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U N I T 8
Gastrointestinal and Hepatobiliary Function
protein synthesis and degradation. It produces proteins
for its own cellular needs, as well as secretory proteins
(e.g., plasma proteins, fibrinogen, and coagulation fac-
tors) that are released into the circulation. One of the
most important of these secretory proteins is albumin.
Albumin contributes significantly to the plasma colloi-
dal osmotic pressure (see Chapter 8) and to the binding
and transport of numerous substances such as hor-
mones, fatty acids, and bilirubin.
Proteins are made up of amino acids. Protein syn-
thesis and degradation involves two major reactions:
transamination and deamination
1
(Fig. 30-4C). In
trans-
amination,
an amino group (NH
2
) is transferred to an
acceptor substance. The process is catalyzed by
amino-
transferases,
enzymes that are found in high amounts
in the liver. As a result of transamination, amino acids
can participate in the intermediary metabolism of car-
bohydrates and lipids. During periods of fasting or
starvation, amino acids are used for producing glucose
(i.e., gluconeogenesis). Most of the nonessential amino
acids are synthesized in the liver by transamination.
Oxidative
deamination
involves the removal of the
amino group and a hydrogen atom from an amino acid.
This yields ammonia (NH
3
). Because ammonia is very
toxic to body tissues, particularly neurons, the ammonia
that is released during the deamination process is rap-
idly removed from the blood by the liver and combined
with carbon dioxide to form urea. Essentially all urea
formed in the body is synthesized by the urea cycle in
the liver and then excreted by the kidneys.
Although urea is mostly excreted by the kidneys,
some diffuses into the intestine, where it is converted
to ammonia by enteric bacteria. The intestinal produc-
tion of ammonia also results from bacterial deamination
of unabsorbed amino acids and proteins derived from
the diet, exfoliated cells, or blood in the gastrointestinal
tract. Ammonia produced in the intestine is absorbed
into the portal circulation and transported to the liver,
Amino acids Glycerol
Lactic acid
Gluconeogenesis
Glycogen
Triglycerides
Bloodstream
Dietary proteins
Amino acid
Tissue protein
Plasma proteins
Glucose synthesis
(gluconeogenesis)
Synthesis of
nonessential
amino acids
Fatty acids
Ammonia
Ketoacids
Acetyl-CoA
Urea
cycle
Citric acid
cycle
ATP
Urea
Dietary fat
Liver
C
B
Glucose
Fatty acid
Acetyl-CoA
Phospholipids
and complex
lipids for
cell structures
Storage as
triglycerols
Beta oxidation
Synthesis
Ketone
bodies
HMG-CoA
Carbohydrates
and amino acids
metabolism
Citric
acid cycle
ATP
Cholesterol
Bile salts
Steroid synthesis
Transamination/
deamination
A
FIGURE 30-4.
Hepatic pathways for
(A)
glucose metabolism,
(B)
lipid metabolism, and
(C)
protein metabolism
and conversion of ammonia to urea. ATP, adenosine triphosphate; HMG-CoA, hydroxymethylglutaryl-CoA.
