部分水解瓜尔豆胶对高脂高糖饮食诱导小鼠代谢紊乱的调节作用

部分水解瓜尔豆胶(partially hydrolyzed guar gum,PHGG)是一种有益于代谢平衡的可溶性膳食纤维,但其对糖脂代谢紊乱的调节效果及其潜在机制尚不明确。利用高脂高糖饮食诱导小鼠16周,使其产生明显的脂代谢紊乱和胰岛素抵抗,进一步通过检测小鼠糖耐量、血清生化指标、脂肪形态、肠道短链脂肪酸及相关mRNA的表达,考察PHGG对模型小鼠的糖脂代谢稳态及肠道环境的调节作用。结果表明:长期高脂高糖饮食条件下,PHGG组小鼠比模型组小鼠的体质量增长率减缓,空腹血糖降低,葡萄糖耐量和胰岛素耐量显著提升；血清中的甘油三酯、总胆固醇、低密度脂蛋白胆固醇和游离脂肪酸可分别降低21.56%、32.67%、25.66%和22.91%,明显抑制了脂肪积累。PHGG将肠道胰高血糖素样肽-1的分泌提升并恢复到67.76pmol/L,盲肠中的丁酸含量比模型组提升了7.14倍。定量PCR显示,PHGG干预后小鼠短链脂肪酸受体GPR43的蛋白表达水平比模型组提升了63.30%。本研究表明,PHGG通过调节短链脂肪酸影响脂联素、胰岛素的分泌,进而改善高脂高糖饮食引起的糖脂代谢紊乱,可以应用于辅助糖脂代谢调控的功能性食品开发中。

Regulating Effect of Partially Hydrolysed Guar Gum on Metabolic Disorder of High Fat High Sugar Diet-Fed Mice

Partially hydrolyzed guar gum (PHGG) as a soluble dietary fiber contributed to maintaining the balance of metabolism. However, the protective effect and potential mechanism on glucose and lipid metabolic disorders were still unclear. In this study, regulation of PHGG on homeostasis and intestinal environment was elucidated in a mouse model of insulin resistance, which was established by feeding a high-fat and high-sugar diet (HFSD) for 16 weeks. The mice were further tested for glucose tolerance,serum biochemical indicators, fat morphology, intestinal short-chain fatty acids and related mRNA expression, to investigate the regulation of PHGG on the glucose and lipid metabolism homeostasis and intestinal environment of model mice. The results showed that PHGG administration not only decreased growth rate of body weight and fasting blood-glucose level, but also improved glucose tolerance and insulin sensibility in HFSD-fed mice. Serum triglyceride, total cholesterol, low-density lipoprotein cholesterol, and free fatty acid were decreased by 21.56%,32.67%, 25.66% and 22.91%, respectively, while adipose tissue pathologic morphology was depleted in HFSD-fed mice. Moreover, PHGG supplementation increased butyric acid in cecal by 7.14 times compared with the model group, while glucagon-like peptide-1 was improved and recovered to 67.76pmol/L in HFSD-fed mice. Quantitative PCR results indicated that expression of G Protein-Coupled Receptor 43 (GPR43) was increased by 63.30% after PHGG supplementation than that of the model group. In conclusion, PHGG might affect the secretion of adiponectin and insulin by regulating short-chain fatty acids, thus improving the disorder of glucose and lipid metabolism caused by HFSD. The results suggested that PHGG could be used as functional food supplement for the delay or prevention of glucose and lipid metabolism disorder.