Physiology 3120 Lecture Notes - Enteropeptidase, Trypsinogen, Tripeptide

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Published on 26 Nov 2011
Department
Professor
Human Physiology
Friday, April 9, 2010
“Gastro IX”
Protein digestion & absorption
Digestion begins in the stomach through the actions of pepsin, which is converted from pepsinogen by
the release of acid, which is in turn stimulated by ACh. Pepsin takes care of 15% of the proteolysis, and
the rest takes place due to pancreatic proteases. The predominant protease is trypsin, and is release as
the inactive precursor trypsinogen for the same reason that pepsin is released as an inactive precursor;
the important thing about these proteases is that they are secreted from the pancreas in response to
secretin, CCK, or ACh stimulation. The inactive enzymes are activated extracellular-ly, but the
mechanism is not by acid because bicarbonate is being released from the pancreatic extralobar duct
cells; they are activated by an enzyme in the brush-border enzyme in the duodenum, and this enzyme is
called enterokinase (activates MOST proteases). Once trypsin is formed, it can auto-catalyze
trypsinogen to make more trypsin, so enterokinase is only required to get the ball rolling.
After the proteases have done their thing, there is a mixture of [mostly] amino acids, and di/tripeptides
in the duodenum, so the proteases are quite efficient. Unlike carbohydrates, you can absorb proteins in
the form of individual amino acids, di- or tri-peptides. For individual amino acids, there is an apical
transporter that is identical to the Na/amino acid transporter just like the Na/glucose transporter except
the stoiciometric relationship is 1:1 instead of 2:1. On the basolateral surface, Na is removed by the Na
ATPase, and the amino acids are moved out via channels or a facilitated diffusion carrier. The four
carriers respond to different types of amino acids (acidic, basic, neutral, imino acids); these carriers are
less specific because 4-7 acids can bind to any carriers. There is also a single carrier (with no specificity)
that takes every di- and tri-peptide; it probably works the same way as the AA carrier.
Lipid digestion & absorption
Digestion
Predominant type of fat in diet is a triglyceride (glycerol backbone + 3 FAs). The major organ
for lipid digestion is the pancreas (just like it was for proteins and carbs); it secretes enzymes
called pancreatic lipases into the proximal small intestine. Unlike the proteases, the lipases DO
NOT have to be activated. They act by chopping off the FA at the 1st and 3rd carbon of TG,
leaving 2 free fatty acids (FFAs) and 2-monoglyceride (2-MG).
The problem with this mechanism is that lipase is water-soluble, but the lipids it digests are not
water-soluble; therefore, the lipase can only act at the water-fat interface if no other mechanism
existed. So to increase the surface area in contact with the water, “shake up” the system using
smooth muscle contractions to break the lipids into smaller droplets (emulsification); this
provides a short-term solution, but eventually the big globules will re-coalesce, so there must be
a way to maintain the emulsion. The stabilizing mechanism is bile acids/salts. They are
synthesized from cholesterol, which is modified in the liver with molecules that are water-
soluble to make an amphipathic molecule; the water-soluble portions ALL end up with the same
net charge, so they repel each other, so different globs of lipids are not going to want to re-
coalesce quickly.
Absorption
Problem is still not solved because the products of digestion are fat-soluble and the predominant
intestinal environment is aqueous. Would like to evenly distribute digested fat over absorptive
surface, but mechanical absorption won’t work because of the contractile properties of the
intestine; the best method would be to solubilise the fat; WELL the bile salts also serve to
solubilise the products of lipid digestion. Initially, to stabilize the emulsion, you don’t need much
bile salt, but as you digest the lipids, more bile salts are released from the gall bladder (stores
bile), and is stimulated by CCK. More bile salts spontaneously form aggregates (spheres of bile
salts called a micelle), and lipid products will be taken into the fat-soluble core of the micelle,
and will therefore become soluble in the water-soluble micelle. What you have done is increased
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