Key result
Diabetes enhanced total fatty acid utilization in perfused mouse hearts, with LPL-derived FA oxidation and esterification increasing up to 3.4-fold and 2.5-fold, respectively.
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Diabetes enhances total fatty acid utilization (oxidation and esterification) in the heart without influencing the supply of LPL-derived fatty acids.
Hydrolysis of triacylglycerols (TG) in circulating chylomicrons by endothelium-bound lipoprotein lipase (LPL) provides a source of fatty acids (FA) for cardiac metabolism. The effect of diabetes on the metabolism of chylomicrons by perfused mouse hearts was investigated with db/db (type 2) and streptozotocin (STZ)-treated (type 1) diabetic mice. Endothelium-bound heparin-releasable LPL activity was unchanged in both type 1 and type 2 diabetic hearts. The metabolism of LPL-derived FA was examined by perfusing hearts with chylomicrons containing radiolabeled TG and by measuring (3)H(2)O accumulation in the perfusate (oxidation) and incorporation of radioactivity into tissue TG (esterification). Rates of LPL-derived FA oxidation and esterification were increased 2.3-fold and 1.7-fold in db/db hearts. Similarly, LPL-derived FA oxidation and esterification were increased 3.4-fold and 2.5-fold, respectively, in perfused hearts from STZ-treated mice. The oxidation and esterification of [(3)H]palmitate complexed to albumin were also increased in type 1 and type 2 diabetic hearts. Therefore, diabetes may not influence the supply of LPL-derived FA, but total FA utilization (oxidation and esterification) was enhanced.
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Neitzel et al. (2003) studied Diabetes. Diabetes (type 1 and type 2) vs. Non-diabetic controls was evaluated on Rates of LPL-derived FA oxidation and esterification (increased up to 3.4-fold (oxidation) and 2.5-fold (esterification)). Diabetes enhanced total fatty acid utilization in perfused mouse hearts, with LPL-derived FA oxidation and esterification increasing up to 3.4-fold and 2.5-fold, respectively.
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