Interaction Between Persistent Organic Pollutants and C-reactive Protein in Estimating Insulin Resistance Among Non-diabetic Adults
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Objectives: Chronic inflammation is now thought to play a key pathogenetic role in the associations of obesity with insulin resistance and diabetes. Based on our recent findings on persistent organic pollutants (POPs) including the lack of an association between obesity and either insulin resistance or diabetes prevalence among subjects with very low concentrations of POPs, we hypothesized that POP concentrations may be associated with inflammation and modify the associations between inflammation and insulin resistance in non-diabetic subjects. Methods: Cross-sectional associations among serum POPs, C-reactive protein (CRP), and homeostasis model assessment of insulin resistance (HOMA-IR) were investigated in 748 non-diabetic participants aged ≥20 years. Nineteen types of POPs in 5 subclasses were selected because the POPs were detectable in ≥60% of the participants. Results: Among the five subclasses of POPs, only organochlorine (OC) pesticides showed positive associations with CRP concentrations, while polychlorinated biphenyls (PCBs) showed inverse associations with CRP concentrations. There were statistically significant interactions between CRP and OC pesticides and between CRP and PCBs, in estimating HOMA-IR (P for interaction <0.01 and < 0.01, respectively). CRP was not associated with HOMA-IR among subjects with low concentrations of OC pesticides or PCBs, while CRP was strongly associated with HOMA-IR among subjects with high concentrations of these POPs. Conclusions: In the current study, OC pesticides were associated with increased levels of CRP, a marker of inflammation, and both OC pesticides and PCBs may also modify the associations between CRP and insulin resistance.
Abstract
Objectives: Chronic inflammation is now thought to play a key pathogenetic role in the associations of obesity with insulin resistance and diabetes. Based on our recent findings on persistent organic pollutants (POPs) including the lack of an association between obesity and either insulin resistance or diabetes prevalence among subjects with very low concentrations of POPs, we hypothesized that POP concentrations may be associated with inflammation and modify the associations between inflammation and insulin resistance in non-diabetic subjects. Methods: Cross-sectional associations among serum POPs, C-reactive protein (CRP), and homeostasis model assessment of insulin resistance (HOMA-IR) were investigated in 748 non-diabetic participants aged ≥20 years. Nineteen types of POPs in 5 subclasses were selected because the POPs were detectable in ≥60% of the participants. Results: Among the five subclasses of POPs, only organochlorine (OC) pesticides showed positive associations with CRP concentrations, while polychlorinated biphenyls (PCBs) showed inverse associations with CRP concentrations. There were statistically significant interactions between CRP and OC pesticides and between CRP and PCBs, in estimating HOMA-IR (P for interaction <0.01 and < 0.01, respectively). CRP was not associated with HOMA-IR among subjects with low concentrations of OC pesticides or PCBs, while CRP was strongly associated with HOMA-IR among subjects with high concentrations of these POPs. Conclusions: In the current study, OC pesticides were associated with increased levels of CRP, a marker of inflammation, and both OC pesticides and PCBs may also modify the associations between CRP and insulin resistance.
