Energy, and built. So we need to eat.

To maintain our selves.

To reproduce.
We have to eat.
To feed and digest is a must.
Digestion is the breaking down of molecules
Absorption is also important.
Secretion of enzymes: to break down the food molecules.
What is digestion all about.
Text goes through them well. I am going to bypass them.
Dont know if he will ask
Lecture 10 - Digestion
December 6, 2013 2:40 PM
BIO270 Page 1
This image: We start at the top. Where we have to sense
the nutrients. We can see it and smell it. Insects can find
the source of the food. There are many mechanisms that
can do that. Secondly, most organisms use some sort of
mechanical digestion here in the tongue is involved in
mech digestion. As food gets released to the intestine
there is chemical processing and break down of
macromolecules and assimilation. And absorption of
those molecules into the body so the body can use them
as building blocks. And then of course egestion.
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Why are some calories not available for animals? This is why.
We have our gross energy. The energy which is there. But
much of it indigestible. They go straight to the digestive tract
and gets released in the feces. The digestible energy which is
left, much of that me even though they are digestible is
unmetabolizable. That is lost in the urine. The left over is
metabolic able energy but even that we don't get all because
of specific dynamic action (SDA). As you eat it is energetically
expensive. It produces a lot of heat. Specific dynamic action.
We use a lot of energy as you eat, you digest, you absorb.
You secrete all these enzymes. You use up energy. When you
eat a full meal you want to lie down and get that warm fuzzy
feeling, that is specific dynamic activity. The amount of heat
produced by digestive system.
So the net energy is nowhere near the gross energy of the
food
There are times when we have lots of food in our body and
times when we dont have lots of food. There is an
imbalance in our eating habits.
So there should be a mechanism to store the contents of the
food.
Some animals can't eat always.
<-- to get proteins you have to eat two times as much of
food to get the same energy as fat.
<-- you take the molecule, put in there, burn it. Oxidize it.
The calorimeter measure the temperature change and
converts it to calorie.
We dont burn food, we oxidize them.
We oxidize food carefully.
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We don't have enough of them so we have lot of significant
important deficiencies.
Vitamin C - scurvy. A connective tissue problem. Can't make
enough collagen.
Vitamin k - required to blood clot. Without it you get
haemophilia. Meaning When you get a cut your blood
vessels cant clot you bleed out.
<00 D, and K can be synthesized in body.
James lind was a physician and British navy. He made a
discovery. He identified a quality in a fruit which gave his
sailors the ability to go and return. The naval ships would left
with 1200 sailors and came after two months with 700 - 800
sailors. Because there was a vitamin deficiency. So he found
this fruit. This was the first clinical trial ever. Gave everyone
some limes, and vinegars, and other fruits and watched what
would happen. The ones who got the limes were fine. The
deficiency of vitamins C is called vimines? The Americans
called the British limens, because they had lot of limes in
their ship/
We dont produce vitamin C. most mammals cant. Most of the research
on vitamin c was done on guinea pigs because they can't synthesize
their vitamin C as well
Have to get for our diets. Most of them are absorbed around
the GI tract.
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12/20 we can produce. The others are called essential AA.
Dogs can only produce 10. so they have 10 essential AA.
Cats have tauring? Which is not an AA, but essential
Cat food doesnt have taurins, and so cant mix cat and dog
food.
We can male palmatate from acetyl CoA.
These must be gotten from the diet.
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We do this by digestive enzymes.
<-- we absorb/ uptake the smaller components.
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How does it happen? It starts very earl on. We release an
enzyme from our salivary glands called salivary amylase
which breaks down starch and glycogen into
oligosaccharides. Occurs in the mouth.
Goes to the stomach and breaks down carbohydrates. Very
little very little carbs. In the Small intestine there's the
release of pancreatic amylase and dischchardases( enzymes
that breaks own disaccharides. Like lactase). That leads to
the monosaccharide's in the small intestine (for absorption.
