Very Triacylglycerols in chylomicrons and LDLs will circulate

Very low density lipoproteins are
not as dense as chylomicrons. These lipoproteins are based on protein
components not as much lipids. Both vldl and ldl are known as bad cholesterols
since their serum concentration levels are responsible for different heart and
artery diseases like strokes. HDL are about half and half when it comes to the
lipid and protein ratio. They are good cholesterols since they to lower the
rate of artery diseases.  

High?density lipoproteins (HDLs) will
contain a different apolipoprotein form, Apolipoprotein A which is different
than those of low density. These proteins are just about half lipid and half
protein by weight. Phospholipids and cholesterol esters are the most important
lipid components. HDL can be sometimes referred to as “good cholesterol”
because a higher ratio of HDL to LDL corresponds to a lower rate of coronary
artery disease.

In summary, these triacylglycerols
from the diet are digested by lipase and associate with bile salts into mixed
micelles. The free fatty acids are absorbed by the cells in the small
intestine, from which they are transported via the lymph system to the liver. From
the liver, they are released as apolipoproteins in the circulation, which can
be used for carrying fatty acids and cholesterol to the cells throughout the
body.

Triacylglycerols in chylomicrons and LDLs will circulate
through the blood system; the former carries dietary lipids while the latter
carries lipids that are synthesized by the liver. These triacylglycerols are used
as substrates for cellular lipases, which hydrolyze them to make fatty acids
and glycerol in several different steps. Many carrier proteins transport the
lipids into the cell in different pathways. There are many different carriers that
exist for different chain?length lipids.

Energy production from triacylglycerols
starts with their hydrolysis into free fatty acids and glycerol. When analyzing
this adipose (fat?storing)
tissue, this hydrolysis will be carried out by a cellular lipase, which
catalyzes the hydrolysis reaction to release the free fatty acids and glycerol.
The fatty acid is carried through the bloodstream by being adsorbed to serum
albumin, while the glycerol goes to the liver. In the liver, glycerol can be
sent to the glycolytic pathway by the action of two enzymes, glycerol kinase
and glycerol?3?phosphate dehydrogenase. Glyceraldehyde?3?phosphate can also be
used as a source of glucose or, after conversion to phosphoenolpyruvate, as a
source of tricarboxylic acid cycle (TCA?cycle) intermediates.

In target tissues, fatty acids are
broken down through the ?? oxidation
pathway that releases 2?carbon units in succession. For example,
palmitic acid has 16 carbons. Its initial oxidation produces eight
acetyl?Coenzyme A (CoA) molecules, eight reduced FAD molecules, and eight NADH
molecules. The fatty acid is first activated at
the outer mitochondrial surface by conjugating it with CoA, then transported through the inner
mitochondrial membrane to the matrix, and then, for each 2?carbon unit, broken
down by successive dehydrogenation,
water addition, dehydrogenation, and hydrolysis reactions. The first reaction will involve the
catalization by the  isoforms of
acyl-CoA dehydrogenase (AD) on the inner-mitochondrial membrane. This reaction
will result in trans double bond, different from naturally occurring
unsaturated fatty acids. Analogous to succinate dehydrogenase reaction in the
citric acid cycle; the electrons from bound FAD transferred directly to the
electron- transport chain via electron-transferring flavoprotein (ETF) which is catalyzed by
two isoforms of enoyl-CoA hydratase. Next, water adds across the double bond yielding
alcohol, analogous to fumarase reaction in the citric acid cycle
with the same stereospecificity. Following this reaction, the one is  catalyzed by b-hydroxyacyl-CoA
dehydrogenase which  uses NAD cofactor
as the hydride acceptor. In this reaction, only L-isomers of hydroxyacyl CoA
act as substrates which is analogous to malate dehydrogenase reaction in
the citric acid cycle. The next reaction is catalyzed by acyl-CoA acetyltransferase
(thiolase) via covalent mechanism: The carbonyl carbon in b-ketoacyl-CoA
is electrophilic, active site thiolate acts as nucleophile and releases
acetyl-CoA, and the terminal sulfur in CoA-SH acts as nucleophile and
picks up the fatty acid chain from the enzyme. This will result in the net
reaction of thiolysis of carbon-carbon bond.