Digestive System: Part 6, The Jejunum

The jejunum is where nutrient uptake really gets going. Up to now, the digestive tract has been obsessed with mashing food up, breaking it down, and purifying it of pathogens, in order to maintain the purity of essence of our precious natural fluids. In the jejunum, digestive juices do continue to work, and there’s some last minute molecular-level destruction happening on the intestinal lining, but the primary focus has shifted from breaking nutrients down to absorbing them safely.

What does it mean to absorb safely? Well, despite its purification by cleansing acid in the stomach, the mashed up, churned up chyme flowing through the jejunum still has some bacteria in it, so the jejunum's lining (and, indeed, the lining of the rest of the intestine) must provide an unbroken barrier between the lumen (the inside of the intestine) and the bloodstream. Nutrients can only cross that barrier by passing (or being pulled) across it. Since only a limited amount of material can pass through a given area, absorption in the jejunum is a game of surface area. More surface area means more cells, means more absorption. Consequently, the jejunum (and the ileum after it) has tiny little projecting folds called villi—from the Latin, meaning “shaggy hair”. As you can see in the figure below, all those little crypts and folds cover more area than a level surface:

Even the cells themselves have their own little folds, creatively called microvilli—from the Latin and Greek, meaning “little shaggy hair,” where "villi" is Latin and "micro" is Greek. At least, I hope micro is Greek, in this case. If micro is Latin, then microvilli means “shaggy urine hair”.

Microvilli

These folds upon folds increase the surface area of the intestines by a factor of 600.¹ Introductory biology textbooks love to point out that, if all those folds were stretched flat, they would have the same surface area as a tennis court—an incredibly gross tennis court.

I mean, seriously, who the fuck would want to play tennis on some poor bastard's small intestine? I hereby formally request that textbook makers think of a size comparison that’s less creepy. Because, casually mentioning that the surface area of the small intestine is equal to a tennis court? That’s the kind of comment that feels right at home next to “basement graveyard” and “chairs made of human skeletons”.

Anyway.

Villi and microvilli are not the only tricks that the small intestine has to increase its surface area. It also increases it the old fashioned way: by being really, really long.

How long, exactly? You may be surprised to learn that this is a matter of some contention. Primary sources that measure the length of the small intestine in cadavers tend to peg the combined length of the jejunum and ileum at about 6 meters, whereas sources relying on live subjects say that it’s more like 3 to 5 meters.²

Why the difference? I haven't found a hard answer, but I suspect it has to do with how far an anatomist is willing to stretch a living patient’s small intestine just to take a measurement. At the very least, you hope that with a live patient, they'd stop at the entrance to the operating theater, so that someone doesn't accidentally slam the door on it. Imagine explaining that to the patient, when they wake up:

"Uh, yeah. So, me and the nurses were kind of playing with your small intestine, and we kind of broke it. But if you ask me, it's Gary from radiology's fault. He's the one that wasn't watching where he was going, and walked straight into the door. If he hadn't come along, I swear I could have stretched it straight into the medical director's office."

The small intestine is, after all, a very stretchy organ, so it's not terribly surprising that its reported length would vary depending on measurement method. It's so stretchy, in fact, that they used to make condoms out of it. (Note: still not creepier than the tennis court thing.)

So, what use is all that surface area put to? Well, the jejunum’s specialty is absorbing sugars, fats, and amino acids (the building blocks of proteins.) It also gets a start at nabbing vitamins, minerals, and water.³ As mentioned, all that good stuff has to get across an unbroken intestinal lining. Making up this lining are cells called enterocytes. They're the final arbiters of what's allowed into the body through the intestines, and what's locked safely outside the castle walls, left to wander the wastelands of the lumen. Passage through the cells takes many forms.

For example, selective channels in the enterocyte cell membranes allow sugars to pass freely, both in and out. But, since the concentration of sugar in the chyme is higher than the concentration in the cell, more sugars move in than out—that’s called a concentration gradient. To visualize a concentration gradient, imagine dropping dye into a glass of water. The spot where you drop it has a high concentration of dye to start with, while the rest of the glass has zero concentration. But, the longer you let it sit, the more the dye spreads out, until it’s distributed evenly through the glass. That’s diffusion. Simple diffusion means that more sugar molecules will move into enterocytes than move out, at least until the concentrations equalize.

The advantage of that method is simplicity. It doesn't require any effort or expenditure of energy. However, you can imagine how slow it is. Nobody wants to wait around for sugar to spread naturally, least of all your greedy body, so enterocytes have a clever little trick to speed the natural process up. They have specialized channels on their surface called cotransporters. These particular cotransporters allow both sodium and glucose to move into the cell together, as a single unit. That way, it's not just the higher concentration of sugar in the lumen that drives the diffusion, but also the much, much higher concentration of sodium.

Think of it like this: there's a movie that you kind of want to see. You know you’re going to see it eventually, but you’re not in any rush. You'll probably just catch it on Netflix in a few months. However, a friend calls you up. They want to see the movie tonight, and they want you to go with them. So you go along, driven more by your friend's interest than your own. In this analogy, you’re the sugar molecule, your friend is the sodium molecule, and the movie is 1987’s smash hit, Mannequin.

