The antibacterial mechanism of carvacrol and thymol against Escherichia coli.

AIMS: To investigate the antibacterial mechanism of carvacrol and thymol against Escherichia coli. METHODS AND RESULTS: The time-kill curve results showed that carvacrol and thymol at 200 mg l(-1) could inhibit the growth of E. coli. Flow cytometry and fluorescent dyes were used to explore the effect of two components on membrane permeability and membrane potential. In membrane permeability experiment, the mean fluorescence intensity of cells treated with 200 mg l(-1) carvacrol or thymol were lower than nonexposed cells. The ratio of red to green fluorescence intensity of DiOC2(3) reflected the change of membrane potential. Carvacrol and thymol at 200 mg l(-1) caused the ratio of red/green decreasing from 0.42 of control to 0.08 and 0.07, respectively. CONCLUSIONS: Carvacrol and thymol had desired antimicrobial effect on E. coli. The antibacterial effects were attributed to their ability to permeabilize and depolarize the cytoplasmic membrane. SIGNIFICANCE AND IMPACT OF THE STUDY: This study showed the potential use of flow cytometry as a suitable method to investigate the mode of antibacterial action of essential oil components.

Effects of fructose and/or fat in the diet on developing the type 2 diabetic-like syndrome in CD-1 mice.

The aim of the present study was to examine the interactions of fructose and fat on glucose regulation and lipid metabolism in CD-1 mice. Mice were assigned in five groups. The control group was provided with tap water and a gavage of vehicle; four experimental groups were treated with 150 g/l fructose solution (FS1), fat emulsion (FE), 150 g/l fructose solution and fat emulsion (FS1+FE), or 70 g/l fructose solution and fat emulsion (FS2+FE) for 12 weeks. At the end of the 8th week, both oral glucose tolerance test and insulin tolerance test were conducted. Lipid profiles in serum, liver, and red gastrocnemius muscle, and serum insulin and glucose concentrations were assessed. The FS1+FE group showed combined glucose intolerance (CGI) and decrease of insulin sensitivity. The low-density lipoprotein cholesterol (LDL-C) concentrations were elevated in all experimental groups (p<0.05). The combined diet groups showed statistically significant (p<0.01) increase in total cholesterol (TC) level in comparison with the control FE (p<0.05), or FS1 (p<0.05) group. Triglyceride levels in liver and red gastrocnemius muscle were significantly increased in FE and combined groups. In conclusion, combination of FE and 150 g/l fructose solution for 8 weeks led to CGI. Fructose enhanced the adverse effect of FE on glucose regulation with increasing percentage in the diet. Furthermore, there was a synergistic effect of fructose and fat on elevating the serum TC level.

A combination of grape seed-derived procyanidins and gypenosides alleviates insulin resistance in mice and HepG2 cells.

This study investigated the effects of grape seed-derived procyanidins (GSP), gypenosides (GPE), and combination procyanidins/gypenosides on insulin resistance in mice and HepG2 cells. ICR mice were randomly divided into 2 control and 4 treatment groups. The control mice were to receive either normal diet (ND) or high-fat diet (HFD), and the treatment groups were fed high-fat diet with either 80 mg/kg of GSP (GSP80), GPE (GPE80), GSP + GPE (1: 1, GSP40 + GPE40), or 500 mg/kg of metformin for a 6-wk period. All the groups of mice except the normal control were on high-fat diet along with fructose (15%) administered in drinking water throughout the period of treatment. An insulin-resistant HepG2 cell model was developed after 24 h of 5 x 10(-7) mol/L insulin incubation. The treatment of GPE80 could significantly reduce the index of insulin resistance (HOMA-IR) and increase hepatic glycogen concentration, compared with HFD group (P < 0.05). When GSP and GPE were administered simultaneously, synergic effects were observed in decreasing the HOMA-IR index and serum total cholesterol (TC) level and enhancing glucose tolerance. All treatment groups showed considerable raise of hepatic glucokinase activity (P < 0.05 compared with HFD group). GSP application increased the consumption of extracellular glucose in HepG2 cells. Our data suggest that the combination of GSP and GPE may have functional efficacy in consumers with insulin resistance.