In vitro metabolic and mitogenic signaling of insulin glargine and its metabolites

PLoS One. 2010 Mar 4;5(3):e9540. doi: 10.1371/journal.pone.0009540.

Abstract

Background: Insulin glargine (Lantus) is a long-acting basal insulin analog that demonstrates effective day-long glycemic control and a lower incidence of hypoglycemia than NPH insulin. After subcutaneous injection insulin glargine is partly converted into the two main metabolites M1 ([Gly(A21)]insulin) and M2 ([Gly(A21),des-Thr(B30)]insulin). The aim of this study was to characterize the glargine metabolites in vitro with regard to their insulin receptor (IR) and IGF-1 receptor (IGF1R) binding and signaling properties as well as their metabolic and mitogenic activities.

Methods: The affinity of human insulin, insulin glargine and its metabolites to the IR isoforms A and B or IGF1R was analyzed in a competitive binding assay using SPA technology. Receptor autophosphorylation activities were studied via In-Cell Western in CHO and MEF cells overexpressing human IR-A and IR-B or IGF1R, respectively. The metabolic response of the insulins was studied as stimulation of lipid synthesis using primary rat adipocytes. Thymidine incorporation in Saos-2 cells was used to characterize the mitogenic activity.

Conclusions: The binding of insulin glargine and its metabolites M1 and M2 to the IR were similar and correlated well with their corresponding autophosphorylation and metabolic activities in vitro. No differences were found towards the two IR isoforms A or B. Insulin glargine showed a higher affinity for IGF1R than insulin, resulting in a lower EC(50) value for autophosphorylation of the receptor and a more potent stimulation of thymidine incorporation in Saos-2 cells. In contrast, the metabolites M1 and M2 were significantly less active in binding to and activation of the IGF1R and their mitogenicity in Saos-2 cells was equal to human insulin. These findings strongly support the idea that insulin glargine metabolites contribute with the same potency as insulin glargine to blood glucose control but lead to significantly reduced growth-promoting activity.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adipocytes / cytology
  • Animals
  • CHO Cells
  • Cricetinae
  • Cricetulus
  • Fibroblasts / metabolism
  • Humans
  • In Vitro Techniques
  • Insulin / analogs & derivatives*
  • Insulin / metabolism*
  • Insulin Glargine
  • Insulin, Long-Acting
  • Mice
  • Phosphorylation
  • Rats
  • Receptor, IGF Type 1 / metabolism
  • Receptor, Insulin / metabolism
  • Signal Transduction*

Substances

  • Insulin
  • Insulin, Long-Acting
  • Insulin Glargine
  • Receptor, IGF Type 1
  • Receptor, Insulin