Roasting improves the hypoglycemic effects of a large-leaf yellow tea infusion by enhancing the levels of epimerized catechins that inhibit α-glucosidase

Abstract

Teas contain bioactive polyphenols, such as (-)-epigallocatechin gallate (EGCG), which is not stable during the processing of tea. EGCG can be epimerized into (-)-gallocatechin gallate (GCG), which is present in very small amounts in fresh tea leaves. An infusion made from roasted large-leaf yellow tea inhibited α-glucosidase more significantly than an infusion of unroasted yellow tea, with IC50 values of 76.08 ± 8.96 and 170.17 ± 33.00 μg mL-1, respectively. After roasting, the content of GCG showed about a 5-fold increase, while EGCG showed a decrease of 56.6%. Of the two main α-glucosidase inhibitors, GCG exhibited a higher inhibitory effect on α-glucosidase than its corresponding epimer (EGCG), whose IC50 value was about 3-fold lower. Modeling of molecular docking suggested that GCG preferably binds to the target α-glucosidase protein; this was confirmed by in vitro protein-polyphenol binding, where GCG had a binding rate about 4 times higher than that of EGCG. Comparative in vivo studies using oral starch tolerance tests in mice verified that GCG exhibited lower postprandial blood glucose compared to EGCG. These results suggest that roasting is a simple and effective way to increase the capacity of large-leaf yellow tea to regulate postprandial blood glucose.

Yellow Tea Stimulates Thermogenesis in Mice through Heterogeneous Browning of Adipose Tissues

“…GCG‐rich catechins were more effective than EGCG‐rich catechins in lowering blood cholesterol and triacylglycerol levels as well as in lowering postprandial blood glucose after consuming starch. [ 17,43 ] Catechin polymers, formed under the high temperature conditions, may also contribute to the activities of YTE; several reports showed that catechin dimers theaflavins lowered body lipid in obese rat, [ 44 ] and theaflavin‐enriched black tea extract protected against obesity‐related inflammation in the obese ZDF rat model. [ 45 ] Careful studies on the active compounds in YTE for the induction of thermogenesis are essential for elucidating the detailed mechanisms involved.…”

“…Using mature fresh tea leaves with stems in the summer and autumn through mechanical harvest and process to yield the final product of YT. [ 17 ] Second, there are two special steps called “sealed yellowing” and “roasting” in the manufacturing process to produce roasted and caramel aromas and flavors similar to coffee and cocoa. The light fermentation and seal turn the leaves to a yellow color, while high‐temperature roasting (140–150 °C for 15 min) brings forth the brown color and the slightly astringent taste of the final YT product.…”

“…[ 19 ] The total content of amino acids decreased and L‐theanine was scarcely detected, while the amounts of two purine alkaloids, caffeine and theobromine were relatively stable during the post‐harvesting processing of YT. [ 17,18,20 ] The thermal degradation, oxidation, epimerization, and polymerization of catechins result in lower levels of total catechins, but higher levels of (‐)‐gallocatechin gallate (GCG, converted from its epimer, EGCG) and catechin polymers in YT. [ 21,22 ]…”

“…In our previous studies, YT exhibited multiple biological activities, such as inhibiting α‐glucosidase activity (possibly lowering blood glucose levels), ameliorating inflammation state, suppressing hepatic lipogenesis, and inhibiting adipose tissue hypertrophy in mice. [ 17,20,23,24 ] However, the detailed actions of YT on DIT and energy metabolism are still unclear. In this study, we used a high‐fat diet (HFD)‐induced obese mouse model to study the effects of YT on thermogenesis.…”

Effects and Mechanisms of Tea for the Prevention and Management of Diabetes Mellitus and Diabetic Complications: An Updated Review

“…Yellow tea could ameliorate glucose intolerance and insulin resistance without dose dependence [70]. Further, the roasted yellow tea could improve insulin sensitivity and reduce fasting blood sugar due to the strong affinity of GCG to target protein-glycosidase, and the strong inhibition effect of GCG on α-glucosidase activity [71].…”