Author: Heikki Savolainen
Position: Professor
Institution: Dept. of Occup. Safety & Hlth., Tampere, Finland
E-mail: heikki.savolainen@stm.fi
Submitted Date: August 08, 2008
Published Date: August 11, 2008
This comment was originally posted as a “Reader Response” on the publication date indicated above. All Reader Responses are now available as comments.

This highly interesting analysis is biologically plausible. Its metabolic mechanisms may include the accumulation of methylglyoxal (MG) from the excessive glucose. MG is known to interfere with signal transmission molecules like Raf-1, a protein ser/thr kinase (1). This could attenuate the macrophage functions.

An analogous example is the increased pulmonary tuberculosis risk in the occupational exposure to silica dust. Phagocytosed quartz particle induce the phagocytic cell death.

An idea of the circulating MG can be had by urinalysis for D-lactate (2).

1 Du J, Zen J, Ou X, et al. Methylglyoxal downregulates Raf-1 protein through a ubiquination-mediated mechanism. Int J Biochem Cell Biol, 2006; 38: 1084

2 Talasniemi JP, Pennanen S, Savolainen H, et al. Analytical investigation: Assay of D-lactate in diabetic plasma and urine. Clin Biochem, 2008, doi:10.1016/j.clinbiochem2008.06.11