참고문헌 (28)
- Lee DH, "Association between serum concentrations of persistent organic pollutants and insulin resistance among nondiabetic adults: results from the National Health and Nutrition Examination Survey 1999-2002", Diabetes Care, 30(3), pp.622~628 (2007)
- Lee DH, "A strong dose-response relation between serum concentrations of persistent organic pollutants and diabetes: results from the National Health and Examination Survey 1999-2002", Diabetes Care, 29(7), pp.1638~1644 (2006)
- Lee DH, "Could low-level background exposure to persistent organic pollutants contribute to the social burden of type 2 diabetes?", J Epidemiol Community Health, 60(12), pp.1006~1008 (2006)
- Porta M, "Persistent organic pollutants and the burden of diabetes", Lancet, 368(9535), pp.558~559 (2006)
- Hotamisligil GS, "Inflammation and metabolic disorders", Nature, 444(7121), pp.860~867 (2006)
- Shoelson SE, "Inflammation and insulin resistance", J Clin Invest, 116(7), pp.1793~1801 (2006)
- Tilg H, "Adipocytokines: mediators linking adipose tissue, inflammation and immunity", Nat Rev Immunol, 6(10), pp.772~783 (2006)
- Ganey PE, "Concurrent inflammation as a determinant of susceptibility to toxicity from xenobiotic agents", Toxicology, 169(3), pp.195~208 (2001)
- Laskin DL, "Role of macrophages and inflammatory mediators in chemically induced toxicity", Toxicology, 160(1), pp.111~118 (2001)
- "National Health and Nutrition Examination Survey: NHANES 1999-2000"[URL]
- "National Health and Nutrition Examination Survey: NHANES 2001-2002"[URL]
- "Fourth national report on human exposure to environmental chemicals, updated tables, February 2011" (2011)[URL]
- Turner W, "A fast universal automated cleanup system for the isotope-dilution HRMS analysis of PCDDs, PCDFs, coplanar PCBs, PCB congeners, and persistent pesticides from the same serum sample", Organohalogen Comp, 31, pp.26~31 (1997)
- Korn EL, "Epidemiologic studies utilizing surveys: accounting for the sampling design", Am J Public Health, 81(9), pp.1166~1173 (1991)
- Graubard BI, "Analyzing health surveys for cancer-related objectives", J Natl Cancer Inst, 91(12), pp.1005~1016 (1999)
- Frampton MW, "Systemic and cardiovascular effects of airway injury and inflammation: ultrafine particle exposure in humans", Environ Health Perspect, 109(Suppl 4), pp.529~532 (2001)
- Hennig B, "Proinflammatory properties of coplanar PCBs: in vitro and in vivo evidence", Toxicol Appl Pharmacol, 181(3), pp.174~183 (2002)
- Puga A, "Activation of transcription factors activator protein-1 and nuclear factor-kappaB by 2,3,7,8- tetrachlorodibenzo-p-dioxin", Biochem Pharmacol, 59(8), pp.997~1005 (2000)
- Castell JV, "Interleukin-6 is the major regulator of acute phase protein synthesis in adult human hepatocytes", FEBS Lett, 242(2), pp.237~239 (1989)
- Chen J, "Association between inflammation and insulin resistance in U.S. nondiabetic adults: results from the Third National Health and Nutrition Examination Survey", Diabetes Care, 27(12), pp.2960~2965 (2004)
- Hak AE, "Markers of inflammation and cellular adhesion molecules in relation to insulin resistance in nondiabetic elderly: the Rotterdam study", J Clin Endocrinol Metab, 86(9), pp.4398~4405 (2001)
- Marques-Vidal P, "Prevalence of insulin resistance syndrome in southwestern France and its relationship with inflammatory and hemostatic markers", Diabetes Care, 25(8), pp.1371~1377 (2002)
- Wannamethee SG, "The metabolic syndrome and insulin resistance: relationship to haemostatic and inflammatory markers in older non-diabetic men", Atherosclerosis, 181(1), pp.101~108 (2005)
- McLaughlin T, "Differentiation between obesity and insulin resistance in the association with C-reactive protein", Circulation, 106(23), pp.2908~2912 (2002)
- Devaraj S, "C-reactive protein increases plasminogen activator inhibitor-1 expression and activity in human aortic endothelial cells: implications for the metabolic syndrome and atherothrombosis", Circulation, 107(3), pp.398~404 (2003)
- Campos SP, "Insulin is a prominent modulator of the cytokine-stimulated expression of acute-phase plasma protein genes", Mol Cell Biol, 12(4), pp.1789~1797 (1992)
- Moran A, "Relation of C-reactive protein to insulin resistance and cardiovascular risk factors in youth", Diabetes Care, 28(7), pp.1763~1768 (2005)
- Matthews DR, "Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man", Diabetologia, 28(7), pp.412~419 (1985)