Association of inflammation with worsening HOMA-insulin resistance

K. Park, Michael W Steffes, D. H. Lee, John H Himes, David R Jacobs Jr

Research output: Contribution to journalArticle

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Abstract

Aims/hypothesis: We examined the cross-sectional and longitudinal relationships between C-reactive protein (CRP), a marker of low-grade inflammation, and insulin resistance and whether the association was independent of obesity and oxidative stress. Methods: CRP and insulin resistance (homeostasis model assessment of insulin resistance [HOMA-IR]) data were obtained in a population-based, prospective observational study, Coronary Artery Risk Development in Young Adults (CARDIA), during 1992-2006. Results: CRP showed a significant positive association with insulin resistance, both cross-sectionally and longitudinally (5 year follow-up). The estimated increment in HOMA-IR was 0.34 log e (pmol/l×[mmol/l]/156.25) (p value for trend <0.0001) in the highest vs lowest CRP quartiles in cross-sectional analysis, whereas the corresponding estimate was 0.12 (p trend <0.0001) in the highest vs lowest CRP quartiles longitudinally over 5 years. The gradient of HOMA-IR across CRP was attenuated but remained statistically significant after controlling for body fat measurements (0.06 in the highest vs lowest CRP in both cross-sectional [p value for trend=0.001] and longitudinal analyses [p value for trend=0.01]), and was little changed by further adjustment for oxidative stress markers (F2-isoprostanes and oxidised LDL). There were consistent increments in the levels of HOMA-IR with increasing concentrations of CRP over time. In contrast, higher HOMA-IR did not predict future increases in CRP. Findings were similar using fibrinogen as the predictor variable. Conclusions/interpretation: Although a substantial portion of this association was explained by obesity, CRP was independently related to concurrent and future insulin resistance.

Original languageEnglish (US)
Pages (from-to)2337-2344
Number of pages8
JournalDiabetologia
Volume52
Issue number11
DOIs
StatePublished - Nov 1 2009

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C-Reactive Protein
Insulin Resistance
Inflammation
Homeostasis
Oxidative Stress
Obesity
F2-Isoprostanes
Fibrinogen
Observational Studies
Adipose Tissue
Young Adult
Coronary Vessels
Cross-Sectional Studies
Prospective Studies

Keywords

  • Inflammation
  • Insulin resistance
  • Obesity

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Association of inflammation with worsening HOMA-insulin resistance. / Park, K.; Steffes, Michael W; Lee, D. H.; Himes, John H; Jacobs Jr, David R.

In: Diabetologia, Vol. 52, No. 11, 01.11.2009, p. 2337-2344.

Research output: Contribution to journalArticle

Park, K. ; Steffes, Michael W ; Lee, D. H. ; Himes, John H ; Jacobs Jr, David R. / Association of inflammation with worsening HOMA-insulin resistance. In: Diabetologia. 2009 ; Vol. 52, No. 11. pp. 2337-2344.
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AB - Aims/hypothesis: We examined the cross-sectional and longitudinal relationships between C-reactive protein (CRP), a marker of low-grade inflammation, and insulin resistance and whether the association was independent of obesity and oxidative stress. Methods: CRP and insulin resistance (homeostasis model assessment of insulin resistance [HOMA-IR]) data were obtained in a population-based, prospective observational study, Coronary Artery Risk Development in Young Adults (CARDIA), during 1992-2006. Results: CRP showed a significant positive association with insulin resistance, both cross-sectionally and longitudinally (5 year follow-up). The estimated increment in HOMA-IR was 0.34 log e (pmol/l×[mmol/l]/156.25) (p value for trend <0.0001) in the highest vs lowest CRP quartiles in cross-sectional analysis, whereas the corresponding estimate was 0.12 (p trend <0.0001) in the highest vs lowest CRP quartiles longitudinally over 5 years. The gradient of HOMA-IR across CRP was attenuated but remained statistically significant after controlling for body fat measurements (0.06 in the highest vs lowest CRP in both cross-sectional [p value for trend=0.001] and longitudinal analyses [p value for trend=0.01]), and was little changed by further adjustment for oxidative stress markers (F2-isoprostanes and oxidised LDL). There were consistent increments in the levels of HOMA-IR with increasing concentrations of CRP over time. In contrast, higher HOMA-IR did not predict future increases in CRP. Findings were similar using fibrinogen as the predictor variable. Conclusions/interpretation: Although a substantial portion of this association was explained by obesity, CRP was independently related to concurrent and future insulin resistance.

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