Effects of xylitol on metabolic parameters and visceral fat accumulation

Abstract

Xylitol is widely used as a sweetener in foods and medications. Xylitol ingestion causes a small blood glucose rise, and it is commonly used as an alternative to high-energy supplements in diabetics. In previous studies, a xylitol metabolite, xylulose-5-phosphate, was shown to activate carbohydrate response element binding protein, and to promote lipogenic enzyme gene transcription in vitro; however, the effects of xylitol in vivo are not understood. Here we investigated the effects of dietary xylitol on lipid metabolism and visceral fat accumulation in rats fed a high-fat diet. Sprague-Dawley rats were fed a high-fat diet containing 0 g (control), 1.0 g/100 kcal (X1) or 2.0 g/100 kcal (X2) of xylitol. After the 8-week feeding period, visceral fat mass and plasma insulin and lipid concentrations were significantly lower in xylitol-fed rats than those in high-fat diet rats. Gene expression levels of ChREBP and lipogenic enzymes were higher, whereas the expression of sterol regulatory-element binding protein 1c was lower and fatty acid oxidation-related genes were significantly higher in the liver of xylitol-fed rats as compared with high-fat diet rats. In conclusion, intake of xylitol may be beneficial in preventing the development of obesity and metabolic abnormalities in rats with diet-induced obesity.

Keywords: lower insulin level; high fat diet; lipid metabolism; visceral fat; xylitol.

Fig. 1

Plasma glucose, insulin, and lipids levels in rats fed three different diets for 8 week. Values are mean ± SEM (n = 6 for each group). *p<0.05 vs HFD group. TG, triglyceride; T-Chol, total cholesterol; NEFA, non-esterified fatty acid.

Fig. 2

Adipose gene expression in rats fed three different diets for 8 week. mRNA levels of genes in the mesenteric fat tissues were determined by quantitative RT-PCR analysis. Values are mean ± SEM (n = 5 for each group). *p<0.05 vs HFD group. The ratio for the data from the HFD group was set arbitrarily at 1. PPARγ, peroxisome proliferator-activated receptor γ; HSL, hormone sensitive lipase; ATGL, adipose triglyceride lipase.

Fig. 3

Hepatic gene expression in rats fed three different diets for 8 week. mRNA levels of genes related to (A) lipogenesis, (B) fatty acid oxidation, and (C) cholesterol metabolism in the liver were determined by quantitative RT-PCR analysis. Values are mean ± SEM (n = 6 for each group). *p<0.05 vs HFD group. The ratio for the data from the HFD group was set arbitrarily at 1. SREBP-1c, sterol regulatory-element binding protein 1c; ChREBP, carbohydrate response-element binding protein; ACC, acetyl coenzyme A carboxylase; FAS, fatty acid synthase; PPARα, peroxisome proliferator-activated receptor α; ACO, acyl coenzyme A oxidase; UCP2, uncoupling protein 2; PGC-1α, peroxisome proliferator-activated receptor-gamma coactivator 1α; CYP7A1, cholesterol 7α hydroxylase; ABCG5, ATP-binding cassette subfamily G member 5.

Fig. 4

Effects of xylitol on gene expression in rat primary hepatocytes. Xylitol stimulation was performed in rat primary hepatocytes, and mRNA levels of genes related to (A) lipogenesis and (B) fatty acid oxidation were determined by quantitative RT-PCR analysis. Values are mean ± SEM, n = 3. *p<0.05 vs control (- xylitol) group.

Fig. 5

Effect of oral sucrose administration with or without xylitol on plasma glucose and insulin levels. After fasting for 18–20 h, the rats were orally administrated sucrose (1 g/kg body weight) either alone or with xylitol or mannitol (0.25 g/kg body weight). Blood samples were taken at 0, 30, 60 and 120 min after administration. (A, B) Time-dependent curve for plasma levels of (A) glucose and (B) insulin. Values are mean ± SEM, n = 4–7. *p<0.05 vs S group. S, sucrose (1 g/kg body weight); SX, sucrose (1 g/kg body weight) with xylitol (0.25 g/kg body weight); SM, sucrose (1 g/kg body weight) with mannitol (0.25 g/kg body weight).