The relationship between plasma adiponectin concentration and insulin resistance is altered in smokers

Fahim Abbasi, Helke M.F. Farin, Cindy Lamendola, Tracey McLaughlin, Eric A. Schwartz, Gerald M. Reaven, Peter D. Reaven

Research output: Contribution to journalArticle

31 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)5002-5007
Number of pages6
JournalJournal of Clinical Endocrinology and Metabolism
Volume91
Issue number12
DOIs
StatePublished - Dec 2006
Externally publishedYes

Fingerprint

Adiponectin
Insulin Resistance
Insulin
Plasmas
pioglitazone
C-Reactive Protein
Observational Studies
Fasting
Healthy Volunteers
Cross-Sectional Studies
Smoking
Outcome Assessment (Health Care)
Inflammation

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Biochemistry
  • Endocrinology
  • Clinical Biochemistry
  • Biochemistry, medical

Cite this

The relationship between plasma adiponectin concentration and insulin resistance is altered in smokers. / Abbasi, Fahim; Farin, Helke M.F.; Lamendola, Cindy; McLaughlin, Tracey; Schwartz, Eric A.; Reaven, Gerald M.; Reaven, Peter D.

In: Journal of Clinical Endocrinology and Metabolism, Vol. 91, No. 12, 12.2006, p. 5002-5007.

Research output: Contribution to journalArticle

Abbasi, Fahim ; Farin, Helke M.F. ; Lamendola, Cindy ; McLaughlin, Tracey ; Schwartz, Eric A. ; Reaven, Gerald M. ; Reaven, Peter D. / The relationship between plasma adiponectin concentration and insulin resistance is altered in smokers. In: Journal of Clinical Endocrinology and Metabolism. 2006 ; Vol. 91, No. 12. pp. 5002-5007.
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abstract = "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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AU - Abbasi, Fahim

AU - Farin, Helke M.F.

AU - Lamendola, Cindy

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AU - Reaven, Gerald M.

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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.

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