Insulin prolongs lifespan and preserves neuronal function under hyperglycemic conditions in C. elegans

Aims: In the nematode Caenorhabditis elegans (C. elegans), the insulin receptor and insulin signal transduction system is highly homologous to the human system and is involved in antioxidative defense and determination of lifespan. Hyperglycemic culture conditions lead to neuronal dysfunction and reduction of lifespan in C. elegans. Aim of this study was to investigate the effects of normal human insulin (Actrapid®) on hyperglycemia-induced neuronal and muscular dysfunction and on lifespan.

Methods: The wild type C. elegans strain N2 was cultivated using standard conditions without glucose and using hyperglycemic conditions (400 mM) without insulin and in the presence of 10 U/ml normal insulin (Actrapid®). Besides investigating the effects on lifespan, neuronal function was assessed by studying defined body movements and lifespan. Equimolar concentrations of sorbitol were used as a control to exclude osmotic effects.

Results: We observed a hyperglycemia-induced neuronal damage reflected by a significant impairment of mobility and a significant reduction of lifespan when compared to standard culture conditions without glucose or using equimolar concentrations of sorbitol. Treatment of C. elegans with insulin improved neuronal function and increased lifespan of C. elegans under hyperglycemic culture conditions while there was no significant effect under normal conditions or when sorbitol was used.

Conclusion: Treatment with normal insulin preserves neuronal function and increases lifespan under hyperglycemic culture conditions in C. elegans.