In 2019, a coffee chain in Taiwan was found to be mixing relatively cheap Robusta beans into products marketed as 100% Arabica. Many studies show 16-OMC is a remarkable marker to distinguish Robusta from Arabica beans, and nuclear magnetic resonance (NMR) is a convenient and efficient technique for 16-OMC quantification. Here, a 500 MHz NMR was employed to determine the content of 16-OMC in coffee for adulterate evaluation. A total of 118 samples were analyzed including products from the coffee chain, raw materials (single coffee beans), and other commercial products. The contents of 16-OMC in single Robusta beans were between 1005.55 and 3208.32 mg/kg and were absent from single Arabica beans. The surveillance results indicate that 17 out of 47 blend products claiming to contain 100% Arabica had 16-OMC quantifications in the range of 155.74–784.60 mg/kg. Furthermore, all 17 products were produced by the same coffee chain. We confirmed that coffee chain adulterated Arabica with Robusta in parts of their products, which claimed to include 100% Arabica. Moreover, this work highlights the free form of 16-OMC was esterified by coffee instantly. The decomposition products of 16-OMC were observed obviously in green Robusta while the mechanisms remain unclear. Future research should focus more on these aspects to further increase our understanding of these mechanisms.

Background: Resveratrol is recognized as a promising nutraceutical with antihypertensive and prebiotic properties; however, its bioavailability in vivo is limited. To enhance its bioactivity, we developed resveratrol butyrate esters (RBEs). This study investigates whether RBEs can mitigate hypertension induced by chronic kidney disease (CKD) and exacerbated by microplastics (MPs) exposure in juvenile rats. Methods: Three-week-old male Sprague Dawley rats were fed either regular chow or 0.5% adenine chow for three weeks. The adenine-fed CKD rats (N = 8 per group) received either 5 μM MPs (10 mg/L) or MPs combined with RBE (25 mg/L) in their drinking water from weeks 3 to 9. Results: Our results indicate that MP exposure worsened CKD-induced hypertension, while RBE treatment resulted in a reduction in systolic BP by 15 mmHg (155 ± 2 mmHg vs. 140 ± 1 mmHg, p < 0.05). The combined exposure to adenine and MPs was associated with nitric oxide (NO) deficiency, which RBE treatment alleviated. Additionally, our findings revealed that RBE modulated both the classical and nonclassical renin–angiotensin system (RAS), contributing to its protective effects. We also observed changes in gut microbiota composition, increased butyric acid levels, and elevated renal GPR41 expression associated with RBE treatment. Conclusions: In conclusion, in this juvenile rat model of combined CKD and MP exposure, RBE demonstrates antihypertensive effects by modulating NO levels, the RAS, gut microbiota, and their metabolites.

Overconsumption of sugar-sweetened beverages increases risk factors associated with cardiometabolic disease, in part due to hepatic fructose overload. However, it is not clear whether consumption of beverages containing fructose as naturally occurring sugar produces equivalent metabolic dysregulation as beverages containing added sugars. We compared the effects of consuming naturally-sweetened orange juice (OJ) or sucrose-sweetened beverages (sucrose-SB) for two weeks on risk factors for cardiometabolic disease. Healthy, overweight women (n = 20) were assigned to consume either 3 servings of 100% orange juice or sucrose-SB/day. We conducted 16-hour serial blood collections and 3-h oral glucose tolerance tests during a 30-h inpatient visit at baseline and after the 2-week diet intervention. The 16-h area under the curve (AUC) for uric acid increased in subjects consuming sucrose-SB compared with subjects consuming OJ. Unlike sucrose-SB, OJ did not significantly increase fasting or postprandial lipoproteins. Consumption of both beverages resulted in reductions in the Matsuda insulin sensitivity index (OJ: −0.40 ± 0.18, p = 0.04 within group; sucrose-SB: −1.0 ± 0.38, p = 0.006 within group; p = 0.53 between groups). Findings from this pilot study suggest that consumption of OJ at levels above the current dietary guidelines for sugar intake does not increase plasma uric acid concentrations compared with sucrose-SB, but appears to lead to comparable decreases of insulin sensitivity.