Pectinase is an enzyme able to degrade pectic substances by hydrolyzing the ester bond between galacturonic acid and methanol or by cleaving the glycosidic bonds of specific

polymers [22]. Indeed, Jin et al [17] used pectinase to hydrolyze ginsenosides and found that compound K is more readily absorbed from HGE compared to non-HGE in human individuals. Compound K has received increasing attention because various pharmacologic actions including anticancer [25], anti-inflammation [26], and antidiabetes [27] were shown to be mediated by this compound. Using pectinase-hydrolyzed ginseng extract, Ramesh et al [28] found an improved antioxidant status and minimized occurrence of oxidative stress-related disorders in aged rats. Moreover, Yuan et al [29] and [30] reported that pectinase-processed ginseng radix had antidiabetic and hypolipidemic effects in high Trametinib fat diet-fed ICR mice. Taken together, pectinase seems to be an effective tool to transform ginsenosides into deglycosylated ginsenosides, thereby enhancing the bioavailability and functionality of ginseng. Our data demonstrate that 8 wk of HGE supplementation causes a significant reduction in FPG (p = 0.017)

and PPG60min (p = 0.01) in IFG individuals. Such reductions may be due to one or a combination of different mechanisms, including intestinal glucose absorption [31] and [32], insulin secretion from pancreatic β-cells see more [33], or peripheral glucose utilization [34]. After the supplementation of HGE, noticeable but not significant difference was found in the glucose level at an earlier time point (PPG30min, p = 0.059) during OGTT. This result suggests that HGE slows the absorption of glucose in the intestinal lumen. Also, our findings of significant decreases in FPG and PPG60min suggest one additional possibility, in which HGE improves glucose intolerance through increasing

the insulin action on the target tissues responsible for glucose uptake. Moreover, FPI (p = 0.063) and PPI60min (p = 0.077) showed a tendency to improve in the HGE group compared to the placebo group. In supporting this possibility, ginsenosides CK and Rg1 have been reported to enhance insulin-mediated glucose uptake in 3T3-L1 adipocytes, which is related to the increased ADAM7 GLUT4 translocation [27] and [35]. Similarly, administration of HGE improves glucose homeostasis and insulin resistance state (or glucose and lipid parameters) in high fat diet-fed mice via activation of AMP-dependent protein kinase in muscle tissue [29] and [30]. In this study, however, there was no significant difference in HOMA-β, suggesting no effect on insulin secretion. In contrast to our results, studies reveal that ginseng significantly stimulates insulin release from pancreatic β-cells [36] and [37]. These discrepancies could be due to the differences in designs (human studies vs. animal studies) and materials (hydrolyzed ginseng vs. nonhydrolyzed ginseng) used in the studies.