(Narrator) This is Armando.
This video was created as part of the Hungry Microbiome Project,
which I made at CSIRO.
Some foods are not digested and absorbed by the small intestine
and so reach the large intestine, also known as the colon.
Resistant starch, for example, is a portion of starch
that escapes digestion in the small intestine
because it is resistant to human digestive enzymes.
However resistant starch still contain energy that our body needs,
and so once resistant starch
reaches the colon the resistant starch will undergo
fermentation by the trillions of bacteria that live there.
Through fermentation the bacteria produces substances
such as short chain fatty-acids,
which our colon cells use as their main source of energy.
In this video we will focus on the process of starch fermentation.
Starch that has resisted digestion
in the small intestine and reached the colon are called resistant starch.
Resistant starch will undergo fermentation by bacteria in the colon.
Resistant starch are made up of amylose and amylopectin,
which are two forms of glucose polymers.
Fermentation of carbohydrates such as resistant starch
lead to the production of short chain fatty-acids.
Let us look at a simple pathway
of how these short chain fatty-acids are produced.
Now within the colon you have primary degraders of resistant starch,
such as bifidobacterium species,
bacteroides species and ruminococcus bromii.
The primary degraders have enzymes
that are important in breaking down resistant starch and fermenting it.
Many products are produced
through the fermentation of resistant starch by the primary degraders.
Glucose can be released thanks to membrane
bound enzymes that cleave off glucose polymers.
Through fermentation of glucose these
primary degraders can produce the two carbon
short chain fatty-acid acetate,
and release formate in the process.
Formate is essentially gases,
carbon dioxide and hydrogen.
These can later be used
by other bacterial species that live in the colon.
Through the fermentation of glucose
the primary degraders can also produce
the three carbon short chain fatty-acid called propionate,
which also forms some gases as a by-product.
Now succinate and lactate
are also produced by these primary degraders,
and are efficiently utilised by certain anaerobic bacteria.
The gases formed through fermentation, such as formate,
can be utilised by methanogens to produce methane.
Interesting fact, methane and other gases,
such as carbon dioxide and hydrogen,
contribute to the chemistry of fart and its smell.
Because these gases are produced in the lumen of the colon
they are often expelled out.
Also if there is sufficient amounts of formate
acetogens are able to utilise formate to produce acetate.
Now back to the degraders.
There are another set of bacteria called the secondary degraders
that also contribute to the fermentation of resistant starch.
However the secondary degraders are considered
to have no enzymes that initiate the cleavage of glucose
from the glucose polymers that make up resistant starch,
and so the secondary degraders, such as the firmicutes species,
rely on the primary degraders to release glucose monomers.
The firmicutes species can utilise the glucose and ferment it,
to produce a four carbon short chain fatty-acid called butyrate.
Some of the secondary degraders can also utilise
acetate to produce butyrate as an end product.
So through the fermentation of starch acetate,
propionate and butyrate are the main short chain fatty-acids produced,
normally in a 3:1:1 ratio,
so more acetate being produced.
At a low pH, about 5.5,
butyrate producing bacteria are known to dominate the colon.
However at a slightly higher pH, about 6.5,
acetate and propionate producing bacteria dominate,
and butyrate producing bacteria seem to be less prominent.
From the lumen these short chain fatty-acids are absorbed by the colon,
they’re absorbed by the colon epithelial cells
known simply as colonocytes.
About 95% of the short chain fatty-acids
are rapidly absorbed by the colon cells,
while the remaining 5% are excreted in the faeces.
After being absorbed by the colon cells
the short chain fatty-acids can enter circulation,
and enter the portal vein, which is blood travelling towards the liver.
Here propionate and acetate enter the portal blood.
Butyrate on the other hand is the major energy source for colon cells,
resulting in low concentrations of butyrate in portal blood.
Now let’s briefly find out the fates of the short chain fatty-acids.
So acetate is the principal short chain fatty-acid in the colon.
It is metabolised in peripheral tissues.
In the liver acetate has shown to stimulate lipogenesis,
the synthesis of fats.
Acetate is also the primary substrate for cholesterol synthesis.
Propionate travels to the liver
and is used as a substrate for gluconeogenesis.
Butyrate is the preferred fuel for colon cells.
About 75% of energy for colon cells come from butyrate,
and because of this there are lower amounts of butyrate in the blood,
compared to the other short chain fatty-acids.
In the liver butyrate is oxidised,
preventing toxic systemic concentrations.
And that concludes this video.
We looked at starch fermentation
and how fermentation of resistant starch by bacteria
produce short chain fatty-acids, such as acetate,
propionate and butyrate, all of which have many...
