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Circulating Adiponectin and Resistin Levels in Relation to Metabolic Factors, Inflammatory Markers, and Vascular Reactivity in Diabetic Patients and Subjects at Risk for Diabetes

¹ Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts
² Microcirculation Laboratory, Beth Israel Deaconess Medical Center West Campus, Harvard Medical School, Boston, Massachusetts
³ Joslin Diabetes Center, Harvard Medical School, Boston, Massachusetts

Address correspondence and reprint requests to Christos S. Mantzoros, MD, Division of Endocrinology, Diabetes and Metabolism, Department of Internal Medicine, Beth Israel Deaconess Medical Center, Harvard Medical School, 99 Brookline Ave., RN 325A, Boston, MA 02215. E-mail: cmantzor{at}bidmc.harvard.edu

OBJECTIVE—Adiponectin and resistin, two recently discovered adipocyte-secreted hormones, may link obesity with insulin resistance and/or metabolic and cardiovascular risk factors. We performed a cross-sectional study to investigate the association of adiponectin and resistin with inflammatory markers, hyperlipidemia, and vascular reactivity and an interventional study to investigate whether atorvastatin mediates its beneficial effects by altering adiponectin or resistin levels.

RESEARCH DESIGN AND METHODS—Associations among vascular reactivity, inflammatory markers, resistin, and adiponectin were assessed cross-sectionally using fasting blood samples obtained from 77 subjects who had diabetes or were at high risk to develop diabetes. The effect of atorvastatin on adiponectin and resistin levels was investigated in a 12-week-long randomized, double-blind, placebo-controlled study.

RESULTS—In the cross-sectional study, we confirm prior positive correlations of adiponectin with HDL and negative correlations with BMI, triglycerides, C-reactive protein (CRP), and plasma activator inhibitor (PAI)-1 and report a negative correlation with tissue plasminogen activator. The positive association with HDL and the negative association with PAI-1 remained significant after adjusting for sex and BMI. We also confirm prior findings of a negative correlation of resistin with HDL and report for the first time a positive correlation with CRP. All of these associations remained significant after adjusting for sex and BMI. No associations of adiponectin or resistin with any aspects of vascular reactivity were detected. In the interventional study, atorvastatin decreased lipid and CRP levels, but adiponectin and resistin were not specifically altered.

CONCLUSIONS—We conclude that adiponectin is significantly associated with inflammatory markers, in part, through an underlying association with obesity, whereas resistin’s associations with inflammatory markers appear to be independent of BMI. Lipid profile and inflammatory marker changes produced by atorvastatin cannot be attributed to changes of either adiponectin or resistin.

Abbreviations: ACH%, acetylcholine chloride with percentage increase over baseline of endothelium-dependent vasodilation • CRP, C-reactive protein • ET1, endothelin-1 • ICAM, intracellular adhesion molecule • NID, nitroglycerin-induced dilation • NNP%, sodium nitroprusside with percentage increase over baseline of endothelium-independent vasodilation • PAI, plasma activator inhibitor • TNF-, tumor necrosis factor- • tPA, tissue plasminogen activator

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