リビトール

139.14 Ų [M+K]+ [CCS Type: TW; Method: calibrated with polyalanine and drug standards]

127.92 Ų [M-H]- [CCS Type: DT; Method: stepped-field]

136.3 Ų [M+Na]+ [CCS Type: DT; Method: single field calibrated with Agilent tune mix (Agilent)]

136.2 Ų [M+Na]+ [CCS Type: DT; Method: single field calibrated with ESI Low Concentration Tuning Mix (Agilent)]

126.1 Ų [M-H]-

There has been evidence of xylitol in dental hygiene in reducing dental caries disease and also reversing the process of early caries. Xylitol increases salivary flow and pH, reduces the levels of _Streptococcus mutans_ in plaque and saliva and reduces the adhesion on the microorganism to the teeth surface. _Streptococcus mutans_ is the main target plaque microorganism, but xylitol may potentially have inhibitory actions against several other bacterial species. It prevents a shift of the bacterial community towards a more cariogenic microflora in oral environment. Oral ingestion of xylitol causes a smaller rise in plasma glucose and insulin concentrations than does the ingestion of glucose in healthy men and diabetics.

Xylitol is initially taken up by the microorganism and accumulates intracellularly. Accumulated xylitol is transported into an energy-consuming cycle, or the inducible fructose transport system. It is converted to non-metabolizable, toxic xylitol-5-phosphate via phosphoenolpyruvate: a constitutive fructose phosphotransferase system by _S. mutans_. This metabolic process of xylitol, without the gain of any energy molecules, results in the development of intracellular vacuoles and cell membrane degradation. _S. mutans_ dephosphorylates xylitol-5-phosphate and expels it from the cell, in which requires energy consumption. This ultimately leading to starving of microorganism and growth inhibition. Long-term exposure to xylitol can cause microorganisms to develop resistance to xylitol. This clinically beneficial selection process creates xylitol-resistant mutans strains that are less virulent and less cariogenic than their parent strains. Xylitol also increases the concentrations of ammonia and amino acids in plaque, thereby neutralizing plaque acids. A study suggests that xylitol may also promote remineralization of deeper layers of demineralized enamel by facilitating Ca2+ and phosphate movement and accessibility.

In mammals, xylitol is mainly metabolized in the liver where it is oxidized to D-xylulose by xylitol dehydrogenase and cofactor NAD. D-xyluose is further phosphorylated and metabolized by xylulose kinase to xylulose 5-phosphate (Xu5P), an intermediate of the nonoxidative branch of the pentose phosphate pathway. Xu5P is reported to activate nuclear transport and the DNA-binding activities of carbohydrate response element binding protein (ChREBP) via activation of activation of protein phosphatase 2A (PP2A) _in vitro_. Activation of ChREBP thereby upregulates the gene transcription of lipogenic enzymes in vitro, which may stimulate lipogenesis in the liver.