Peng Bing Jie, Zhu Qi, Zhong Ying Li, Xu Shi Hao, Wang Zheng
College of Bioscience and Biotechnology, Hunan Agricultural University, Changsha 410128, Hunan, China.
Biomed Environ Sci. 2015 Dec;28(12):894-903. doi: 10.3967/bes2015.123.
To reveal the effects and related mechanisms of chlorogenic acid (CGA) on intestinal glucose homeostasis.
Forty male Sprague-Dawley rats were randomly and equally divided into four groups: normal chow (NC), high-fat diet (HFD), HFD with low-dose CGA (20 mg/kg, HFD-LC), and HFD with high-dose CGA (90 mg/kg, HFD-HC). The oral glucose tolerance test was performed, and fast serum insulin (FSI) was detected using an enzyme-linked immunosorbent assay. The mRNA expression levels of glucose transporters (Sglt-1 and Glut-2) and proglucagon (Plg) in different intestinal segments (the duodenum, jejunum, ileum, and colon) were analyzed using quantitative real-time polymerase chain reaction. SGLT-1 protein and the morphology of epithelial cells in the duodenum and jejunum was localized by using immunofluorescence.
At both doses, CGA ameliorated the HFD-induced body weight gain, maintained FSI, and increased postprandial 30-min glucagon-like peptide 1 secretion. High-dose CGA inhibited the HFD-induced elevation in Sglt-1 expression. Both CGA doses normalized the HFD-induced downregulation of Glut-2 and elevated the expression of Plg in all four intestinal segments.
An HFD can cause a glucose metabolism disorder in the rat intestine and affect body glucose homeostasis. CGA can modify intestinal glucose metabolism by regulating the expression of intestinal glucose transporters and Plg, thereby controlling the levels of blood glucose and insulin to maintain glucose homeostasis.
揭示绿原酸(CGA)对肠道葡萄糖稳态的影响及相关机制。
将40只雄性Sprague-Dawley大鼠随机等分为四组:正常饮食(NC)组、高脂饮食(HFD)组、低剂量CGA高脂饮食(20 mg/kg,HFD-LC)组和高剂量CGA高脂饮食(90 mg/kg,HFD-HC)组。进行口服葡萄糖耐量试验,采用酶联免疫吸附测定法检测空腹血清胰岛素(FSI)。使用定量实时聚合酶链反应分析不同肠段(十二指肠、空肠、回肠和结肠)中葡萄糖转运蛋白(Sglt-1和Glut-2)和胰高血糖素原(Plg)的mRNA表达水平。利用免疫荧光对十二指肠和空肠中的SGLT-1蛋白及上皮细胞形态进行定位。
两种剂量的CGA均改善了高脂饮食诱导的体重增加,维持了FSI水平,并增加了餐后30分钟胰高血糖素样肽1的分泌。高剂量CGA抑制了高脂饮食诱导的Sglt-1表达升高。两种剂量的CGA均使高脂饮食诱导的Glut-2下调恢复正常,并提高了所有四个肠段中Plg的表达。
高脂饮食可导致大鼠肠道葡萄糖代谢紊乱并影响机体葡萄糖稳态。CGA可通过调节肠道葡萄糖转运蛋白和Plg的表达来改变肠道葡萄糖代谢,从而控制血糖和胰岛素水平以维持葡萄糖稳态。