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A prior study (Dasari et al., 2010) revealed that 27-OH induced toxicity in RPE cells via the stimulation of A142 peptide production, elevation of stress markers specific to the endoplasmic reticulum (cysteinyl asparaginase-12 and C/EBP homologous protein), reduction in dysregulation of Ca 2+ homeostasis, mitochondrial membrane potential, oxidative stress (as indicated by glutathione depletion and reactive oxygen species (ROS) production), and apoptosis

Ketone bodies may increase UCP expression through regulating Sirtuin 1 activity (58), potentially via altered NAD+ levels (59), although the precise mechanisms are not yet known

point-of-care (finger-prick) HbA1c testing is not recommended for confirming a diagnosis

Mol Ther 9(3):355-67, 2004

Interestingly, when this reaction was studied in enzymes whose Fe(II) atoms are liganded by a cysteine residue, the cysteine ligand itself was left untouched by the nascent Fe(III)-OOH (Gu and Imlay, 2013)