Propolis contains a variety of bioactive components and possesses many biological properties. This study was designed to evaluate potential effects of Brazilian green propolis on glucose metabolism and antioxidant function in patients with type 2 diabetes mellitus (T2DM). In the 18-week randomized controlled study, enrolled patients with T2DM were randomly assigned to Brazilian green propolis group (900 mg/day) (n = 32) and control group (n = 33). At the end of the study, no significant difference was found in serum glucose, glycosylated hemoglobin, insulin, aldose reductase or adiponectin between the two groups. However, serum GSH and total polyphenols were significantly increased, and serum carbonyls and lactate dehydrogenase activity were significantly reduced in the Brazilian green propolis group. Serum TNF-α was significantly decreased, whereas serum IL-1β and IL-6 were significantly increased in the Brazilian green propolis group. It is concluded that Brazilian green propolis is effective in improving antioxidant function in T2DM patients.

Introduction Propolis is a natural product with many biological activities. The present study was designed to evaluate the effects of Chinese propolis on glucose metabolism, antioxidant function, and inflammatory cytokines in patients with type 2 diabetes mellitus (T2DM). Methods In the 18-week study, recruited T2DM patients were randomly divided into a Chinese propolis group (900 mg/day) (n = 31) and a control group (n = 30) according to fasting serum glucose levels at baseline. Results At the end of the study, no significant difference was found between the groups in serum glucose, glycosylated hemoglobin, insulin, aldose reductase, or adiponectin. However, serum GSH, flavonoids, and polyphenols were significantly increased, and serum lactate dehydrogenase activity was significantly reduced in the Chinese propolis group. Meanwhile, serum IL-6 was significantly increased in the Chinese propolis group. Conclusion Chinese propolis is effective at improving antioxidant function in T2DM patients, partly by increasing serum antioxidant parameters.

Quercetin has a wide range of biological properties that can be used to prevent or decrease particular inflammatory diseases. In this study, we aimed to investigate the gene expression profile and metabolic pathway of the gut microbiota of an antibiotic-treated mouse model administered quercetin. Blood, feces, and intestinal tissue samples were collected and metagenomic sequencing, enzyme-linked immunosorbent assay, and western blot analysis were used to detect variations. The results showed that the quercetin-treated group exhibited increased levels of health beneficial bacterial species, including Faecalibaculum rodentium (103.13%), Enterorhabdus caecimuris (4.13%), Eggerthella lenta (4%), Roseburia hominis (1.33%), and Enterorhabdus mucosicola (1.79%), compared with the model group. These bacterial species were positively related to butyrate, propionate, and intestinal tight junction proteins (zonula occludens-1 and occludin) expression, but negatively related to serum lipopolysaccharide and tumor necrosis factor-α level. In addition, the metabolic pathway analysis showed that dietary quercetin significantly enhanced spliceosomes (111.11%), tight junctions (62.96%), the citrate cycle (10.41%), pyruvate metabolism (6.95%), and lysine biosynthesis (5.06%), but decreasing fatty acid biosynthesis (23.91%) and N-glycan (7.37%) biosynthesis. Furthermore, these metabolic pathway changes were related to relative changes in the abundance of 10 Kyoto Encyclopedia of Genes and Genomes genes (K00244, K00341, K02946, K03737, K01885, k10352, k11717, k10532, K02078, K01191). In conclusion, dietary quercetin increased butyrate-producing bacterial species, and the acetyl-CoA-mediated increased butyrate accelerated carbohydrate, energy metabolism, reduced cell motility and endotoxemia, and increased the gut barrier function, thereby leading to healthy colonic conditions for the host.

The role of glucose transporters in the transport of flavonoids remains ambiguous. In this study, we examined whether quercetrin would be uptaken and transported intactly in modeled Caco-2 cells, as well as to determine the involvements of sodium-dependent glucose transporter 1 (SGLT1) and glucose transporter 2 (GLUT2) in its transmembrane transport. The uptake experiment was conducted in Caco-2 cells 24 hours after seeded and the transport experiment was conducted in Caco-2 cells after 21 days of culturing in a Millicell system. Quercetrin was administered at 3, 9 or 18 µg/mL; and the timepoints of sampling were 30, 60, 90, 120, and 150 min. In the uptake experiment, the highest intracellular quercetrin concentration was observed in the cells treated with 18 µg/mL quercetrin at 60 min, with a bell-shaped kinetic curve. Quercetin, isorhamnetin, and tamarixetin were detected inside the cells, particularly when treated with the high dose. In the transport experiment, quercetrin was transported from the apical to basolateral side and vice versa; its concentrations depended on dose, time, and transport direction. Only trace amounts of isorhamnetin and tamarixetin were detected in the apical chamber when quercetrin was added to the basolateral chamber. Phloridzin and phloretin, a potent inhibitor of SGLT1 and GLUT2, respectively, significantly diminished quercetrin transport from the apical to basolateral side; and phloretin had a larger inhibitory effect than phloridzin. In conclusion, our results demonstrate that quercetrin is absorbed intactly and then effluxed out of Caco-2 cells through both apical and basolateral membranes probably via SGLT1 and GLUT2.