![]() ![]() Metabolically challenged Decr −/− mice turned on ketogenesis, but unexpectedly developed hypoglycemia. In line with this expectation, fasted Decr −/− mice displayed increased serum acylcarnitines, especially decadienoylcarnitine, a product of the incomplete oxidation of linoleic acid (C 18:2), urinary excretion of unsaturated dicarboxylic acids, and hepatic steatosis, wherein unsaturated fatty acids accumulate in liver triacylglycerols. In Decr −/− mice, the mitochondrial β-oxidation of unsaturated fatty acids with double bonds is expected to halt at the level of trans-2, cis/trans-4-dienoyl-CoA intermediates. ![]() To elucidate the role of 2,4-dienoyl-CoA reductase (DECR) as an auxiliary enzyme in the mitochondrial β-oxidation of unsaturated fatty acids, we created a DECR–deficient mouse line. Enzyme defects in this pathway cause fatty acid oxidation disorders. The mitochondrial β-oxidation system is one of the central metabolic pathways of energy metabolism in mammals. ![]()
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