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 http://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, firstname.lastname@example.org).
Requests for Single Reprints: Frank Hu, MD, PhD, Department of Nutrition, Harvard School of Public Health, 665 Huntington Avenue, Boston, MA 02215; e-mail, email@example.com.
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.
Heidemann C, Sun Q, van Dam RM, Meigs JB, Zhang C, Tworoger SS, 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: 10.7326/0003-4819-149-5-200809020-00005
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Published: Ann Intern Med. 2008;149(5):307-316.
Excess adiposity is a major modifiable risk factor for type 2 diabetes (1). Adipose tissue is an important metabolically active endocrine organ that secretes various hormones and cytokines, known as adipokines(2). These adipokines, particularly adiponectin and resistin, may provide a molecular link between adiposity and type 2 diabetes (3, 4).
Adiponectin is a collagen-like protein that is exclusively synthesized by adipocytes (5) and circulates at relatively high concentrations of 2 to 30 μg/mL in blood (3, 6). Unlike other adipokines, concentrations of adiponectin are paradoxically reduced in persons who are obese compared with lean persons (3, 6). There is no clear explanation for this inverse association, but in vitro and in vivo studies suggest that endogenous inflammatory cytokines, such as interleukin-6, interleukin-8, and tumor necrosis factor-α, which are elevated in obesity, may inhibit the production of adiponectin (7). In addition, prospective studies have consistently found a decreased risk for type 2 diabetes with increasing concentrations of total adiponectin (8–18). However, adiponectin exists in plasma as a trimer, a hexamer, and a high-molecular-weight form (2, 6). Recent evidence suggests that high-molecular-weight adiponectin is the most biologically active form of the hormone (6), but few epidemiologic studies have investigated high-molecular-weight adiponectin separately from total adiponectin (18–20).
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Cardiology, Endocrine and Metabolism, Diabetes, Coronary Risk Factors.
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