Almost all absorption takes place here) Are absorbed in the
small intestine by a special epithelium cells called
enterocytes. Enterocytes are absorptive these cells in the GI
tract. Cellulose, for most organisms, including us do not have
any environment to break down cellulose. We don't have the
enzymes to break it down.
Two situations to look at
1) low glucose in the lumen of the GI tract.
When there is low glucose, We don't have a strong gradient
for glucose to move into the cell . Even if we had a
transporter in these low glucose conditions Na/glucose
transporter is key. It drags the glucose in along with its
electrochemical gradient.
Glut 5 transporters bring fructose into these enterocytes.
Fructose can exit across the basolateral membrane via glut
5 and glut 2 transporter. Both are shown in the baso lateral
membrane. This is how we can get glucose even if we have
low glucose situations. Na/ glucose co transporter.
2) high glucose levels.
In high glucose levels why use Na/glucose transporter which
requires ATP secondary active transporter. Doesn't use much
of the Na/glucose transporter. What it does is It incorporates
free form of glut two into the apical membrane. Now we
have a high conc of glucose in the lumen lower in the cell.
Now the glucose is going to freely pass. Facilitated diffusion.
these glut 2 transporters are stored in vesicle within
enterocytes. No energy required, especially when you cut
these glut two transporters stored in vesicles. The Na
glucose co transporter apparently signals these vesicles to
move to the apical membrane.
If that is the case what transporter is missing in this thing in
the figure? It should be there. We saw the Na glucose co-
transporter. How does it function? It makes no sense like
this. Na K ATPase which will be in the basolateral membrane.
If you don't this you don't have the electrochemical, gradient
to pull glucose into the cell. It is a secondary active
transporter, Na k ATP Ase.
Lmd n
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More people have lactose intolerance these days.
We reduce the amount of lactase as we move into
adulthood.
Congenital:
If we dont have lactase we can't break down lactose.
Lactose goes to the large intestine, the gut flora acts on
it --> produces gas, produces muscle contraction.
Because lactose is a carbohydrate and it holds onto
a lot of water and water cannot be reabsorbed and
results in diarrhoea.
It also produces diarrhoea --> for lactose intolerant
people

Reading: lactose is not increasing in coagulation. What

happens is that lots of people mix, and those with
lactase has been brought up with milk. Lots of places in
the world doesnt use cow's milk.
<--no peptidases in the saliva so starts in the stomach.
Enzyme called pepsin the active enzyme is released initially
as a pepsinogen which is inactive. This is the pro enzyme.
This is important because same as in the pancreatic
enzymes, you dont want this enzyme active in the cells.
Because they will start breaking down proteins in the PM in
the gut or in other organelles so they are as proenzymes.
Amino acid Na+ co transporters are in eh small intestine
Trypsin, chymotrypsin, Carboxypeptidase: they are initially
as trypsionge, chymotrypsinogen, and procarboxypesinogen.
The same as before. Dont want to harm the lumen of the GI
tract
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GI tract has to secrete bile --> composed of amphipathic
molecules. Positive and negative regions. This is very
important. There are bile acids, and also phosphor lipids
which are secreted with bile. These leads to emulsification.
emulsify, mix up and break into smaller components fat
molecules. This is really important. These are large fat
globules, They have a really small surface area on the
outside in which lipase can break down. If you emulsify,
break them into fat globules, essentially then you are
increasing the surface area to in which lipase can break
down that fat. Or the fat is going to flow straight through
and not going to be able break it down and take it in. so bile
is important to break down and absorption of lipids.
physical properties of lipids determines on how its
transported. If you have short chains of fatty acids or
glycerol It can be taken up, moved across the PM to the
directly to blood. They are hydrophilic they can be moved
that way. The most of these large triglycerides, cholesterols,
they are much more hydrophobic. They are absorbed across
the apical membrane, by simple diffusion, hydrophobic
molecules so can cross the PM, then they are incorporated
into the ER> thorough the Golgi. Through that transport you
have the building of chylomicrons. They are label? Proteins.
