LECTURE "Lack of mitochondrial acyl-coenzyme A synthetase Acsm3 may contribute to hypertriglyceridemia in PD rat"
The rat inbred strain PD/Cub is a model of diet-sensitive metabolic syndrome, with marked elevation of triacylglycerols, especially in chylomicron and VLDL fractions, after feeding high sucrose or high fat diet. We compared liver transcriptome of PD rats with control BN (no metabolic syndrome) and SHR (metabolic syndrome with hypertension, but without striking hypertriglyceridemia) after 4 weeks of high fat diet.
We used microarrays with subsequent qPCR confirmation. Acsm3 (acyl-CoA synthetase medium chain family member 3, also known as SAH = Spontaneously hypertensive rat-clone A-Hypertension associated), coding for mitochondrial acyl-coenzyme A synthetase, which activates medium chain fatty acids for beta-oxidation, was completely absent from PD while BN and SHR had comparable mRNA levels. We hypothesize that Acsm3 absence can lead to impaired activation of fatty acids, which in turn can decrease fatty acid utilization with subsequent hypertriglyceridemia.