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Circulating Resistin Levels Are Not Associated with Obesity or Insulin Resistance in Humans and Are Not Regulated by Fasting or Leptin Administration: Cross-Sectional and Interventional Studies in Normal, Insulin-Resistant, and Diabetic Subjects

Division of Endocrinology, Diabetes, and Metabolism (J.H.L., J.L.C., C.O., C.S.M.), Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts 02215; Harokopio University (N.Y., M.K.), Athens, Greece 17671; Division of Endocrinology (E.E.), Connecticut Children’s Medical Center, University of Connecticut School of Medicine, Hartford, Connecticut 06106; and Preventative Cardiology Program (R.S.), Division of Cardiology, Hartford Hospital, Hartford, Connecticut 06102

Address all correspondence and requests for reprints to: Christos S. Mantzoros, M.D., Division of Endocrinology, Diabetes, and Metabolism, Department of Internal Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Stoneman 816, Boston, Massachusetts 02215. E-mail: cmantzor{at}bidmc.harvard.edu.

Resistin is a novel adipocyte-secreted hormone proposed to link obesity with diabetes. Studies in mice have revealed conflicting data however, and the physiological role of circulating resistin in humans remains unknown. We conducted cross-sectional studies in 123 middle-aged women and 120 healthy young subjects and found that serum resistin levels did not correlate with markers of adiposity, including body mass index, waist-to-hip ratio, or fat mass, or insulin resistance assessed by homeostasis model, lipid profile, or serum leptin levels; but females had higher resistin levels than males (P < 0.02). We also found no difference in serum resistin levels between lean healthy and obese insulin-resistant nondiabetic and type 2 diabetic adolescents. Finally, to evaluate the effect of food deprivation and/or leptin administration on resistin levels, we performed interventional studies that revealed no significant difference in resistin levels after 48 h of fasting and/or leptin administration at either physiological or pharmacological doses. We conclude that circulating resistin is unlikely to play a major role in insulin resistance or energy homeostasis in humans.

This work was supported by National Institute of Diabetes and Digestive and Kidney Diseases Grant DK 58785; National Institutes of Health Grants MO1-RR01032, K30-HL04095, and 5T32DK07516-18; Amgen grant (to C.S.M.); and an Eli Lilly and Co. fellowship award.

Abbreviations: BIA, Bioelectrical impedance analysis; BMI, body mass index; CV, coefficient of variation; DEXA, dual-energy x-ray absorptiometry; FM, fat mass; %FM, percent fat mass; HOMA, homeostasis model assessment; IR, insulin resistance; RELM, resistin-like molecule; r-metHuLeptin, recombinant methionyl human leptin; T2DM, type 2 diabetes; TZD, thiazolidinedione; WC, waist circumference; WHR, waist-hip ratio.

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