Homocysteine-induced impairment of insulin secretion from clonal pancreatic BRIN-BD11 beta-cells is not prevented by catalase

Steven Patterson*, Peter R. Flatt, Neville H. McClenaghan

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

15 Citations (Scopus)


Objectives: Although detrimental effects of homocysteine attributed to homocysteine auto-oxidation and generation of hydrogen peroxide (H2O2) have been reported in various cell types, such actions have not been considered in pancreatic beta-cells. This study investigates the acute effects of homocysteine on beta-cell integrity and regulation, in particular, the role of H2O2 generated by auto-oxidation.

Methods: Assessment of beta-cell function was examined during acute 20- or 40-minute incubations with homocysteine using clonal BRIN-BD11 beta-cells.

Results: Homocysteine (50-1000 micromol/L) inhibited basal and glucose-induced insulin secretion in a concentration-dependent manner. Insulinotropic responses to alanine, arginine, 2-ketoisocaproate, elevated Ca, tolbutamide, potassium chloride (KCl), forskolin, and phorbol 12-myristate 13-acetate were also significantly reduced by homocysteine. Likewise, preincubation with homocysteine caused a reduction in the insulinotropic responses to glucose and each of the secretagogues tested. Notably, excess catalase (100 microg/mL) in the buffer, although sufficient to remove homocysteine-derived H2O2, did not alleviate the detrimental effects of homocysteine.

Conclusions: Collectively, these data suggest that homocysteine impairs insulin secretory function by mechanisms independent of H2O2 generation. Although homocysteine may give rise to reactive oxygen species, these observations indicate detrimental non-oxidative pancreatic beta-cell actions of homocysteine.
Original languageEnglish
Pages (from-to)144-151
Number of pages8
Issue number1
Publication statusPublished - Jan 2007


  • auto-oxidation , homocysteine , hydrogen peroxide , insulin secretion , pancreatic β-cells


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