Abstract
In diabetes there is a decrease in membrane arachidonic (AA) and docosahexaenoic (DHA) acids and a concomitant increase in linoleic (LA) and alpha-linolenic (ALA) acids. This metabolic perturbation is thought to be due to impaired activity of Δ 6- and Δ 5-desaturases. Triacylglycerols are the major lipid pool in plasma and liver tissue and have a significant influence on fatty acid composition of membrane and circulating phospholipids. Data on the distribution of n-6 and n-3 polyunsaturated fatty acids of triacylglycerols in diabetes are sparse. We investigated whether streptozotocin-induced diabetes in Sprague–Dawley rats alters fatty acid composition of triacylglycerols and free fatty acids of liver tissue. The animals were fed a breeding diet prior to mating, during pregnancy and lactation. On days 1–2 of pregnancy, diabetes was induced in 10 of the 25 rats. Liver was obtained at post partum day 16 for analysis. Relative levels of LA ( P=0.03), dihomo-gamma-linolenic acid (DHGLA) ( P=0.02), AA ( P=0.049), total n-6 ( P=0.02), ALA ( P=0.013), eicosapentaenoic acid (EPA) ( P=0.004), docosapentaenoic acid (22:5n-3, DPA) ( P=0.013), DHA ( P=0.033), n-3 metabolites ( P=0.015) and total n-3 ( P=0.011) were significantly higher in the triacylglycerols of the diabetics compared with the controls. Similarly, liver free fatty acids of the diabetics had higher levels of LA ( P=0.0001), DHGLA ( P=0.001), AA ( P=0.001), n-6 metabolites ( P=0.002), total n-6 ( P=0.0001), ALA ( P=0.003), EPA ( P=0.015), docosapentaenoic (22:5n-3, P=0.003), DHA ( P=0.002), n-3 metabolites ( P=0.005) and total n-3 ( P=0.001). We conclude that impaired activity of desaturases and/or long chain acyl-CoA synthetase could not explain the higher levels of AA, DHA and n-6 and n-3 metabolites in the diabetics. This seems to be consistent with an alteration in the regulatory mechanism, which directs incorporation of polyunsaturated fatty acids either into triacylglycerols or phospholipids.
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