Intrinsic cardiac dysfunction during the diabetic state has been causally l
inked to changes in myocardial lipid metabolism. However, the precise alter
ations in the molecular species of myocardial polar and non-polar lipids du
ring the diabetic state and their responses to insulin have not been invest
igated. Herein we demonstrate four specific alterations in rat myocardial l
ipid molecular species after induction of the diabetic state by streptozoto
cin treatment: (i) a massive remodelling; of triacylglycerol molecular spec
ies including a > 5-fold increase in tripalmitin mass and a 60% decrease in
polyunsaturated triacylglycerol molecular species mass (i.e. triacylglycer
ols containing at least one acyl residue with more than two double bonds);
(ii) a 46 % increase in myocardial phosphatidylinositol mass; (iii) a 44 %
increase in myocardial plasmenylethanolamine mass and (iv) a 22 % decrease
in 1-stearoyl-2-arachidonoyl phosphatidylethanol-amine content. Each of the
changes in phospholipid classes, subclasses and individual molecular speci
es were prevented by insulin treatment after induction of the diabetic stat
e. In sharp contrast, the alterations in triacylglycerol molecular species
were not preventable by peripheral insulin treatment after induction of the
diabetic state. These results segregate diabetes-induced alterations in my
ocardial lipid metabolism into changes that can be remedied or not by routi
ne peripheral insulin treatment and suggest that peripheral insulin therapy
alone may not be sufficient to correct all of the metabolic alterations pr
esent in diabetic myocardium.