RESUMEN
Objective: To investigate the mechanisms of chlorogenic acid (CGA) on regulating carbohydrate metabolism in skeletal muscle of SD rats fed on high-fat diet. Methods: Forty male SD rats were randomly divided into five groups: normal control (NC), high-fat diet (HFD), HFD with low-dose-CGA (20 mg/kg, HFD-LC), HFD with high-dose-CGA (90 mg/kg, HFD-HC), and Rosiglitazone (HFD-ROS) groups. NC rats were fed with normal chow diet, while the other rats were fed with HFD. The rats were killed after 12 weeks, and the real-time PCR method was used to measure the expression levels of GLUT-4, PKA, Akt, AMPKα2, IRS-1, PI3K, and PPARs mRNA in skeletal muscle. Results: The expression levels of GLUT-4, AMPKα2, and PPARβ in HFD group were more dramatically decreased than those in the NC group (P<0.05); Compared with the HFD group, CGA increased genes involved in carbohydrate metabolism, particularly Akt, PI3K, IRS-1, GLUT-4, PKA, AMPKα2, PPARα, and PPARβ in HFD-HC group (P<0.05). Conclusion: High-dose CGA could significantly slow the weight gain induced by HFD, as well as improve carbohydrate metabolism in skeletal muscle through regulating PI3K/Akt and AMPK signaling pathways, and insulin sensitivity.
RESUMEN
<p><b>OBJECTIVE</b>To reveal the effects and related mechanisms of chlorogenic acid (CGA) on intestinal glucose homeostasis.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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.</p><p><b>CONCLUSION</b>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.</p>