No abstract

The sugar alcohol xylitol inhibits the growth of some bacterial species including Streptococcus mutans. It is used as a food additive to prevent caries. We previously showed that 1.5–4.0 g/kg body weight/day xylitol as part of a high-fat diet (HFD) improved lipid metabolism in rats. However, the effects of lower daily doses of dietary xylitol on gut microbiota and lipid metabolism are unclear. We examined the effect of 40 and 200 mg/kg body weight/day xylitol intake on gut microbiota and lipid metabolism in mice. Bacterial compositions were characterized by denaturing gradient gel electrophoresis and targeted real-time PCR. Luminal metabolites were determined by capillary electrophoresis electrospray ionization time-of-flight mass spectrometry. Plasma lipid parameters and glucose tolerance were examined. Dietary supplementation with low- or medium-dose xylitol (40 or 194 mg/kg body weight/day, respectively) significantly altered the fecal microbiota composition in mice. Relative to mice not fed xylitol, the addition of medium-dose xylitol to a regular and HFD in experimental mice reduced the abundance of fecal Bacteroidetes phylum and the genus Barnesiella, whereas the abundance of Firmicutes phylum and the genus Prevotella was increased in mice fed an HFD with medium-dose dietary xylitol. Body composition, hepatic and serum lipid parameters, oral glucose tolerance, and luminal metabolites were unaffected by xylitol consumption. In mice, 40 and 194 mg/kg body weight/day xylitol in the diet induced gradual changes in gut microbiota but not in lipid metabolism.

Isolated adipocytes were prepared from epididymal adipose tissues removed from rats which had been fed or starved for 48 h (fed adipocytes or fasted adipocytes). These cells were incubated at 37 degrees C for 90 min in media containing 0, 3, or 30 mM glucose, with or without norepinephrine (1.0 mug/ml). Then the concentrations of free fatty acids (FFA) and free glycerol (FG) in the total mixture (medium plus cells) and in the medium alone were measured. Addition of glucose to the medium increased the total PG, presumably by increasing the basal lipolysis, and it decreased the intracellular retention ratio of FG (the ratio of intracellular FG to total FG). Addition of glucose did not change the total FFA, but decreased the FFA/FG ratio, presumably by increasing reesterification. The increase in FG and decrease in the FFA/FG ratio on addition of glucose were greater in fed than in fasted adipocytes. The intracellular retention ratio of FFA also decreased on addition of glucose. Glucose enhanced norepinephrine-induced lipolysis (release of free glycerol), and this effect of glucose was greater in fasted adipocytes. However, the increase in FFA in fasted adipocytes induced by norepinephrine was not altered by addition of glucose. In fed adipocytes norepinephrine decreased the total FFA in the presence of glucose. Reesterification of FFA following norepinephrine was increased by addition of glucose. Norepinephrine decreased the intracellular retention ratios of FG and FFA in the presence of glucose. These results suggest that the passage of the lipolytic products, FFA and FG, through the cell membranes may not occur by simple diffusion, but may require energy.

enhanced macrophage foam cell formation associated with scavenger receptors (CD36 and SR-A) and acyl-CoA:cholesterol acyltransferase-1 downregulation and ATP-binding cassette transporter A1 up-regulation, and increased cell proliferation and collagen-1 and-3 expression via PI3K/AKT/c-Src/NF-kB/ERK1/2 pathways in HASMCs" is corrected as follows: "Fetuin-A enhanced macrophage foam cell formation associated with scavenger receptors (CD36 and SR-A) and acyl-CoA:cholesterol acyltransferase-1 up-regulation and ATP-binding cassette transporter A1 down-regulation, and increased cell proliferation and collagen-1 and-3 expression via PI3K/AKT/c-Src/NF-kB/ERK1/2 pathways in HASMCs." The authors would like to apologize for any inconvenience caused.