Tso many proteins are added to the lipids creating the
chylomicrons. This is the mechanism in which triglyceride,
monoglycerids and cholesterol get into the blood supply.
They are released into the lactilc, which leads to the venous
system and then circulates through the body. The small,
short chain fatty acid of glycerol can get into the blood. But
larger glycerol's such as triglycerides they get incorporated
into chylomicrons, glycoproteins, they then move into the
blood stream --> they are processed at peripheral tissues -->
bind to specific receptors --> as those fats are moving
through the ER and Golgi ,proteins are incorporated. The
proteins binds into the specific receptors on the peripheral
tissues. And can break down the triglyceride into fatty acids
and glycerol. They can take up cholesterol
Ultimately what's left of the chylomicrons are taken up by
liver, and reincorporated into a bunch of molecules such a
LDL , HDL. (not talking about it too much)
The image you see a chylomicron: in the central core you see triglycroles and cholesterols. You see the
materials that want to be incorporated into cells. Can be used To build membranes. can be used for energy.
but they are hydrophobic and they are surrounded by an outer layer of phospholipids which are amphipathic.
They are positive and negative . Hydrophobic and hydrophilic. Hydrophobic region is interacting with the
triglyceroled and cholesterol esters? Hydrophilic interacting with the aqueous extracellular fluid allowing those
factors to be transported to the peripheral tissues. Then able proteins that are mentioned are receptors with
peripheral protein to bind to them. Allowing the break down/incorporation into those cells of triglyceroils and
cholesterol
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<-- separating different function into different regions of the
gut.
<-- food goes in , waste goes out exactly from the same
opening. This is a huge advance in evolution so now you can
secrete your digestive enzymes into the isolated
environment, in this case the gastrovascular cavity. Before
that they secreted the enzymes into the extracellular fluid or
find a way to take them up, the large molecules, and
process them inside a vacuole which was not the best way to
do them.
These organisms developed further and developed
direticulum. They increases in the surface area. Secondly,
they can allow the organism to specialize. So in one region of
the gut you have an acidic region and in the other you may
have basic region. This is not perfect, but this is better
because there is one flow through.
Hydra: is an cnidarian. They are constantly feeding
organisms. Capture food with tentacles, have a mucus
stream which delivers food into the mouth, and into the
gastro vascular cavity if the mouth is open. In the epithelium
the gastrodremis they have two primary types of cells.
Enzymatic cells and neutral cell. enzymatic cell releases
enzymes into the gastrovasular cavity breaking down
macromoelcules. Nutritive cells phagocytose, takes up the
somewhat broken down food molecules into the cell. In the
food vacuoles there is more cleavage Of the macrmoelcules.
In the end these vesicles move through the nutritive cell,
released into the epidermis and providing energy to the
epidermal cells, the muscle, neuronal cells. This is the two
way gut
This is also called the GI tract. Very distinct functionally and
anatomically separate regions. You have pharynx the
esophagus, involved in the chemical breakdown of food, the
stomach which is in the acidic regions which is important for
the enzymes functioning in that regions.
<-- further digestion. Almost all the absorption via the
enterocytes
<-- mostly absorption of water, some ions.
<--- release of indigestible material
Note that there are sphincters: they separate some of the
anatomical regions, because enzyme in the stomach
function at low pHs. Enzymes in the intestine will not
function at low pH. So they separate these regions and
create micro environments. The stomach of the horse for
example create these regions. Sphincters can be controlled
by the nervous system.
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This is one of the evolutionary advances --> Increase in
surface area of GI tract.
More surface area --> more transporters you can have -->
the more time food spend in the gut --> the more nutrients
you can absorb and break down. You dont want the food to
go too quickly through the gut or you won't be able to
absorb nutrients. But on the other hand you dont want this
indigestible material hanging around.
