Is acetylcholinesterase inhibition in Caenorhabditis elegans at sub-lethal concentrations predictive of hyperglycemic potential of anticholinesterase agents?

We explored the hypothesis that strong inhibition of acetylcholinesterase (AChE) in Caenorhabditis elegans after acute exposure (4h) to sub-lethal concentrations could serve as a model for predicting hyperglycemic potential of anti-cholinesterase toxicants. Acute exposure to sub-lethal concentrations of acephate and monocrotophos elicited significant inhibition of AChE in C. elegans. Sub-chronic exposure (90 days) to acephate (280mg/kg b.w./d) and monocrotophos (3.6mg/kg b.w./d) to male Wistar rats caused inhibition of brain AChE and increased blood glucose. Literature survey as well as previous work from our laboratory suggests that toxicants with ability to cause AChE inhibition in C. elegans also cause hyperglycemia in experimental mammalian models. This suggests that strong inhibition of C. elegans AChE after acute exposure to sub-lethal concentrations could help in predicting the ability of xenobiotics to cause disruption of glucose homeostasis in mammalian system due to AChE inhibition and cholinergic stress.