Syringaldehyde promoting intestinal motility with suppressing α-amylase hinders starch digestion in diabetic mice

• Main Authors: Lebin Weng, Ting-Hsu Chen, Qingyan Zheng, Wei-Hao Weng, Liyue Huang, Dong Lai, Yaw-Syan Fu, Ching-Feng Weng
• Format: Article
• Language: English
• Published: Elsevier 2021-09-01
• Series: Biomedicine & Pharmacotherapy
• Subjects: Syringaldehyde; M2 receptor; Acetylcholinesterase; Intestinal contractility; DPP4; PPAR gamma
• Online Access: http://www.sciencedirect.com/science/article/pii/S0753332221006478

The antihyperglycemic potential of syringaldehyde has been previously investigated; however, the underlying mechanism remains unclear. In this study, we performed a postprandial glucose test (in vivo) including oral glucose tolerance test (OGTT) and oral starch tolerance test (OSTT) in fructose-induced diabetic mice on a high-fat diet for mimicking type 2 diabetes to explore the hypoglycemic efficacy of syringaldehyde and the underlined molecular involvement of syringaldehyde in a glucose-lowering effect. The results revealed that syringaldehyde dose-dependently suppressed blood glucose in both the OSTT and OGTT when referenced to acarbose and metformin, respectively. Surprisingly, syringaldehyde triggered jejunum motility (ex vivo) via activation of the muscarinic-type acetylcholine receptor. By performing virtual screening with molecular docking, the data showed that syringaldehyde nicely interacted with glucagon-like peptide 1 receptor (GLP-1R), peroxisome proliferator-activated receptor (PPAR), dipeptidyl peptidase-IV (DPP-4), acetylcholine M2 receptor, and acetylcholinesterase. These results showed that syringaldehyde can potentiate intestinal contractility to abolish the α-amylase reaction when concurrently reducing retention time and glucose absorption to achieve a glucose-lowering effect in diabetic mice, suggesting its potential therapeutic benefits with improvement for use as a prophylactic and treatment.