ABSTRACT
Holman first reported an abnormality of essential fatty acid (EFA) metabolism in diabetes (1). Diabetic animals required much higher amounts of linoleic acid to counteract EFA deficiency compared with normal animals. The possible explanation for this was provided by Brenner, who observed that the mechanism for conversion of linoleic acid to γ-linolenic acid was defective in diabetic animals (2). Thus, much higher amounts of linoleic acid may be required in the diabetic state to provide the long-chain, highly unsaturated EFAs, dihomo-γ-linolenic acid (DGLA) and arachidonic acid (AA).
