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

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 alpha-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.

Automated summary

The study demonstrated that syringaldehyde can lower blood glucose levels in diabetic mice by enhancing intestinal contractility and reducing glucose absorption, suggesting its potential therapeutic benefits.