Most organisms increase the surface area or increase the
length or both.
So the tissue levels, the circular folds. At the tissue level
there is villi. Increasing the surface area again.
Blow the villi: on top of the enterocytes on the villi there are
microvilli. These are formed by microfilaments. Important
for the structure. This is called the brush order within the
intestine,. Significantly increasing the surface area for the
secretion of enzymes into the gut or absorption of small
molecules.
Specialize dcompaortnets
<-- increase the efficiency of digestion Because you can close
off one region from another sequentially. You can't do this
easily in a two way gut.
<-- alter pH: Also specific enzymes are released in one
region, mucus is released in one region.
<-- and complexity : of gut morphology significantly is varies.
Real Complexity at the ease of digestion (like upon what they
eat): like plant eaters they have much longer stomachs with
larger surface area because it is much harder to extract
energy from them than in animals.
<-- gut morphology changes within taxa too: the insects have
larva stage, which is an eating machine eating green leafy
plant material, it pupates and become a nectar eater. So
completely different guts. There is difference within and
between guts. Female mosquitoes drink blood, males feed
on nectar. So there is different in the gut morphology.
Talked about humans, start off with nutrients crossing the
placenta, then you get only milk then you only get different
types of diets. There is significant variation within taxa on
what you eat developmentally. Great differences.
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This is the guts of various animals.
Lots of variation.
Have a simple straight gut and is way shorter than the
animal
Sharks: have a spiral valve, food has to go through the spiral
surface and this increases the surface area, slows down the
movement of food so you can enzymatically break down the
foods or nutrients can be absorbed.
1. Increase surface area so there is more area for secretion
of enzymes and absorption of molecules
2. Microbes: house microbes. Bacteria is not the only one
that can be housed. Protozoans can also be housed. So
should be microbes.
Many organisms have ceca: have two functions
Chickens/ birds : have a very interesting traits, They have a
crop which is an extension of the esophagus. Which does
stores food. The proventiculus is the active stomach of the
birds.
Pigs: huge stretch which could go half way round this hall.
Significant increasing the length and microvilli.
(and microbes)
The fact is that we can't break down cellulose. But Some
organisms can. They can do that because they have specific
microbes within certain regions of the gut/ ceca. Bacteria ,
fungi, photosynthetic organisms.
<-- most common well studied. Found within the lumen of
the GI tract/ ceca. The first mage is a termite: they eat
wood, but they can't eat wood on their own. But they store
protozoans (second image) in the gut which can cleave the
bond in cellulose (beta-1,4 bond on cellulose) we can only
cleave the alpha 1,4 bond in starch.
<-- actively structure symbioses outside of the body. The leaf
cutter ants. They bring that back to the fungal garden and
they take care of the fungus that breaks down the leaves and
then the leaves and fungus they have double?? They can
break cellulose down and able to incorporate.
<-- much more less common, but they are out there. Deep
sea vents, (rifts of large worms in the bottom of the ocean)
they have symbiotic relationship between organisms that
can oxidize H2S.
And symbiotic theory: mitochondria was thought to be
phagocytosed into a cell, a bacteria, and incorporated into
it. Now, symbiotic relationship in everyone.
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<-- so ceca is a modification that improves the digestion. this
is an accessory region in the gut. But ruminant is slightly
different. They have a digastric stomach. Two regions in the
stomach. The rumen in the reticulum, the first two regions in
the stomach where initially the food goes. thats where they
found the fermentative bacteria in the stomach. You take
the food in very quickly --> very little chemical breakdown is
done --> goes into the rumen and the reticulum where they
keep the fermented bacteria which breaks down the
cellulose. They would reverge the food back into the
mouth --> chew it and then after it is been partially broken
down by the bacteria--> goes back down the esophagus but
now it goes to the omasum and the abomasum.
Abomasum is the glandular stomach, the acidic region of the
stomach.
