Video summary
Iron in the diet exists primarily in two forms: heme iron, found in non-vegetarian foods, and non-heme iron, which is less efficiently absorbed. The body absorbs approximately 25% of dietary heme iron compared to only about 5% of non-heme iron. Absorption mainly occurs in the duodenum and the proximal part of the small intestine, where specific cellular mechanisms determine how much iron enters the bloodstream. Once inside the intestinal epithelial cell, non-heme iron must first be converted from its ferric form to the ferrous form by an enzyme called duodenal cytochrome B, allowing it to cross cell membranes via the divalent metal transporter 1. In contrast, heme iron bypasses this initial conversion step and enters the cell directly through a specific heme transporter before being broken down into its iron component inside the cell.
Once inside the intestinal cell, the fate of the iron depends on the body's current needs. If iron stores are sufficient or demand is low, the iron remains within the cell, where it is stored as ferritin. When these cells eventually shed from the intestinal lining due to rapid turnover, this trapped iron is lost in the feces rather than being excreted through a dedicated pathway. Conversely, when the body requires more iron, such as during increased red blood cell production, erythroblasts produce hepcidin-inhibiting factors that prevent the release of hepcidin. This allows the ferroxidase enzyme hephaestin to function alongside ferroportin at the basolateral membrane, facilitating the export of iron from the cell into the plasma where it binds to transferrin for transport to tissues like the liver or bone marrow.
The regulation of iron absorption is critical because the human body lacks an active excretory mechanism to remove excess iron; therefore, controlling how much is absorbed is the primary method of maintaining iron balance. Several factors influence this absorption process, with increased demand being a key driver that suppresses hepcidin levels to enhance uptake. Nutritional components also play a significant role, as vitamin C helps maintain non-heme iron in its absorbable ferrous state, whereas substances like milk, phytates found in tea and coffee, and tannates can bind to iron or alter its chemical state, forming insoluble compounds that prevent absorption. Additionally, adequate gastric acidity is essential for converting dietary ferric iron into the more absorbable ferrous form, highlighting how diet and physiological conditions collectively determine the body's iron status.
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Iron in diet is present basically in two
forms either in heem iron form. Hemiron
is present in non-vegetarian diet or as
non-heam iron. So this hem iron actually
is better absorbed than non-heem iron.
So non-veg diet whatever iron is there
as hem iron that is better absorbed and
approximately 25% of this iron is
absorbed but in non-heem iron only 5% of
the iron in diet is absorbed. Now the
absorption takes place in jodinum mostly
and some part of proximal small
intestine other part of small intestine
as well. Okay but mostly it is covered
uh it is happening in durina. Okay. So
here this is the luminal side of
intestine and this is the basolateral
side. So here what we see that uh this
is the dural epithelial cell and there
is vi projecting on this intestinal uh
border we have the this reductase enzyme
is there. It is also known as gyc
basically diodinal cytochrome B. Okay,
doden cytochrome B enzyme is there which
converts the feric form of iron into the
ferrris form. Now this is important.
Why? Because it is the ferrris form of
iron which can cross the membranes. So
always you see it will be the ferrris
forms of iron which will be crossing the
membranes. But it is transported and
stored as feric forms right. So by this
enzyme dural cytochrome B the feric ion
is converted to ferosion and then this
ferrraion moves into the cell in the
intracellular compartment via another
transporter that is dalent metal
transporter one. Okay, divalent because
this is two valencies there, right? So
dalent metal iron is a metal dalent
metal transporter one. So this moves
inside into the intracellular
compartment of the cell. Now he iron
hemiron there is another transporter
direct hem transporter. So it will
directly transport he from the lumininal
site to the intracellular compartment
and within the intracellular compartment
there is a enzyme heem oxygenase which
will act on this he and remove the
globin part and the ferris part
separately. Okay. Now this ferris has
two pathways either it can go out of the
cell that is one or it can remain within
the cell right now that depends on the
requirement of the iron. So if the iron
requirement is more this iron will go
out of the cell. If body doesn't need
iron then the iron remains
intracellularly in this intestinal
epithelial cell. Okay. So what I'm
trying to tell you here that absorption
of iron
absorption of iron is regulated
depending on the requirements. So how
this regulation is brought about. So
first let us see how it is getting
absorbed. So on the basolateral side of
this intestinal epithelial cell we see
there is a transporter that is
feropotin. So this feropotin basically
transports this ferris form outside and
along with this feropos uh feropotin
there is another protein attached
heestin. Okay. So here it is shown
separately but you will see other books
it will be like this. So if this is
feropotin
you will see that they will show one
diagram where heestin another protein is
associated with this feropotin and this
is much better way of depicting why that
you see that as the transport of iron
occurs in the ferrris form by the
feropotin immediately this iron is
converted into the feric form. So it is
associated movements uh they are
occurring simultaneously iron is moving
out and this ferrris form is getting
converted to feric form immediately and
uh this heestin is responsible for
conversion of ferrus to feric form. Then
this feric binds to the protein
transferin which is present in the
plasma. So iron is transported aspheric
form combined with transferin and this
transferin either goes to the cells
where it is required where the iron is
required or it goes to the storage site
and the main storage site for iron is
liver. Okay. So either it is taken by
the epito cells or it goes to the
iththroidid marrow because the iron is
present in the hemoglobin. So where it
will go? It will go to the developing
cells which will form ithroytes the RBC.
