Chlorogenic Acid Maintains Glucose Homeostasis through Modulating the Expression of SGLT-1, GLUT-2, and PLG in Different Intestinal Segments of Sprague-Dawley Rats Fed a High-Fat Diet.
- Author:
Bing Jie PENG
1
;
Qi ZHU
1
;
Ying Li ZHONG
1
;
Shi Hao XU
1
;
Zheng WANG
1
Author Information
- Publication Type:Journal Article
- Keywords: Chlorogenic acid; GLP-1; GLUT-2; Glucose homeostasis; High-fat diet; Intestine; PLG; SGLT-1
- MeSH: Animals; Chlorogenic Acid; pharmacology; Diet, High-Fat; adverse effects; Glucagon-Like Peptide 1; metabolism; Glucose; metabolism; Glucose Tolerance Test; Glucose Transporter Type 2; metabolism; Homeostasis; Insulin; blood; Intestines; drug effects; metabolism; Male; Proglucagon; metabolism; Random Allocation; Rats, Sprague-Dawley; Sodium-Glucose Transporter 1; metabolism; Weight Gain; drug effects
- From: Biomedical and Environmental Sciences 2015;28(12):894-903
- CountryChina
- Language:English
-
Abstract:
OBJECTIVETo reveal the effects and related mechanisms of chlorogenic acid (CGA) on intestinal glucose homeostasis.
METHODSForty 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.
RESULTSAt 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.
CONCLUSIONAn 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.