But what happens when the sodium runs out, too? No more cotransport, right? Wrong. Because enterocytes pump sodium out into the lumen, just so it can diffuse right back in again, dragging sugar with it. In the above analogy, this would be like you and your friend going to see Mannequin, but having your friend leave to bring someone else in to watch it with you. Then they leave again, to bring yet another person in. And so on and so forth, until you're all watching Mannequin in bitter harmony.

Model of cotransport from "The road to ion-coupled membrane processes" by Robert K. Crane

There are a few other tricks for getting sugars through the enterocytes. Some involve the expenditure of energy to actively pump them through. Some involve breaking double sugars (like sucrose or maltose) in two, and using the energy of that reaction to pump glucose (the most prolific simple sugar) into the enterocyte.⁴ Whatever the method, once sugars move across the enterocytes (literally going in one end and out the other,) they proceed into hepatic blood vessels, which all lead to the liver.

Fat has an equally interesting trip through the enterocytes. Smaller fats and fatty acids (a constituent of fat) will cross into and out of enterocytes without much fuss, passing directly through the cell membranes. That’s because the cell membranes are made out of lipids. Fats are just a type of lipid, so the small ones dissolve right into the lipid membrane without a problem, melting through it like hot butter through more butter. Larger fats have to be broken down into fatty acids before they’ll go through, but the bile from the duodenum will do exactly that.

A triglyceride fat.

Once inside the enterocytes, many of the smaller fats are taken apart the same way their larger cousins were out in the lumen, being broken down into fatty acids and glycerol. These short fatty acids can then travel directly into the bloodstream. The bigger fatty acids, which can't melt through the lipid membrane on their own, are pasted back together with a glycerol, rebuilding the same fats that the duodenum just got finished breaking down. Why bother with that? Well, the thing is, fatty acids are toxic.⁵ They’re great at storing chemical energy for later use in the body, but the little fuckers also want to kill you. That’s why our cells package them, whenever possible, into triglycerides (fats,) a more innocuous storage solution.

But there's a catch. Once the long fatty acids are reassembled inside the enterocyte... Well, do you remember why they had to be broken down in the first place? Because they were too big to get in. So what happens to them when they're reassembled? Yeah, exactly. Now they're too big to get into the bloodstream. (Cue sad trombone.)

Like Winnie the Pooh, Triglyceride made it inside, but got stuck in the door on its way out. But, unlike Pooh, Triglyceride’s friends actually help out, instead of just wandering by and generally being assholes about the whole affair. Triglyceride joins up with its friend Cholesterol, and they're both surrounded by a scaffold of proteins.

Exocytosis.

The protein scaffold and its contents are then excreted from the enterocyte in a process called exocytosis. Essentially, the scaffold and its cargo stuff themselves into a little bubble of lipid called a vesicle (see image to right.) This vesicle melts into to the cell membrane (which is made out of the same lipids,) thus releasing its contents out the back end of the enterocyte. From there, the triglyceride is still too big to cross over into the blood stream (encore sad trombone,) so it hangs out in the lymph fluid, until the lymph does what lymph eventually does, and drains into the bloodstream.

It's a kludgy, stupidly complex process, but it's required to keep naked fatty acids from poisoning you.

Which leaves amino acids, the building blocks of proteins. Mind you, the protein in your intestines, by this time, isn't just the protein that you ate. It also includes protein from your own body: digestive enzymes secreted in the saliva, the stomach, and especially the duodenum. It took significant resources to make those enzymes, so they too are broken down into their constituent amino acids, bravely laying down their lives for the good of the body. The amino acids, whatever their origin, are absorbed by cotransport with sodium, much like sugars are. Amino acids, however, come in twenty-two biologically critical flavors, each of which have different chemical properties. There are therefore four categories of transporter, that each serve one class of amino acid.⁶

The jejunum also starts the absorption of vitamins, minerals, and water, but we’ll save that for the ileum and the large intestine, which we'll be exploring in the coming months.

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Want to learn more about the digestive system? Check out the other articles in this series:

Digestive System, Part 1: Teeth and Spit   
Digestive System, Part 2: Swallowing
Digestive System, Part 3: Down the Tubes
Digestive System, Part 4: B-12 as Temptress
Digestive System, Part 5: The Duodenum    
Digestive System, Part 6: The Jejunum
Digestive System, Part 7: The Ileum
Digestive System, Part 8: Liver and Cecum
Digestive System, Part 9: The Colon
Digestive System, Part 10: The Bitter End 

Citations and References:

1. Human Biology, 5th Edition, pg 98
2. Anatomy of General Surgical Operations, 2nd Edition, pg 56
3. Nutrition & Diet Therapy, 7th Edition, pg. 542
4. Understanding Medical Physiology: A Textbook for Medical Students, 4th Edition, pg. 333
5. Nogueira de Sousa Andradea, et al. Toxicity of fatty acids on murine and human melanoma cell lines. Toxicology in Vitro. Volume 19, Issue 4. June 2005, Pages 553–560.
6.  Understanding Medical Physiology: A Textbook for Medical Students, 4th Edition, pg. 336