So that is eriththroidid mar. Okay. So
that's what we discussed that how iron
is absorbed. Peropin associated with
feesin. Right. Now if the storage form
of iron is more. So here say suppose
liver has already lot of storage of iron
is there. So in that case liver releases
a protein that is hepsidin. Hepsidin it
releases. Now this heepsidin goes and
blocks this feropin one. Okay. So if
this feropotin transporter is blocked,
will iron move from the intracellular
compartment to the basil site? No, it
won't be able to move. So it will remain
intracellularly and intracellularly it
will be converted from ferrris to feric
form and it will be stored as mucosal
feritin here. Right now in some time
there will be loss of this epithelial
cells. So there is shedding of dural
epithelial cells and the intestinal
cells turnover is very high. So with the
loss of this intestinal epithelial cells
the iron which is present here that will
also be lost. Okay, understanding. So
very important fundamental concept it is
that absorption of iron is regulated in
our body. We don't have any excrettory
regulated pathway for iron. It is the
absorption which is regulated and this
here with the iron which is trapped here
if the iron requirement is fulfilled in
the body if there are adequate stores
and the iron which is trapped here this
is also lost along with the epithelial
cell. So this is known as there is a
term for this mucosal trap mucosal trap
of iron. Okay. So that was about the
iron absorption. We saw that intestinal
epithelial cell there are transporter
for hem hem transporter is there. Then
for non-heam iron first it is converted
from feric to ferrus by dycb enzyme
jodal cytochrome B and then ferrus is
transported intracellularly by talent
metal transporter one and then it moves
from the intracellular site to the
vasolator site by feropotin one which is
associated with hephestin and this
feropotin one can be blocked by another
protein that is hepsidin. Now this is
very important to know because it has
significance in another disease that is
hemocchromattosis that we are going to
discuss later. Okay. So that was about
the iron absorption we have discussed.
So what are the factors which affect
iron absorption. There are factors which
increase the iron absorption and there
are factors which decrease the iron
absorption. So increased iron absorption
occurs based on the demand. Okay. So
when there is increased demand for
example if there is increased synthesis
of RBC so the eriththroidid precursor
cells which are there that is the
pronormal blast they will divide more so
that means iron requirement will be more
so in that case these ariththroblast
produce a protein that is
okay and thiserone actually inhibits
hepsidin so this hepsidin which we
talked before okay which is inhibiting
feropotin so it is not allowing iron
absorption to occur. So this
ariththroblast actually produce
ariththreron which blocks uh which
inhibits hepsidin. So that heepsidin is
not able to act on parapotin and iron
absorption can continue. Okay. So that's
how ethoid hyperplasia increases iron
absorption. Then next component is
vitamin C. Vitamin C actually keeps
dietary iron in ferris state. Okay. So
it is keeping it in reduced state in the
fer state and we have seen that
non-hemir iron is absorbed in fer state.
Then the factors which decrease iron
absorption include milk. Okay. So
suppose you have given iron
supplementation to somebody and they
take milk along with that then iron will
not be absorbed. Okay. Then phitates and
tanates these are basically present in
tea coffee and these phitates tanates
bind to non-hem iron and form
nonabsorbable insoluble compounds. So
obviously iron will not be absorbed.
Then decreased gastric acidity. So that
is also important because acidic
environment actually facilitates the
conversion of feric to ferrus form. So
if acidity is less this is not going to
take place and the dietary iron will
remain in feric form so it will not be
absorbed. So that was about the iron
absorption in the diodnum and the
factors affecting the iron absorption.
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