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Salivary glands begins the breakdown of carbohydrates. They
are collection of several exocrine glands: secreted by ducts
outside the body into the GI tract. Ducts open to the mouth,
and multicellular.
Have mucus secreting serous cells which is a clear fluid with
enzymes in it. Such as salivary amylase.
This is important because it lubricates food and dissolves
food and food can bind to receptors and stimulates the
signal transdcution pathway. Cleanses the mouth with
antimicrobial properties.
< salivation is controlled by parasympathetic nervous
system. Stimulates the production of saliva.
Sympathetic nervous system also stimulates the production
of the saliva. Clear fluid with more salivary amylase.
Sympathetic nervous system inhibits and also stimulates the
salivation. 29. 00
Image: dogs have 4 sets of glands. We dont have the orbital
gland but we have the other three. All of these contribute to
the production of saliva. Serving these functions.
Surface involves the columnar epithelium cells joined by
tight junctions. This is important in the gut because it has a
very acidic gastric juice in the stomach. And dont want to
leak.
4 cells are found within gastric pits or the walls of the
stomach.
Mucous neck cells.
Pariteal cells
Chief cells - pepsin is secreted as an inactive precursor
pepsinogen by this cell. This is activated by the HCL
produced by the parietal cells.
G cells: called this because synthesize and release
gastrin.
And they are enterochromatin cells which release
histidine.
Enterendocrine cells: endocrine is secreted into the blood.
The first three secrete into the lumen of the gut. This
secretes into the blood.
This guys ( I think showing an image) : they are bacteria
found within the gut. The acidic compartment kills about
everything and the pH there is 1-2.
But this bacterium finds a way to survive. This is what
produces gastritis, peptic ulcers and is associated with
hylubacterim? This is found in the maze of this pit. It escapes
the high acidity of the stomach.
Also the gastric pruning frog? - (shows image): there were
only two species found they both are extinct. They lived in
Australia. The parents takes the young embryos into the
stomach and the embryos secrete prostaglandin E2. which
actually inhibits the production of HCL and allows this
organisms to develop within the stomach of the gastric
brooding frog. There is project called Lazarus project trying
to bring them back again in university if new south wales.
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Intestines:
Structure - most nutrients are absorbed here. Forms the
mucosa where you found the villi and the crypts. This is
where the important cells are produced.
Sub mucosa is where you find the blood lymphatic vessels
and the nerves which supply ?
Circular smooth muscle and longitudinal muscle: have two
forms of smooth muscle allowing the gut to shorten and
lengthen and allowing the circular diameter to change.
length longitudinal.
Number of mucosal cells:
Histologically:
enterocytes are the primary absorptive cells in the GI. Have
lots of microvilli increasing surface area.
Into the
blood
<--- secrete antimicrobial molecules important in protecting
stem cells produced at the bottom of the crypt of
lieberkuhn.
Cells in the GI tract, stomach and the intestine generally are
there about 3 days. They are constantly been swapped off
and reproduced by stem cells.
<--- goblet cells: secreting mucus
<-- secrete into the blood
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Another secretion:
Into the duodenum, the upper portion of the small intestine.
And phospholipids which
are also amphipathic
<-- this shows what the amphipathic molecules can do.
Hydrophobic side shields from the aqueous extracellular
fluid. Hydrophilic meets the aqueous side.
This is easy to get rid of hydrophilic waste
products can send them straight to the urine.
But hydrophobic ones are harder. One of the important ones we have to get rid of
are breakdown of red blood cells. Break down of bilirubin. This is hydrophobic
molecule and it is secreted with bile and released by desiccation?
Pancreases ducts is also released into the duodenum. The
upper small intestine.
Secretes as inactive pro enzyme protecting the cells which
produce these enzymes. Activated upon release.
<--- these are released by the pancreatic juice.
Trypsiongen is released to the small intestine. This is acted
upon by membrane bound enterokinase producing trypsin.
Which then goes to activate chymotrypsin and
Carboxypeptidase. Which were in the precursor form
chymotripsinogen and procarboxypeptidase.
