Platelets from diabetics in acidosis incorporate significantly less C-14 into fatty acids than do platelets from control subjects. This decrease in incorporation of C-14 into fatty acids is not uniform. Incorporation of C-14 into myristic and palmitic acids, fatty acids presumably made by de novo synthesis, is suppressed to a much greater extent than is incorporation into other fatty acids.
Since some of these abnormalities of incorporation of C-14 by platelets from comatose diabetics could represent isotope dilution effects, we have been particularly interested in the analysis of these data in terms of percentage of total fatty acid C-14 incorporated into the various groups of fatty acids. Platelets from diabetics in acidosis have a pattern of incorporation of C-14 into platelet fatty acids which is much different from that of normal platelets. There is a great decrease in percentage of C-14 in myristic and palmitic acid with a relative increase in percentage of C-14 in fatty acids with retention time corresponding to arachidic acid (20:0) or greater. A significant increase in relative percentage of C-14 in fatty acids containing ten carbons or less is also seen. These findings presumably mean that the cytoplasmic or malonyl CoA pathway, which is involved primarily in synthesis of palmitic and myristic acids, is suppressed greatly in diabetic acidosis, while the mitochondrial or chainlengthening pathway is suppressed to a much smaller degree, or is actually stimulated. It is, therefore, important to consider qualitative as well as quantitative alterations in fatty acid synthesis in diabetes.