Journal
PLOS ONE
Volume 9, Issue 3, Pages -Publisher
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0092238
Keywords
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Categories
Funding
- Federal Ministry of Science, Germany [01 EA 9401]
- European Union [SOC 95201408 05F02]
- German Cancer Aid [70-2488-Ha I]
- European Community [SOC 98200769 05F02]
- National Institutes of Health [CA87969, CA4449, DK58845, DK58785, P30 DK46200]
- National Heart, Lung, and Blood Institute [K99HL098459]
- Pilot and Feasibility program
- Boston Obesity Nutrition Research Center [DK46200]
- German Research Foundation (DFG) [KFO 114, STE 1096/3-1]
- German Federal Ministry of Education and Research
- Diabetes Stiftung [270-07-10]
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Background: 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 Tubingen 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 < 1.8x10(-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.
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