Geertruida J van Woudenbergh1, Despoina Theofylaktopoulou, Anneleen Kuijsten, Isabel Ferreira, Marleen M van Greevenbroek, Carla J van der Kallen, Casper G Schalkwijk, Coen D A Stehouwer, Marga C Ocké, Giel Nijpels, Jacqueline M Dekker, Ellen E Blaak, Edith J M Feskens. 1. Division of Human Nutrition, Wageningen University, Wageningen, Netherlands (GJvW, DT, AK, and EJMF); the CARIM School for Cardiovascular Diseases (IF, MMvG, CJvdK, CGS, and CDAS), the Department of Human Biology (EEB) and the NUTRIM School for Toxicology, Metabolism, and Nutrition (EEB), Maastricht University, Maastricht Netherlands; the Departments of Internal Medicine (IF, MMvG, CJvdK, CGS, and CDAS) and Clinical Epidemiology and Medical Technology Assessment (IF), Maastricht University Medical Center, Maastricht, Netherlands; the National Institute for Public Health and the Environment, Bilthoven, Netherlands (MCO); and the Departments of General Practice (GN) and Epidemiology and Biostatistics (JMD), EMGO Institute for Health and Care Research, Vrije Universiteit University Medical Center, Amsterdam, Netherlands.
Abstract
BACKGROUND: Diet may be associated with the development of type 2 diabetes through its effects on low-grade inflammation. OBJECTIVES: We investigated whether an adapted dietary inflammatory index (ADII) is associated with a summary score for low-grade inflammation and markers of glucose metabolism. In addition, we investigated the mediating role of inflammation in the association between ADII and markers of glucose metabolism. DESIGN: We performed cross-sectional analyses of 2 Dutch cohort studies (n= 1024). An ADII was obtained by multiplying standardized energy-adjusted intakes of dietary components by literature-based dietary inflammatory weights that reflected the inflammatory potential of components. Subsequently, these multiplications were summed. Six biomarkers of inflammation were compiled in a summary score. Associations of the ADII (expressed per SD) with the summary score for inflammation and markers of glucose metabolism were investigated by using multiple linear regression models. Inflammation was considered a potential mediator in the analysis with markers of glucose metabolism. RESULTS: A higher ADII was associated with a higher summary score for inflammation [β-adjusted = 0.04 per SD (95% CI: 0.01, 0.07 per SD)]. The ADII was also adversely associated with insulin resistance [homeostatic model assessment of insulin resistance (HOMA-IR): β-adjusted = 3.5% per SD (95% CI: 0.6%, 6.3% per SD)]. This association was attenuated after the inclusion of the summary score for inflammation [β-adjusted+inflammation = 2.2% (95% CI: -0.6%, 5.0%)]. The ADII was also adversely associated with fasting glucose and postload glucose but not with glycated hemoglobin. CONCLUSION: The significant mediating role of low-grade inflammation in the association between the ADII and HOMA-IR suggests that inflammation might be one of the pathways through which diet affects insulin resistance.
BACKGROUND: Diet may be associated with the development of type 2 diabetes through its effects on low-grade inflammation. OBJECTIVES: We investigated whether an adapted dietary inflammatory index (ADII) is associated with a summary score for low-grade inflammation and markers of glucose metabolism. In addition, we investigated the mediating role of inflammation in the association between ADII and markers of glucose metabolism. DESIGN: We performed cross-sectional analyses of 2 Dutch cohort studies (n= 1024). An ADII was obtained by multiplying standardized energy-adjusted intakes of dietary components by literature-based dietary inflammatory weights that reflected the inflammatory potential of components. Subsequently, these multiplications were summed. Six biomarkers of inflammation were compiled in a summary score. Associations of the ADII (expressed per SD) with the summary score for inflammation and markers of glucose metabolism were investigated by using multiple linear regression models. Inflammation was considered a potential mediator in the analysis with markers of glucose metabolism. RESULTS: A higher ADII was associated with a higher summary score for inflammation [β-adjusted = 0.04 per SD (95% CI: 0.01, 0.07 per SD)]. The ADII was also adversely associated with insulin resistance [homeostatic model assessment of insulin resistance (HOMA-IR): β-adjusted = 3.5% per SD (95% CI: 0.6%, 6.3% per SD)]. This association was attenuated after the inclusion of the summary score for inflammation [β-adjusted+inflammation = 2.2% (95% CI: -0.6%, 5.0%)]. The ADII was also adversely associated with fasting glucose and postload glucose but not with glycated hemoglobin. CONCLUSION: The significant mediating role of low-grade inflammation in the association between the ADII and HOMA-IR suggests that inflammation might be one of the pathways through which diet affects insulin resistance.
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