What this doesnt show is that trypsin can also cleave
trypsiongen.one trypsin molecule and activate
chrymptrypsiongen and and procarboxypeptidase and also
other protrypsin molecule. This can now break down
proteins in the small intestine.
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Enzymes feed into wild animals: requires and energy and
puts the animal at risk. This risk has to be waived. How much
risk is there, and how badly I need the food. This is
controlled by the CNS. The signal is sent to the
hypothalamus. To feed. When you can't provide the fuel
required for the circulation fuels we tend not to use the
storage forms of the fuel unless we have to. We go back and
eat so we have more circulation fuels.
There are three which are found to be
particularly important in humans in
controlling appetite and feeding. Leptin,
peptide Yy and ghrelin.
Leptin: secreted by
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Leptin is considered to be as an white adipose stat? lots of
lipids in adipose tissue and Leptin is released to inhibit
appetite. Leptin is secreted by white adipose tissue when
the lipid content of the white adipose tissue is high.
Which is different from brown adipose tissue.
<-- peptide YY is secreted when the colon is full
<-- ghrelin stimulates appetite. Released when stomach is
empty.
Leptin mouse: the one on the right is a normal mouse
with normal Leptin.
The left one has no Leptin. And can't stop eating. And gets
enormous. Thought that when You pump in Leptin you
can stop the appetite. But unfortunately this doesnt
work. Leptin doesnt have the direct effect we want to
have. So its long term adipose stat. Regulating the amount
of stored fuel supply in terms of fat.
When lots of lipid is stored
you dont want to eat anymore
These hormones have an effect on the arcuate nucleus? On
the hypothalamus where you find a number of cells which
have receptors on for these hormones. These hypothalamic
neurons release neurotransmitters in response. So there are
synapses on the neurons, higher centers in the brain which
influence the feeding behavior. Some of these
neurotransmitters stimulate appetite. Pre
neurotransmitters which are released from one type of
neurons on the brain. from the same neurons you get all the
peptides ( on slide)
But we concentrate only on peptide Y.
There are neurotransmitters releases in response which
inhibits appetite:
POMC is not a neurotransmitter: its a pro hormone. There
are three or four peptides which are released from
proopiomelanocortin to differential cleavage in tissues.
Important ones for us is alpha MHS: alpha melanocyte
stimulating hormone.
One of the
cleavage products of precursor POMC.
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Brown in the top is the hypothalamus arcuate nucleus.
You have two types of neurons
Neuropeptide Y releasing hormones and POMC relsing
hormones.
Neuropeptide Y is an appetite stimulant. POMC is specifically
alpha MSH is appetite depressant.
Leptin which is released from white adipose tissue when
there is lot of lipids stored in the white adipose tissue. Leptin
inhibits neuropeptide Y releasing hormones reducing the
release of neuropeptide Y. this reduces Y and depress
appetite.
This also has a positive effect on POMC releasing neurons.
Releasing alpha MHS which is an appetite depressant.
Stomach when releasing ghrelin, stimulates receptors on the
neuropeptide Y releasing hormones to release neuropeptide
Y to stimulate appetite.
The colon, if it is full, releases peptide YY and inhibits
neuropeptide Y. releasing neurons and reducing the release
of neuropeptide Y and reducing appetite.
Putting it all together: we have ghrelin and peptide YY which
controls the desire to eat between meals. Whether or not
the stomach is empty or full. Whether or not the colon is
empty or full. Whereas Leptin is more long term controlling
the amount of lipid stored in the adipose tissue. Leptin is
appetite depressant by reducing the release of neuropeptide
Y from neuropeptide Y releasing neurons In the
hypothalamus and also stimulating the release of alpha MHS
from the POMC precursor. As the peptide YY from the colon,
ghrelin from the stomach antagonizes one another. One
stimulates appetite and the other depresses it.
Ghrelin is released when the stomach is empty so it is a
stimulant.
