In this study, in a multi-ethnic Singaporean population, coffee consumption was inversely associated with IR independent of plasma CRP or adiponectin concentrations. This association appeared to be consistent for overweight and non-overweight participants and for Chinese, Malay, and Asian Indian participants. We also noted an inverse relationship between green tea and plasma CRP concentrations, but found no evidence for an association between tea consumption and basal glucose metabolism.
To the best of our knowledge this is the first study to examine the extent to which inflammatory markers such as CRP and adiponectin explain the association between coffee consumption and IR. Data from other clinical and cross-sectional studies suggest a beneficial effect of coffee consumption on insulin sensitivity. However few studies have examined coffee in relation to insulin sensitivity  or inflammation [13, 15, 19, 20] in Asian populations and these studies were all conducted in Japan. These cross-sectional studies found inverse associations between coffee and serum CRP concentrations [13, 15], and either no association  or a direct association  with serum adiponectin concentrations. Both adiponectin and CRP have been associated with Type-2 DM risk [38, 39]. Adiponectin can also decrease IR, independent of its anti-inflammatory properties, via the AMP-activated protein kinase pathway .
Although we observed an inverse association between coffee consumption and IR, we found no significant associations between coffee intake and inflammatory markers and these markers did not explain the association between coffee and IR. These results suggest that the putative protective effect of coffee consumption against the development of Type-2 DM, which has been previously reported in Singapore Chinese , is at least partly mediated by its effects on IR. However, this inverse association between coffee consumption and IR is probably not mediated by anti-inflammatory effects. Nevertheless, there are some caveats that are worth considering. First, although CRP is a well-established marker of systemic inflammation , it is possible that coffee alters other measures of inflammation that were not examined in this study. Second, the relatively low amounts of coffee consumed in this population, may have been insufficient to exert a biological effect on CRP and adiponectin. In a cross-sectional study of U.S. women, only consuming four or more cups of coffee per day, but not lower consumption, was associated with higher adiponectin concentrations . However, the literature on this topic is not consistent with a few other studies suggesting associations with concentrations of CRP and adiponectin at intakes as low as one cup per day [13, 19].
Apart from its anti-inflammatory effects, phenolic compounds in coffee have been postulated to affect glucose metabolism through various mechanisms including intestinal glucose absorption and incretin secretion , and reduction of hepatic triglyceride accumulation . Consistent with several intervention studies, no associations were noted between black or green tea, and fasting glycemic parameters in this investigation [23, 24, 26]. In contrast, a Japanese intervention study, noted reduced fasting plasma glucose and fructosamine concentrations in diabetic participants who consumed 1 L per day of Oolong tea for four weeks . The difference in diabetes status or amount of tea consumed may have contributed to the difference in results as compared with our study.
Tea consumption was not associated with adiponectin concentrations in our study. This is consistent with studies that showed no associations between green tea and plasma adiponectin concentration even at relatively high intake levels of four cups/day [19, 43], but contrasts with one randomized trial in which consumption of one L of Oolong tea per day increased adiponectin concentrations in 22 persons with coronary artery disease .
The inverse association between green tea and CRP is a finding that stands in contrast to several other studies which observed no such association [25, 43, 45, 46]. However, these studies were all clinical trials that examined either the acute  or short-term (4-8 weeks) [25, 43, 45] effects of green tea intake. A longer duration may be needed for the beneficial effects of green tea on CRP to be manifested. Interestingly, we found no associations between black tea and glycemic parameters or inflammatory markers. These findings were inconsistent with those of a prospective cohort study in Singaporean Chinese that found an inverse association between black tea consumption and Type-2 DM risk . It is possible that black tea alters post-prandial aspects of glucose metabolism, which were not examined in this study.
The large multi-ethnic study population and detailed assessments of potential confounders are strengths of this study. Because of the cross-sectional design, the sequence of events cannot be inferred from this study. However, we excluded people with known diseases who may have exhibited differential recall of lifestyle exposures or were on medications that may have obscured the effects of coffee or tea on the markers of interest. Also, measurement error in the assessment of lifestyle exposures is unavoidable and makes the possibility of residual confounding a concern. However, as coffee consumption was associated with less health-conscious lifestyle behaviors, it is less likely that un-measured confounders would weaken the inverse association between coffee and IR. Green tea intake was associated with some favorable lifestyle behaviors and higher education, and it is thus possible that green tea may have served as a proxy for an unmeasured or imperfectly measured beneficial exposure in this study.