Emetic Response to T-2 Toxin Correspond to Secretion of Glucagon-like Peptide-17-36 Amide and Glucose-Dependent Insulinotropic Polypeptide.

Abstract

The T-2 toxin, a major secondary metabolite of Fusarium Gramineae, is considered a great risk to humans and animals due to its toxicity, such as inducing emesis. The mechanism of emesis is a complex signal involving an imbalance of hormones and neurotransmitters, as well as activity of visceral afferent neurons. The T-2 toxin has been proven to induce emesis and possess the capacity to elevate expressions of intestinal hormones glucagon-like peptide-17-36 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), both of which are important emetic factors. In addition, the activation of calcium-sensitive receptor (CaSR) and transient receptor potential (TRP) channels are engaged in intestinal hormone release. However, it is unknown whether hormones GLP-1 and GIP mediate T-2 toxin-induced emetic response through activating CaSR and TRP channels. To further assess the mechanism of T-2 toxin-induced emesis, we studied the hypothesis that T-2 toxin-caused emetic response and intestinal hormones GLP-1 and GIP released in mink are associated with activating calcium transduction. Following oral gavage and intraperitoneal injection T-2 toxin, emetic responses were observed in a dose-dependent manner, which notably corresponded to the secretion of GLP-1 and GIP, and were suppressed by pretreatment with respective antagonist Exending9-39 and Pro3GIP. Additional research found that NPS-2143 (NPS) and ruthenium red (RR), respective antagonists of CaSR and TRP channels, dramatically inhibited both T-2 toxin-induced emesis response and the expression of plasma GLP-1 and GIP. According to these data, we observed that T-2 toxin-induced emetic response corresponds to secretion of GLP-1 and GIP via calcium transduction.

• Authors: Jie Zhang, Tushuai Li, Qinghua Wu, Zihui Qin, Ben Wei, Ran Wu, Xinyi Guo, Huiping Xiao, Wenda Wu
• Journal: Toxins (Toxins (Basel)) Vol. 14 Issue 6 (06 02 2022) ISSN: 2072-6651 [Electronic] Switzerland
• PMID: 35737050 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)

Chemical References

• Amides
• Emetics
• Insulin
• Peptide Fragments
• Receptors, G-Protein-Coupled
• Gastric Inhibitory Polypeptide
• Glucagon-Like Peptide 1
• T-2 Toxin
• Glucose
• Calcium

Topics

• Amides
• Animals
• Calcium
• Emetics
• Gastric Inhibitory Polypeptide (metabolism, pharmacology)
• Glucagon-Like Peptide 1 (metabolism)
• Glucose (pharmacology)
• Insulin
• Peptide Fragments (pharmacology)
• Receptors, G-Protein-Coupled
• T-2 Toxin (toxicity)
• Vomiting