How are secretions controlled?
Neurotransmitters, hormones control the secretions of acid.
Bicarbonate is important to raise the pH of the bowl of food
entering intestine from the stomach where the all the acid is
secreted into the stomach.
Also digestive enzymes to break down macromolecules to
absorbable materials.
In respond to both the anticipation of the food( when an
animal perceive the prey.) You get that feeling when you see
that cake you salivate. Also from the presence of food in the
digestive system.
The
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The anticipation of the food stimulates the parasympathetic
neuron --> they have direct effect on the parietal cells which
releases acid into the stomach.
Parasympathetic neurons also activate G cells which release
gastrin hormone --> stimulating enterochromofine cells
which release histamine which also stimulate parietal cells to
release acid.
Gastrin also stimulates chief cells to release pepsinogen
which gets activated in the stomach to pepsin by HCL. (pH
1-2)
Also when you ingest food it activates chemoreceptors and
mechanoreceptors, in the gut, esophagus, mouth etc.
This has two effects:
Can directly stimulate the G cells. ( gastrin)
Can Also affect the enteric nerves which are inherent in the
gut. The gut has its own nervous system, a physiological
system which has its own nervous system.
These enteric nerves can also effect G cells. G cells are the
commanders . Everything goes through the G cells.
Second image: how does this work? Talked something like
this in osmoregulation. We talked about proton ATPase. But
in this the important pump is the K/H pump. This is an
ATPase. Pumping protons into the lumen of the stomach in
exchange for K. it also has Cl- channels. Cl- (negative)
following the K+ (positive) into the stomach. Thats how we
have the HCL secretions into the stomach. What's so
important is the regulation of pH. Is the presence of the
enzyme carbonic anhydrase. Hydrates Co2. producing
carbonic acid which dissociates into protons and
bicarbonate. Protons which supplies K/ H pump so that it
doesn't run out of protons and bicarbonate which is
exchanged for Cl- making sure you have enough Cl- to get
into the stomach. Carbonic anhydrase is able to hydrate Co2
producing that proton, this is what supplies the proton and
the bicarbonate is exchanged for Chloride. Of course we
have the Na/K ATPase in the basolateral membrane.
Acid reflux: you may have taken papsidase C or anti? How do they work? They inhibit and binds to histamine
receptors on parietal cells. The histamine released from the enetrochromaphin cells cannot stimulate the parietal
cells to release acid to stomach. There are also other medicine which specifically targets the K/H ATPase. They fncion
by inhibiting that pump which reduces the prodcutionof acid by parietal cells.
From the intestine we start to break down molecules. So we
have acid and food entering the duodenum, the first section
after the stomach.
1. Vasoactive intestinal peptide - works on the pancreas to
release HCO3- to increase pH. Why? Important because
the enzymes whicha re going to function in the intestine
is not going to work in acdic level.
2. Secretin - stimualtes the prodcution and release of bile.
Bile also has bicarbonate so contributes to the icnrease
of pH. This stimulates the liver to produce bile.
Acids stimulate the enteroendocrine cells to stimulate two
hormones:
Digestive products( AA, FA, small peptides) stimuatles the
endocrine cells to release CCK (cholysictokinenie)
1. Stimulates the smooth muscle in the gallbladder to
release the bile into the duodenum into the upper
intestine.
2. Stimuatles the pancrease to release enzymes. Also the
trypsinogen, chrymotrypsiogens, lipasess, nuclease
Has two effects:
Because all of the secretions are aquesou solutions and body is losing a lot of water as it
secretes them in the digestive tract. Osmotically we have to recover most of those water.
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Gut is controlled by muscles. Muscles which are controlled
by neurons.
Food moves along the GI tract in contractile waves. This is
called peristalsis. This occurs because of intrinsic myogenic
activity. Similar to pacemaker cells which spontaneously
depolarize and dont need signals.
Receives signal from CNS but not directly to the muscle.
