Comparative in vivo and in vitro Study of the Influence of Experimental Diabetes on Rat Liver Linoleic Acid Δ6- and Δ5-Desaturation

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Abstract
Rats with experimental diabetes were administered in vivo a tracer dose of either [1-14C]-linoleic, [1-14C]-.gamma.-linoleic or [2-14C]-dihomo-.gamma.-linolenic acid and sacrificed 48 h later. With all three radioactive precursors, the radioactivity incorporated into arachidonic acid was lower in experimental diabetes, compared to nondiabetic rats similarly treated, while the weights of hepatic arachidonic acid were not significantly affected by the diabetic state. Streptozotocin-treated rats were administered moderate or excessive quantities of protamine-zinc-insulin. Streptozotocin diabetes inhibits rat liver homogenate [2-14C]-dihomo-.gamma.-linolenic acid .DELTA.5-desaturation; only moderate injections of protamine-zinc-insulin restore the in vitro .DELTA.5-desaturation. These results suggest that experimental diabetes, a reported inhibitor of .DELTA.6-desaturation, also causes partial inhibition of .DELTA.5-desaturation in rat liver; this suggests that dihomo-.gamma.-linolenic acid desaturation, a secondary regulatory step in linoleic acid metabolism, may be restored through an optimum insulin therapy.

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