Regulation of Organic Metabolism and Energy Balance
569
(glycerol linked to one fatty acid chain) and fatty acids by the
enzyme
lipoprotein lipase.
This enzyme is located on the
blood-facing surface of capillary endothelial cells, especially
those in adipose tissue. In adipose tissue capillaries, the fatty
acids generated diffuse across the capillary wall and into the adi-
pocytes. There they combine with
α
-glycerol phosphate, sup-
plied by glucose metabolites, to form triglycerides once again.
Thus, most of the fatty acids in the VLDL triglycerides origi-
nally synthesized from glucose by the
liver
end up being stored
in triglyceride in
adipose tissue.
The monoglycerides formed in
the blood by the action of lipoprotein lipase in adipose tissue
capillaries circulate to the liver, where they are metabolized.
To summarize, the major fates of glucose during the
absorptive phase are utilization for energy, storage as glycogen
in liver and skeletal muscle, and storage as fat in adipose tissue.
Absorbed Triglycerides
As described in Chapter 15, absorbed chylomicrons enter
the lymph, which fl ows into the systemic circulation. The
biochemical processing of these chylomicron triglycerides in
plasma is quite similar to that just described for VLDLs pro-
duced by the liver. The fatty acids of plasma chylomicrons are
released, mainly within adipose tissue capillaries, by the action
of endothelial lipoprotein lipase. The released fatty acids then
enter adipocytes and combine with
α
-glycerol phosphate, syn-
thesized in the adipocytes from glucose metabolites, to form
triglycerides.
The importance of glucose for triglyceride synthesis in
adipocytes cannot be overemphasized. Adipocytes do not
have the enzyme required for phosphorylation of glycerol, so
α
-glycerol phosphate can be formed in these cells only from
glucose metabolites and not from glycerol or any other fat
metabolites.
In contrast to
α
-glycerol phosphate, there are three major
sources of the fatty acids found in adipose tissue triglyceride:
(1) glucose that enters adipose tissue and is converted to fatty
acids; (2) glucose that is converted in the liver to VLDL triglyc-
erides, which are transported via the blood to the adipose tis-
sue; and (3) ingested triglycerides transported to adipose tissue
in chylomicrons. As we have seen, sources (2) and (3) require
the action of lipoprotein lipase to release the fatty acids from the
circulating triglycerides.
This description has emphasized the
storage
of ingested
fat. For simplicity, Figure 16–1 does not include the fraction
of the ingested fat that is not stored, but is oxidized during the
absorptive state by various organs to provide energy. The rela-
tive amounts of carbohydrate and fat used for energy during the
absorptive period depend largely on the content of the meal.
Absorbed Amino Acids
Some absorbed amino acids enter liver cells. They are used to
synthesize a variety of proteins, including liver enzymes and
plasma proteins, or they are converted to carbohydrate-like
intermediates known as
`
-ketoacids
by removal of the amino
group. This process is called deamination. The amino groups
are used to synthesize urea in the liver, which enters the blood
and is excreted by the kidneys. The
α
-ketoacids can enter the
Krebs tricarboxylic acid cycle and be catabolized to provide
energy for the liver cells. They can also be converted to fatty
acids, thereby participating in fat synthesis by the liver.
Most ingested amino acids are not taken up by the liver
cells, however, but instead enter other cells (see Figure 16–1),
where they may be used to synthesize proteins. All cells
require a constant supply of amino acids for protein synthesis
and participate in protein metabolism.
Protein synthesis is represented by a dashed arrow in
Figure 16–1 to call attention to an important fact: There is
a net synthesis of protein during the absorptive period, but
this basically just replaces the proteins catabolized during the
postabsorptive period. In other words, excess amino acids are
not stored as protein in the sense that glucose is stored as gly-
cogen or that both glucose and fat are stored as fat. Rather,
ingested amino acids in excess of those needed to maintain
a stable rate of protein turnover are merely converted to car-
bohydrate or fat. Therefore, eating large amounts of protein
does not in itself cause increases in body protein. Increased
daily consumption of protein does, however, provide the
amino acids needed to support the high rates of protein syn-
thesis occurring in growing children or in adults who increase
muscle mass by weight-lifting exercise.
Table 16–1
summarizes nutrient metabolism during the
absorptive period.
Postabsorptive State
As the absorptive period ends, net synthesis of glycogen, fat, and
protein ceases, and net catabolism of all these substances begins
to occur. The overall signifi cance of these events can be under-
stood in terms of the essential problem during the postabsorp-
tive period: No glucose is being absorbed from the intestinal
tract, yet the plasma glucose concentration must be maintained
because the brain normally utilizes only glucose for energy. If
plasma glucose concentration decreases too much, alterations
of neural activity can occur, ranging from subtle impairment of
mental function to seizures, coma, and even death.
The events that maintain plasma glucose concentration
fall into two categories: (1) reactions that provide sources of
blood glucose, and (2) cellular utilization of fat for energy,
thus “sparing” glucose.
Table 16–1
Summary of Nutrient Metabolism
During the Absorptive Period
1.
Energy is provided primarily by absorbed carbohydrate in a
typical meal.
2.
There is net uptake of glucose by the liver.
3.
Some carbohydrate is stored as glycogen in liver and muscle,
but most carbohydrates and fats in excess of that used for
energy are stored as fat in adipose tissue.
4.
There is some synthesis of body proteins, but some of
the amino acids in dietary protein are used for energy or
converted to fat.
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