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The Relationship between Plasma Adiponectin Concentration and Insulin Resistance Is Altered in Smokers

Department of Medicine (F.A., H.M.F.F., C.L., T.M., G.M.R.), Stanford University School of Medicine, Stanford, California 94305; and Medical Research Service (E.A.S., P.D.R.), Division of Endocrinology and Metabolism, Department of Medicine, Carl T. Hayden Veterans Affairs Medical Center, Phoenix, Arizona 85012

Address all correspondence and requests for reprints to: Peter Reaven, M.D., Division of Endocrinology and Metabolism, Department of Medicine (CS-111E), Carl T. Hayden Veterans Affairs Medical Center, 650 East Indian School Road, Phoenix, Arizona 85012. E-mail: peter.reaven{at}med.va.gov.

Context: Low plasma adiponectin concentrations in smokers may contribute to the adverse consequences that occur in these individuals.

Objective: The objective of the study was to define the relationship among smoking, plasma adiponectin concentrations, insulin resistance, and inflammation.

Design: This was a cross-sectional, observational study with a 2 x 2 factorial design and a prospective longitudinal arm.

Setting: The study was conducted at a general clinical research center.

Participants: Apparently healthy smokers (n = 30) and nonsmokers (n = 30), subdivided into insulin resistant (IR) (n = 15) and insulin sensitive (IS) (n = 15) subgroups participated in the study.

Intervention: Intervention included pioglitazone administration for 3 months to 12 IR smokers and eight IS smokers.

Main Outcome Measures: Measures included fasting plasma adiponectin and C-reactive protein (CRP) concentrations and changes in adiponectin after pioglitazone treatment in IR and IS smokers.

Results: Being either a smoker or having insulin resistance was independently associated with lower adiponectin concentrations (P = 0.046 and 0.001, respectively). The difference in mean adiponectin concentration between smokers and nonsmokers did not depend on the insulin resistance status of the subjects. No difference was detected in average CRP concentrations between smokers and nonsmokers (P = 0.18) and between IR and IS subjects (P = 0.13). CRP concentrations were unrelated to adiponectin in smokers (r = –0.05, P = 0.78) and nonsmokers (r = 0.03, P = 0.86). Finally, pioglitazone treatment increased adiponectin concentrations in both IR (P < 0.001) and IS smokers (P = 0.001).

Conclusions: Plasma adiponectin concentrations are lower in smokers and IR subjects and are unrelated to CRP concentrations. These findings suggest that low levels of adiponectin in smokers may be independent of both insulin resistance and a generalized inflammatory response.

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