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Do it yourself intestinal remodeling
You eat it…….. you absorb it.
That’s the way we think about nutrition. We don’t often think about, how it happens and/or the players.
So let me introduce you to the body part of the moment…………
An intestinal villi.
You’ve got lots of them.
Butting out from intestinal surface…..
In charge of absorption
They’re quite a complex structure. Each villus is approx 0.5 mm – 1.6 mm in length and composed of many enterocytes. These enterocytes have microvilli projecting from their surface. Enterocytes are the cells that are tasked with mopping up the goodies, you eat.
Well that’s the day job of the enterocytes. It pays the bills.
But, what every enterocyte dreams of, is to bungee jump, into the abyss.
They are born daredevils.
They live fast and die young.
And living faster, is their REAL objective.
In the beginning….
It all begins in the base station of the villi. Specialized intestinal stem cells, birth baby enterocytes.
They jostle each other, for a place on “the travelator”.
The unlucky ones, get pushed down, not up…..
Keeping good cells down
Some end up, trapped in the base station, which is for the most part, is a BIG disappointment, but not a hopeless situation. The opportunity to float free, is delayed, not obliterated.
If you’re in the base station, you are required to “go forth and multiply”.
But multiplication has perks……
There is always the possibility of escape. Cells that can position themselves, just right, can push their way out of the base station and hop on the travelator, and head for glory.
The hell of being a Paneth cell
The really unlucky ones, get pushed into the basement of the travelator and put to work, as Paneth cells.
It is hard labour.
Paneth cells are in charge of travelator, maintenance and security.
Both worthy jobs, but from an intestinal cell perspective, this is like being banished to “hell”. The problem, you live a whole lot longer, work hard everyday and never get to float free.
The highs and lows of being an enterocyte
Don’t get me wrong, the “lucky” enterocytes, also WORK HARD.
As they climb onto the travelator, bound for their moment of glory, they are expected to pull finger and fuel the machinery. They reach out and grab, all the nutrients, you have provided, sugars, fats, amino acids, vitamins and minerals.
The nutrients are processed and then passed on.
Using the supply lines that run beneath the travelator. Water soluble items get loaded into blood capillaries, fat soluble items, are shoved into lacteals.
It’s hard work………… but rewarding.
Reaching the goal
The more nutrients grabbed, the faster and further the travelator moves.
And everyone WINS.
Well the enterocytes do, the fat cells might feel differently.
This is what a team of researchers from ………………… discovered.
The team investigated villi construction, in genetically disadvantaged mice (db/db mice). The disadvantage these mice were suffering from, is they NEVER FEEL FULL.
Which means, they eat and eat and eat.
And if you eat non-stop, you end up being fat and diabetic.
Ag shame !
So what happens to your villi, in this situation ?
The Long villi
Well, since the cells are receiving more nutrients, they are able to extend their reach and move along faster.
This can be seen here…..
The first panel, shows what happens in a normal mouse. The second panel, shows the villi in the genetically disadvantaged mice, who eat non-stop.
The continuous grazing, causes the villi to be about one third longer.
So what ?
Longer villi are more efficient, OR NOT
Well it is a vicious cycle………..
The longer your villi are, the more nutrients you’ll absorb. And the more nutrients you absorb, the longer you villi will be.
And…………………. THE FATTER YOU WILL BE.
Because, more calories in, mean there are more calories available.
To use and TO STORE.
Driven by catenin signalling
Now the team, being science types, wanted to know, why the villi were longer.
And how to stop the process.
Using radiographic probes and inhibitors, they established that the process was being driven by catenin signalling, inside the base station.
Basically the cells in the base station, were being told to speed up their “go forth and multiply”.
So what was sparking catenin signalling ?
Food, glorious food…………
It really didn’t matter what the food was.
Carbs did. So did fats.
Would curtailing nutrient supply, shorten the villi ?
Shortening the villi
The team put their genetically disadvantaged mice ON DIET.
By taking away the food.
The mice were fed twice daily, instead of being allowed to eat whenever they felt like it.
It was HARD on the mice, remember these little guys, NEVER FEEL FULL. NEVER ! But within a short space of time, the villi, returned to “normal” levels.
Of course, as an added bonus, the mice lost weight.
This research suggests…………
Not a genetic disadvantage is behind the extra weight.
We know INTESTINAL REMODELING can help melt away the pounds…..
In fact, this is the premise behind bariatric surgery.
Surgeons, re-wire the gut, to stop, nutrients passing through much of the small intestine. Ouch !
But, you don’t have to re-wire the gut, to get the benefit.
DYI intestinal remodeling
You can do a little intestinal remodelling, without going under the knife. Since the presence of nutrients in the small intestine, IS THE TRIGGER.
Make sure, nutrients aren’t PRESENT 24/7.
Try restricting your eating to a defined time period, shoot for an 8 to 12 hour window, so you give the little guys at the base station, a breather and keep your villi in shape.
Your dustbin men sit tight, when you’re insulin resistant. So cleaning up barely happens. Wastes pile up and this has health consequences – diabetes, CVD, NASH
When meal frequency shifts away from the magic number of 3 meals a day – weight changes. People eating lots of small meals per day, get bigger.
It might sound counterintuitive, but when you’re battling insulin resistance, you don’t want to aim to eat like a bird, you want to eat like a horse. Go BIG.