Maintenance of the Body
Nearly all products of fat digestion enter the lymph in the form
of chylomicrons, which are hydrolyzed to fatty acids and glyc-
erol before they can pass through the capillary walls.
, the enzyme that catalyzes fat hydrolysis, is particularly
active in the capillaries of muscle and fat tissues.
Adipose cells, skeletal and cardiac muscle cells, and liver cells
use triglycerides as their primary energy source, but when die-
tary carbohydrates are limited, other cells begin to oxidize more
fat for energy. Although some fatty acids and glycerol are used
for anabolic purposes by tissue cells, most enter adipose tissue
to be reconverted to triglycerides and stored.
Absorbed amino acids are delivered to the liver, which deami-
nates some of them to keto acids. Te keto acids may ﬂow into
the Krebs cycle to be used for A±P synthesis, or they may be
converted to liver fat stores. Te liver also uses some of the
amino acids to synthesize plasma proteins, including albumin,
clotting proteins, and transport proteins.
However, most amino acids ﬂushing through the liver sinu-
soids remain in the blood for uptake by other body cells, where
they are used to synthesize proteins. Figure 24.18 has been sim-
pliﬁed to show nonliver amino acid uptake only by muscle.
Hormonal Control of the Absorptive State
Insulin directs essentially all events of the absorptive state
. A²er a meal, rising blood glucose and amino
acid levels stimulate the beta cells of the pancreatic islets to se-
crete more insulin (see Figure 16.19). Te GI tract hormone
glucose-dependent insulinotropic peptide (GIP) and parasym-
pathetic stimulation also promote the release of insulin.
Insulin binds to membrane receptors of its target cells. Tis
stimulates the translocation of the glucose transporter (GLU±4)
to the plasma membrane, which enhances the carrier-mediated
facilitated diﬀusion of glucose into those cells. Within minutes,
the rate of glucose entry into tissue cells (particularly muscle and
adipose cells) increases about 20-fold. Te exception is brain and
liver cells, which take up glucose whether or not insulin is present.
Once glucose enters tissue cells, insulin enhances glucose
oxidation for energy and stimulates its conversion to glycogen
and, in adipose tissue, to triglycerides. Insulin also “revs up” the
active transport of amino acids into cells, promotes protein syn-
thesis, and inhibits liver export of glucose and virtually all liver
enzymes that promote gluconeogenesis.
As you can see, insulin is a
mik). It sweeps glucose out of the blood into tissue cells,
lowering blood glucose levels. It also enhances glucose oxida-
tion or storage while inhibiting any process that might raise
blood glucose levels.
Homeostatic Imbalance 24.3
is a disorder of inadequate insulin production
or abnormal insulin receptors. Without insulin or receptors
that “recognize” it, glucose is unavailable to most body cells.
energy fuel. Dietary amino acids and fats are used to remake de-
graded body protein or fat, and small amounts are oxidized to
provide A±P. Excess metabolites, regardless of source, are trans-
formed to fat if not used for anabolism. Let’s look at the fate and
hormonal control of each nutrient group during this phase.
Absorbed monosaccharides are delivered directly to the liver,
where fructose and galactose are converted to glucose. Glucose,
in turn, is released to the blood or converted to glycogen and
fat. Glycogen formed in the liver is stored there, but most fat
synthesized there is packaged with proteins as
very low density
) and released to the blood to be picked up
by adipose tissues for storage.
Bloodborne glucose not sequestered by the liver enters body
cells to be metabolized for energy. Excess glucose is stored in
skeletal muscle cells as glycogen or in adipose cells as fat.
Targets tissue cells
Beta cells of
of amino acids
into tissue cells
of glucose into
Insulin directs nearly all events of the
(Note: Not all effects shown occur in all cells.)