obesity measures considerably attenuated the association of adiponectin, but not of fetuin-A. Subjects with low adiponectin and concomitantly high fetuin-A had the highest risk. Whereas both proteins were independently (both p<1.8×10−7) associated with insulin sensitivity, circulating fetuin-A (r = −0.37, p = 0.0004), but not adiponectin, associated with insulin secretion in subjects with impaired glucose tolerance. Conclusions: We provide novel information that adiponectin and fetuin-A independently of each other associate with the diabetes risk. Furthermore, we suggest that they are involved in the development of type 2 diabetes via different mechanisms, possibly by mediating effects of their source tissues, expanded adipose tissue and nonalcoholic fatty liver.en
dc.language.isoen_USen
dc.publisherPublic Library of Scienceen
dc.relation.isversionofdoi:10.1371/journal.pone.0092238en
dc.relation.hasversionhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC3958485/pdf/en
dash.licenseLAAen_US
dc.subjectBiology and Life Sciencesen
dc.subjectBiochemistryen
dc.subjectHormonesen
dc.subjectInsulinen
dc.subjectNutritionen
dc.subjectPhysiologyen
dc.subjectPhysiological Parametersen
dc.subjectBody Weighten
dc.subjectObesityen
dc.subjectEndocrine Physiologyen
dc.subjectMedicine and Health Sciencesen
dc.subjectEndocrinologyen
dc.subjectDiabetic Endocrinologyen
dc.subjectMetabolic Disordersen
dc.subjectDiabetes Mellitusen
dc.subjectType 2 Diabetesen
dc.subjectEpidemiologyen
dc.subjectBiomarker Epidemiologyen
dc.subjectCardiovascular Disease Epidemiologyen
dc.subjectGastroenterology and Hepatologyen
dc.subjectLiver Diseasesen
dc.subjectNonalcoholic Steatohepatitisen
dc.titleImpact of the Adipokine Adiponectin and the Hepatokine Fetuin-A on the Development of Type 2 Diabetes: Prospective Cohort- and Cross-Sectional Phenotyping Studiesen
dc.typeJournal Articleen_US
dc.description.versionVersion of Recorden
dc.relation.journalPLoS ONEen
dash.depositing.authorSun, Qien_US
dc.date.available2014-04-11T14:11:03Z
dc.identifier.doi10.1371/journal.pone.0092238*
dash.authorsorderedfalse
dash.contributor.affiliatedSun, Qi
dash.contributor.affiliatedHu, Frank


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