Diabetes-induced changes in specific lipid molecular species in rat myocardium

Citation
Xl. Han et al., Diabetes-induced changes in specific lipid molecular species in rat myocardium, BIOCHEM J, 352, 2000, pp. 79-89
Citations number
48
Categorie Soggetti
Biochemistry & Biophysics
Journal title
BIOCHEMICAL JOURNAL
ISSN journal
02646021 → ACNP
Volume
352
Year of publication
2000
Part
1
Pages
79 - 89
Database
ISI
SICI code
0264-6021(20001115)352:<79:DCISLM>2.0.ZU;2-K
Abstract
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.