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Published on: January 4, 2018
Association of inflammation with worsening HOMA-insulin resistance
1Division of Epidemiology and Community Health, School of Public Health, University of Minnesota, 1300 South 2nd Street, Suite 300, Minneapolis, MN 55454, USA.
Insights
C-reactive protein (CRP) is linked to insulin resistance. Even after accounting for obesity, CRP independently predicts current and future insulin resistance, highlighting its role in metabolic health.
Area of Science:
- Biomedical research
- Metabolic health
- Inflammation markers
Background:
- Low-grade inflammation, indicated by C-reactive protein (CRP), is increasingly recognized as a factor in metabolic dysfunction.
- Insulin resistance is a key precursor to type 2 diabetes and cardiovascular disease.
Purpose of the Study:
- To investigate the cross-sectional and longitudinal associations between C-reactive protein (CRP) and insulin resistance.
- To determine if these associations are independent of obesity and oxidative stress.
Main Methods:
- Utilized data from the Coronary Artery Risk Development in Young Adults (CARDIA) study (1992-2006).
- Measured C-reactive protein (CRP) and insulin resistance via homeostasis model assessment (HOMA-IR).
- Employed cross-sectional and longitudinal (5-year follow-up) analyses, controlling for body fat and oxidative stress markers.
Main Results:
- A significant positive association was observed between CRP and insulin resistance, both cross-sectionally and longitudinally.
- The association between CRP and HOMA-IR remained statistically significant after adjusting for body fat and oxidative stress.
- Higher CRP levels consistently predicted increased HOMA-IR over time, but not vice versa.
Conclusions:
- C-reactive protein (CRP) is independently associated with concurrent and future insulin resistance.
- Obesity explains a significant portion of the CRP-insulin resistance link, but does not fully account for it.
- Findings suggest CRP is a valuable marker for predicting insulin resistance beyond its association with adiposity.
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 x [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 (F(2)-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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