Xiangyang Qi

Microcapsule technology can effectively prevent the core material from losing functional activity due to external influences while reducing undesirable characteristic odor or taste (D. L. Li et al....

BACKGROUND: Non‐nutritive sweeteners (such as sucralose) bind to sweet receptors Tas1r2/Tas1r3 on intestinal endocrine L cells after diets to upregulate blood glucose. However, the mechanism by which sucralose regulates postprandial blood glucose (PBG) has not been clarified to date. We hypothesized that the gut sweet taste receptor was one of the targets for sucralose to regulate PBG. The aim of this study was to examine the effect of sucralose on PBG based on the gut sweet taste receptor signaling pathway and to explore the mechanism. Therefore, we examined PBG, genes, and proteins associated with the gut sweet receptor pathway in sucralose‐exposed mice.RESULTS: The results showed that after 12 weeks of sucralose exposure the PBG of mice increased significantly, and the expression of intestinal sweet taste receptors increased correspondingly. Within the concentration range of this experiment, a significant increase of PBG was observed in mice fed on sucralose with a concentration equal to or higher than 0.33 g L⁻¹.CONCLUSION: Long‐term consumption of sucralose may increase body weight and the risk of elevated PBG, resulting in overexpression of sweetness receptors and glucose transporters. The mechanism of these effects might be the result of non‐nutritive sweeteners binding to sweetness receptors Tas1r2/Tas1r3 in gut endocrine cells and upregulating Slc5a1 and Slc2a2. But we cannot rule out that the rise in PBG is the result of a combination of sweet receptors and gut microbes. Therefore, the effect of gut microbes on PBG needs to be studied further. © 2023 Society of Chemical Industry.

Summary: Simulated gastric fluid (SGF) and intestinal fluid (SIF) digestion were used to evaluate the effects of digestion on the composition of phenolic compounds and antioxidant capacities of the pulp of six lychee cultivars. Caffeic acid, ferulic acid, procyanidin B2, epicatechin, A‐type procyanidin trimer, procyanidin A2, quercetin‐3‐rutinose‐7‐rhamnoside, rutin and isoquercitrin were quantified using HPLC‐DAD. Lychee pulp had high concentrations of procyanidin B2 (0.30~15.53 mg g⁻¹), procyanidin A2 (0.29~0.52 mg g⁻¹) and quercetin‐3‐rutinose‐7‐rhamnoside (0.16~0.45 mg g⁻¹). SGF and SIF Digestion, which significantly decreased the concentration of procyanidin B2, epicatechin and quercetin‐3‐rutinose‐7‐rhamnoside. But observably increased the concentration of procyanidin A2. Compared with deionized water treatment (DW), the total phenolic content (TPC) and total flavonoid content (TFC) of different lychee pulps significantly increased after SGF and SIF digestion. After SGF digestion, the ferric ion reducing antioxidant power (FRAP) of lychee pulps increased while the ABTS+ free radical scavenging ability (ABTS) had a slight decline. This shows that simulated digestion improves the bioactive component and antioxidant activity of different varieties of lychee pulp.

Previous studies suggested the anti-diabetic effect of mogrosides in type 1 diabetes. To evaluate the potential effect of mogrosides in type 2 diabetes, we herein investigated the hypoglycemic and hypolipidemic effects and the underlying mechanism of mogroside-rich extract (MGE) using a high-fat diet in combination with streptozotocin (STZ)-induced diabetic model. MGE feeding for 5 weeks did not result in any obvious impact on the body weight and energy intake, but caused a moderate decrease of organ index in diabetic mice. MGE-supplemented diabetic mice showed a notable reduction of fasting blood glucose (FBG), glycated serum protein (GSP), serum insulin, homeostasis model assessment-insulin resistance (HOMA-IR), and serum atherogenic lipid profiles in a dose-dependent manner, whereas significant increases in the anti-atherogenic lipid profile, insulin sensitivity, glucose and insulin tolerance capacity with high dose (300 mg kg⁻¹) MGE were observed (P < 0.01). Besides, hepatocyte polymorphism, lipid accumulation and steatosis were ameliorated and restored to near normal at the high dose. Furthermore, hepatic 5′AMP-activated protein kinase (AMPK) signaling was dose-dependently activated. Accordingly, the mRNA levels of hepatic gluconeogenic and lipogenic genes were downregulated and fat oxidation-associated genes were upregulated. These findings suggest that the hypoglycemic and hypolipidemic activities of MGE are probably attributed to the attenuation of insulin resistance and activation of hepatic AMPK signaling.