CD59 and diabetes mellitus: The same holds true for human GPIHBP1 and CD59 with its complement regulatory function in nerves, kidney and vasculature which become impaired in the course of diabetes [239,240,241,242,243], presumably as a result of its non-enzymic glycation in dependence on the glucose concentration as well as exposure time [242,243] and lipolytic release from cell surfaces into interstitial fluids, serum [244,245] and urine [246].