TY - JOUR
T1 - The relationship between plasma adiponectin concentration and insulin resistance is altered in smokers
AU - Abbasi, Fahim
AU - Farin, Helke M.F.
AU - Lamendola, Cindy
AU - McLaughlin, Tracey
AU - Schwartz, Eric A.
AU - Reaven, Gerald M.
AU - Reaven, Peter D.
N1 - Funding Information:
This work was supported by the Tobacco-Related Disease Research Program (12RT-0159), the National Insitutes of Health/Stanford Vascular Biology and Medicine Training Grant (5 T32 HL07708), Grant RR-00070 from the National Institutes of Health, and resources and use of the facilities at the Carl T. Hayden Veterans Affairs Medical Center (Phoenix, Arizona).
PY - 2006/12
Y1 - 2006/12
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=33845484032&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=33845484032&partnerID=8YFLogxK
U2 - 10.1210/jc.2006-0419
DO - 10.1210/jc.2006-0419
M3 - Article
C2 - 17003098
AN - SCOPUS:33845484032
SN - 0021-972X
VL - 91
SP - 5002
EP - 5007
JO - Journal of Clinical Endocrinology and Metabolism
JF - Journal of Clinical Endocrinology and Metabolism
IS - 12
ER -