Please use this identifier to cite or link to this item: https://doi.org/10.1186/1475-2891-10-61
Title: Coffee and tea consumption in relation to inflammation and basal glucose metabolism in a multi-ethnic Asian population: A cross-sectional study
Authors: Rebello, S.A. 
Chen, C.H.
Naidoo, N. 
Xu, W.
Lee, J. 
Chia, K.S. 
Tai, E.S.
Van Dam, R.M. 
Issue Date: 2011
Citation: Rebello, S.A., Chen, C.H., Naidoo, N., Xu, W., Lee, J., Chia, K.S., Tai, E.S., Van Dam, R.M. (2011). Coffee and tea consumption in relation to inflammation and basal glucose metabolism in a multi-ethnic Asian population: A cross-sectional study. Nutrition Journal 10 (1) : -. ScholarBank@NUS Repository. https://doi.org/10.1186/1475-2891-10-61
Abstract: Background: Higher coffee consumption has been associated with a lower risk of type 2 diabetes in cohort studies, but the physiological pathways through which coffee affects glucose metabolism are not fully understood. The aim of this study was to evaluate the associations between habitual coffee and tea consumption and glucose metabolism in a multi-ethnic Asian population and possible mediation by inflammation. Methods. We cross-sectionally examined the association between coffee, green tea, black tea and Oolong tea consumption and glycemic (fasting plasma glucose, HOMA-IR, HOMA-beta, plasma HbA1c) and inflammatory (plasma adiponectin and C-reactive protein) markers in a multi-ethnic Asian population (N = 4139). Results: After adjusting for multiple confounders, we observed inverse associations between coffee and HOMA-IR (percent difference: - 8.8% for ≥3 cups/day versus rarely or never; P trend= 0.007), but no significant associations between coffee and inflammatory markers. Tea consumption was not associated with glycemic markers, but green tea was inversely associated with plasma C-reactive protein concentrations (percent difference: - 12.2% for ≥1 cup/day versus < 1 cup/week; Ptrend= 0.042). Conclusions: These data provide additional evidence for a beneficial effect of habitual caffeinated coffee consumption on insulin sensitivity, and suggest that this effect is unlikely to be mediated by anti-inflammatory mechanisms. © 2011 Rebello et al; licensee BioMed Central Ltd.
Source Title: Nutrition Journal
URI: http://scholarbank.nus.edu.sg/handle/10635/108302
ISSN: 14752891
DOI: 10.1186/1475-2891-10-61
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