Fatty Acid Lipolysis and Oxidation
By:
Derek Charlebois
The main energy reserve
in the human body is stored as adipose tissue triglycerides (glycerol
bonded to three fatty acid chains), which is commonly referred to
as fat. Triglycerides (TG) are also stored in skeletal muscle cells
as intramuscular triglycerides (IMTG), between muscle fibers as
extramyocellular triglyceride (EMTG), and circulate in the plasma.
The total amount of triglycerides stored in the body far exceeds
the amount of stored glucose (in the form of muscle and liver glycogen),
the body’s other main source of energy. Storing calories as fat
is more than twice as efficient as storing them as glycogen since
one gram of fat provides about nine calories of useable energy while
one gram of glucose provides about four grams of useable energy.
Due to fats high energy storing capacity, it is vital for human
life.
The manipulation of ones body fat percentage, specifically reducing
it, is of prime interest to researchers studying obesity and the
general public looking to “get in shape.” Understanding the interworking
of triglyceride lipolysis and oxidation will allow for exercise
and dietary intervention to be implemented in the most efficient
manner.
Lipolysis
Lean adults have more
than 80,000 kcals of potential energy stored as adipose tissue triglycerides
(Horowitx 2003). Before the body can harness this energy, the triglycerides
must be hydrolyzed into glycerol and three fatty acid chains. First,
hormones, specifically epinephrine and norepinephrine, stimulate
the adipocytes. Next, the enzyme hormone sensitive lipase acts on
the triglyceride molecule, which releases two FFA and one monoacylglycerol
(MAG) molecule. MAG is metabolized by monoacylglycerol lipase producing
a FFA molecule and glycerol, resulting in a total of three FFA and
one glycerol (Ronallo & Rhodes 1998). After triglyceride hydrolysis
has occurred, the resulting fatty acids must be transported in the
bloodstream to active tissues (skeletal muscle, liver, heart) by
the protein albumin to be oxidized. The glycerol enters the bloodstream
and is metabolized into glucose in the liver.
Transport
Blood flow is of prime
importance to transport of FFA away from adipocytes and through
the circulation to active tissues. This is especially important
during exercise where energy requirements are heightened.
Low blood flow could cause the accumulation of FFA within adipose
tissue (Coppack et al 1994) resulting in less available FFA to be
oxidized and a greater chance of FFA reesterification into trigylcerides.
Oxidation
Fat can be oxidized in the mitochondria and the peroxisomes of
cells, with the majority of this oxidation occurring in skeletal
muscle cells and the liver. Carnitine palmitolyltransferase-I (CPT-I),
the rate-limiting enzyme in beta-oxidation of long-chain fatty acids
(LCFA) in skeletal muscle and liver cell mitochondria, is found
on the outer membrane of mitochondria and carries long chain fatty
acids across the membrane and into the mitochondria by binding to
them. Medium-chain fatty acid (MCFA) oxidation is less inhibited
than LCFA oxidation because part of the MCFAs can freely diffuse
into the mitochondria and they use the enzyme carnitine octanoyl
transferase, which is less regulated that CPT (Achten & Jeukendrup,
2004).
References:
Achten, J. Jeukendrup, AE. Optimizing Fat Oxidation through exercise
and diet. Nutrition 2004;20:716 –727.
Coppack SW, Jensen MD, Miles JM. In vivo regulation of lipolysis
in humans.
J Lipid Res. 1994 Feb;35(2):177-93.
Horowitz, JF. Fatty acid mobilization from adipose tissue during
exercise.
Trends Endocrinol Metab. 2003 Oct;14(8):386-92.
Ranallo RF, Rhodes EC. Lipid metabolism during exercise. Sports
Med. 1998 Jul;26(1):29-42.
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