Berries and their functional components have been put forward as an alternative to pharmacological treatments of type 2 diabetes mellitus (T2DM), and more attention has been paid to the gut microbiome in the pathophysiology of T2DM. Thus, we tried to examine the metabolic impact of red bayberry-derived cyanidin-3-O-glucoside (C3G) and investigate whether the antidiabetic effects of C3G were associated with the gut microbiome. As a result, C3G administration was found to reduce blood glucose levels of diabetic db/db mice, accompanied by increased levels of glucagon-like peptide (GLP-1) and insulin. Moreover, 16S rRNA analysis showed that the dominant microbiota modulated by C3G were pivotal in the glucose metabolism. Furthermore, the modulation of C3G on metabolic activities of gut bacteria leads to an increase in intestinal levels of key metabolites, particularly short-chain fatty acids. This contribution helps in promoting the secretion of GLP-1, which in turn increases insulin release with the purpose of reducing blood glucose levels. Overall, these findings may offer new thoughts concerning C3G against metabolic disorders in T2DM.
Acrolein (ACR) derives from the external environment and the endogenous metabolism of organisms. It has super-reactivity and can induce various diseases. We investigated the capacity of cyanidin-3-O-glucoside (C3G) and its degradants/metabolites to capture ACR during thermal processing or in vivo. Our results indicated that both C3G and its degradants, including phloroglucinaldehyde (PGA) and protocatechuic acid (PCA), could efficiently trap ACR to form adducts, such as C3G–ACR, C3G–2ACR, PGA–ACR, PGA–2ACR, PCA–ACR, and PCA–2ACR. Additionally, these adducts were detected in commercial canned red bayberry products. The adducts of C3G and its metabolites conjugated with ACR, such as C3G–ACR, C3G–2ACR, PGA–ACR, and 4-hydroxybenzoic-acid–ACR (4-HBA–ACR), were also detected in mice feces treated with C3G by oral gavage, where the adduct level was dose-dependent. A similar pattern was observed in tests on human consumption of red bayberry. In human urine, only PGA–2ACR and 4-HBA–ACR, were found, whereas C3G–ACR, C3G–2ACR, myricetin-3-O-rhamnoside–ACR (M3R–ACR), PGA–2ACR, 4-HBA–ACR and ferulic acid–ACR (FA–ACR) were detected in human feces following administration of red bayberry. Our results are the first demonstration that C3G and its metabolites can capture ACR in vitro and in vivo (mice and humans) and present a novel strategy, the development of C3G as a promising ACR inhibitor.
危险品化学品经营许可证（带存储）