Small intestine 3: Absorption | Gastrointestinal system physiology | NCLEX-RN | Khan Academy

Small intestine 3: Absorption | Gastrointestinal system physiology | NCLEX-RN | Khan Academy

Voiceover: All right, great. So, now we have all of our
monomers ready to be absorbed. How does the absorption process
work? Let’s take a look. So, now we’re so close. We’ve got all of our monomers, but we need to figure out how the heck are we going to get them
inside our blood stream. Well, starting with our amino acids here. These guys are going to be shuttled into cells using what’s called primary active transport,
primary active transport. Now, if I say primary here, what does that specifically indicate as used? Now, you might recall when we use active transport, that means
we need a little bit of energy to get something to happen. And the form of energy that we use in primary active transport comes from ATP, the energy, the unit of life, adenosine tri as an three, phosphate. And so if we look at a
single enterocyte or an intestinal cell, there would be a protein that’s here on the cell membrane. This protein would break apart our ATP, cleaving off one of the phosphate groups to release adenosine diphosphate, so that’s two, diphosphate. And in doing so, would
allow our amino acid to enter into our enterocyte
or our intestinal cell. From there, the amino acid could undergo a couple of different
steps, but eventually will leave the enterocyte
and go to a blood capillary, where it enters the blood stream and then can be shuttled anywhere
else in the body for use. Monosaccharides are sugars, sort of have a similar thing going on,
but instead of primary active transport, we have what’s called secondary active transport going on. So, if we use the ATP for
primary active transport, what do we use for secondary? Well, the fact that we’re
saying this is still active transport means
that there was some energy that was used at some
point, and the energy actually was invested in
sending up an ion gradient. And so the ion gradient then
could be used by allowing something like sodium to
flow down its gradient, to go from the place of high concentration to low concentration where it can relax. And by allowing that to occur, energy is then harnessed allowing a monosaccharide or a sugar to
enter into our enterocyte. And just to make sure we’re complete, I’m going to draw the protein transporter we have here as well as
one on the other side, and show that there is a sodium ion that’s flowing into our enterocyte down its concentration gradient to end up in the enterocyte with the sugar. And sort of the same thing happens on the other side, except
as the sugar leaves, sodium on this side is entering. So, the sodium is still flowing down its concentration gradient, but it ends up inside the enterocyte
while the sugar leaves and goes to the blood capillary. So this also ends up in our blood stream and can go anywhere in
the body to be used. The nucleoside in the base sort of use the same mechanism that amino acids do. So, I’m just going to write primary active transport right here. And you can take a look above
to see how that happens. And by doing that, you can imagine where they are going to end up. That’s right, the blood capillary as well. And that takes us to our
last macro molecule, fat. Now, the thing about fat that’s rather redonkulous is that because it’s got this really nonpolar tail. If it ever shows up next to
an enterocyte like this guy, all it has to do is just
diffuse across the membrane, and then it ends up on the inside. In the enterocyte, all of our fatty acids are going to be reorganized into what are called
chylomicrons, chylomicrons. And like the name, chylomicrons
themselves are too big to fit directly into a blood capillary. I couldn’t even fit it
here in this enterocyte. So, it doesn’t actually directly go into the blood capillary. It is too big to do that. Too big to go to the blood capillary. Instead, chylomicrons will be absorbed into what are called lymphatic, lymphatic capillary, also known as a lacteal, a lymphatic capillary. And these are big enough to
accommodate our chylomicrons. Here, they’re going to be further digested and broken down into smaller
bits, and by the time that happens, they will end up in veins. That will send the digested fat through the heart and
eventually to arteries. That can then distribute them wherever they need to go in the body. And so you can appreciate
a lot it’s going on here. We’ve talked about how
all four of our major macromolecules are
digested in the duodenum, the place where the most
digestion occurs in the GI tract. And now, we just talked
about how they are absorbed, most likely in the jejunum, right. Because the jejunum is where the most absorption occurs
anywhere in the GI tract. And that’s how our small intestine works.

12 thoughts on “Small intestine 3: Absorption | Gastrointestinal system physiology | NCLEX-RN | Khan Academy

  1. Secondary transport in the way you present it for carbohydrate absorption would result in an enterocyte filled to the brim with sodium.. The enterocyte actually pumps sodium out of the cell with sodium potassium ATPase, not as an antiport with glucose as shown in the video. This is important, since to create the concentration gradient needed for the secondary transport of glucose from the lumen, the sodium concentration in the enterocyte MUST be lower in the enterocyte than in the intestinal lumen. I really like these videos and you're a great tutor, but this is a rather big error.

  2. I think there is something wrong here.. amino acids can transport inside the cell the same as glucose.
    resource :
    Guyton and hall medical physiology .

  3. I am also confused, shouldn't amino acid transport be secondary active transport energised by sodium gradient? This is what Constanzo book says.

  4. Sugar is transported to the enterocytes by co-transportation which is aginst concentration gradient But Not from high to low concentration gradient.

  5. the stomach parietal cell also secretes intrinsic factor for vit b12 absorption, and chief cell also secretes gatric lipase

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