Christin Heidemann, DrPH, MSc; Qi Sun, MD, ScD; Rob M. van Dam, PhD; James B. Meigs, MD, MPH; Cuilin Zhang, MD, PhD; Shelley S. Tworoger, PhD; Christos S. Mantzoros, MD, DSc; Frank B. Hu, MD, PhD
Grant Support: By the National Institutes of Health and the Intramural Research Program of the National Institute of Child Health & Human Development (grants CA87969, DK58845 and DK58785). Dr. Heidemann was supported by fellowships of the German Academic Exchange Service and the Hans & Eugenia Juetting Foundation. Dr. Meigs received a Career Development Award from the American Diabetes. Dr. Mantzoros was supported by discretionary grants from the Tanita Corporation and Beth Israel Deaconess Medical Center.
Potential Financial Conflicts of Interest: None disclosed.
Reproducible Research Statement:Study protocol: Available at www.channing.harvard.edu/nhs. Statistical code and data set: Available subject to approval by the Nurses' Health Study committees by contacting Dr. Hu (e-mail, email@example.com).
Requests for Single Reprints: Frank Hu, MD, PhD, Department of Nutrition, Harvard School of Public Health, 665 Huntington Avenue, Boston, MA 02215; e-mail, firstname.lastname@example.org.
Current Author Addresses: Dr. Heidemann: Department of Epidemiology & Health Reporting, Robert Koch Institute, Seestrasse 10, 13353 Berlin, Germany.
Drs. Sun, van Dam, and Hu: Department of Nutrition, Harvard School of Public Health, 665 Huntington Avenue, Boston, MA 02115.
Dr. Meigs: General Medicine Division, Massachusetts General Hospital, 50 Staniford Street, Boston, MA 02114.
Dr. Zhang: Division of Epidemiology, Statistics & Prevention Research, National Institute of Child Health & Human Development, National Institutes of Health, 6100 Executive Boulevard, Room 7B03, MSC 7510, 9000 Rockville Pike, Bethesda, MD 20892-7510.
Dr. Tworoger: Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, 181 Longwood Avenue, 3rd Floor, Boston, MA 02115.
Dr. Mantzoros: Division of Endocrinology, Diabetes and Metabolism, Beth Israel Deaconess Medical Center and Harvard Medical School, ST 816, 330 Brookline Avenue, Boston, MA 02215.
Author Contributions: Conception and design: C. Heidemann, R.M. van Dam, J.B. Meigs, C.S. Mantzoros, F.B. Hu.
Analysis and interpretation of the data: C. Heidemann, Q. Sun, S.S. Tworoger, F.B. Hu.
Drafting of the article: C. Heidemann, C. Zhang, F.B. Hu.
Critical revision of the article for important intellectual content: Q. Sun, R.M. van Dam, J.B. Meigs, S.S. Tworoger, C.S. Mantzoros, F.B. Hu.
Final approval of the article: C. Heidemann, Q. Sun, R.M. van Dam, J.B. Meigs, C. Zhang, S.S. Tworoger, C.S. Mantzoros, F.B. Hu.
Provision of study materials or patients: S.S. Tworoger, C.S. Mantzoros.
Statistical expertise: C. Heidemann, Q. Sun, S.S. Tworoger.
Obtaining of funding: J.B. Meigs, F.B. Hu.
Administrative, technical, or logistic support: F.B. Hu.
Collection and assembly of data: S.S. Tworoger, C.S. Mantzoros, F.B. Hu.
Adiponectin and resistin are recently discovered adipokines that may provide a molecular link between adiposity and type 2 diabetes.
To evaluate whether total and high-molecular-weight adiponectin and resistin are associated with future risk for type 2 diabetes, independent of obesity and other known diabetes risk factors.
Prospective, nested, case–control study.
1038 initially healthy women of the Nurses' Health Study who developed type 2 diabetes after blood sampling (1989 to 1990) through 2002 and 1136 matched control participants.
Plasma concentrations of total and high-molecular-weight adiponectin and resistin.
In multivariate models including body mass index, higher total and high-molecular-weight adiponectin levels were associated with a substantially lower risk for type 2 diabetes (odds ratio [OR] comparing the highest with the lowest quintiles, 0.17 [95% CI, 0.12 to 0.25] for total adiponectin and 0.10 [CI, 0.06 to 0.15] for high-molecular-weight adiponectin). A higher ratio of high-molecular-weight to total adiponectin was associated with a statistically significantly lower risk even after adjustment for total adiponectin (OR, 0.45 [CI, 0.31 to 0.65]). In the multivariate model without body mass index, higher resistin levels were associated with a higher risk for diabetes (OR, 1.68 [CI, 1.25 to 2.25]), but the association was no longer statistically significant after adjustment for body mass index (OR, 1.28 [CI, 0.93 to 1.76]).
The findings apply mainly to white women and could be partly explained by residual confounding from imperfectly measured or unmeasured variables.
Adiponectin is strongly and inversely associated with risk for diabetes, independent of body mass index, whereas resistin is not. The ratio of high-molecular-weight to total adiponectin is related to risk for diabetes independent of total adiponectin, suggesting an important role of the relative proportion of high-molecular-weight adiponectin in diabetes pathogenesis.
Heidemann C, Sun Q, van Dam RM, et al. Total and High-Molecular-Weight Adiponectin and Resistin in Relation to the Risk for Type 2 Diabetes in Women. Ann Intern Med. 2008;149:307–316. doi: https://doi.org/10.7326/0003-4819-149-5-200809020-00005
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Published: Ann Intern Med. 2008;149(5):307-316.
Cardiology, Coronary Risk Factors, Diabetes, Endocrine and Metabolism.
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