Most tissues are able to degrade FA to C[O.sub.2] and [H.sub.2]O, but the liver has the unique capacity to synthesise ketone bodies, acetoacetate and 3-hydroxybutyrate from
acetyl-CoA, supplying an important fuel to other organs, mainly the brain (9).
Unlike normal cells that preferentially use dietary (exogenous) lipids for synthesis of endogenous lipids, cancer cells prefer de novo synthesis.[sup.4] Consequently, cancer cells have elevated expression and activity of key enzymes in this process that can serve as a therapeutic target.[sup.4] The first step of fatty acid synthesis is the formation of malonyl-CoA by condensation of
acetyl-CoA and CO[sub.2] catalyzed by
acetyl-CoA carboxylase, which is the major site of the regulation of fatty acid synthesis.
Acetyl-CoA carboxylase and fatty acid synthase activity and immunodetectable protein in adipose tissues of ruminants: Effect of temperature and feeding level.
The universal starting points are acetate (
acetyl-CoA), pyruvate, phosphoenol pyruvate, oxaloacetate, and 2-oxoglutarate.
The present study was designed to investigate the effect of feeding triacylglycerols on milk fat composition, lipogenesis and polymer-protomer transition of
acetyl-CoA carboxylase in rat mammary gland.
Pyruvate is converted (through the actions of the thiamine-dependent enzyme pyruvate dehydrogenase) into a molecule called
acetyl-CoA, which can then be fed into the second set of reactions, the citric acid cycle (also known as the tricarboxylic acid [TCA] cycle).
Acetyl-CoA is an essential metabolic intermediate in the carbon metabolism of all organisms.
The monomeric composition of PHA polymers is determined by the substrate specificities of [beta]-ketothiolase and PHB synthase and by the availability of
acetyl-CoA and propionyl-CoA.
These acids are made from acetyl-coenzyme A (
acetyl-CoA), which is also the starting material for biosynthesis of waxes, flavonoids, certain amino acids and other compounds.
This enzyme binds to both serotonin and a molecule called
acetyl-CoA, then attaches a fragment of
acetyl-CoA to serotonin.
Second, the fact that detoxification of the two products seems to occur along the same metabolic pathway leading to
acetyl-CoA production, although ADH is not involved in acetic acid tolerance.
It has also been shown that the AD brain has decreased activity of pyruvate dehydrogenase complex which generates
acetyl-CoA, the precursor of acetylcholine from pyruvate [41, 42], decreased activity of phosphofructokinase [43], and alpha-ketoglutarate dehydrogenase [44] but increased cerebral release of ammonia and amino acids [39, 40].