Signals from the CNS go to the myentric plexus which is part
of the enteric nervous system which controls the gut alone.
CNS signals the gut VIA enteric nervous system.
sturcturE: you have the intestinal vili, circular smooth muscle
and longitudinal smooth muscle. In between that you see
the myenteric plexus. Neurons which controls the actiivty of
gut. They also control thesecretion of digestive enzymes.
What is important: controls the speed of contracions. If
contracts too fast cant acsoprb nutrients.
Too slow, then there is indegesible food so there shoulde a
perfect balance. This happens because of the interstitial cells
of cajal and also the effects of CNS on those cells.
How does it work: smooth and longitudinal muscles. So
smooth muscles show rhythmic cycles that move along tract
through peristalsis.
( From interstitial cells.
If you look at step 1: you see contrction of circular mucsles.
Circular muscles are invovled in controlling the diamtere.
Logitudinal muscles : length.
So contraction of circula smooth musclesinfront of the food.
Step 2: contraction of longitudinal muscles shortening the
gut. At the same time you have relazation of the smooth
muscles. (figure doesnt show). Contraction of circulat
infront of the food, relaxation behind the food, and
contraction of the longitudinal muscles shortening the gut
and reuslting in movement.
This is peristalsis.
BIO270 Page 22
How does the body control metabolic transtiions between
meals?
Postprandial period can vary froms seconds to months.
Depending on the orgnaism type and how often you feed.
<-- whatever you need immediately are used, excess are
stored.
<--endocrine pancreas: iseltes of langhaerns. Releasing
digestive enzymes into the gut. When we talked about the
uptake of glucose across the GI tract involving GLUT 2
transporters, skeleton muscles insulin stimulates the
transport of GLUT 4 tranpsorters to the membrane. So you
have lot of glucose after a meal, you put the glucose
tranpsoeters into the PM of skeltel muscle cells and glucose
is take up.
Steroid
hormone
<-- released from alpha cells from the endocrine pancres.
Stimulates glucose release from liver. Steroid hormones are
released from the adrenal cortex. Stimulates
glucoenogenesis.
Gluconeogenesis: Produced from the non carbohydrate
presurosrs from the liver.
Insects:
Homrones are secreted by the gland called Corpra cardiaca,
Is a gland associated with the brain of insects. Corpra allata:
releases juvenile hormones which Stimulates the release of
FA from the fat body.
Fat body is like the white adipose tissue in humans and
stores triglyceride.
There is a second messenger pathway: the pathway is very
similar. You should recognize this very much. You have the
adipokinetic hormone receptor a GPCR. Heterotrimeric G
protein is associated with this receptor. Binding of AdK
stimulates the release of GDP and binding of GTP and the
alpha subunit moves along the membrane stimulating
phspholipase C. this phospholipase does more than is shown
here. Phsopholipase C --> cleave
phosphptilinositolbisphosphate membrane phsopholipid
into IP3 and triecyloglycerol. Inositolbisphosphate is soluble
on aqueous cytoplasm. It diffuses to the cytoplasm binds to
receptors on the sarcoplasmic reticulum releasing Ca.
Ca has a number of effects: stimulates the activation of
glycogen phosphorylation breaking down glycogen and
releasing glucose. And triglycerid lipase, breaks down lipase
releasing FA. Also stimualtes the moement of PKC to the
membrnae where diacylglycerola ctivates it and PKC can go
an phsophprylate someone. Dont forget the second
messenger pathways.
BIO270 Page 23
<--if that postprandial? Happens too long it leads to
starvation where you have the reorganization of
metabolism.
We have tissues that function only with glucose: e.g.: brain
and red blood cells.
Muscles shift to lipid metabolism. If there is lots of glucose
muscles select glucose but in starvation response they
switch to lipids saving glucose.
Then when these stores are depleted body starts using
proteins. We dont have a store of protein in our body like
glycogen and lipids. But it is stored in our skeleton muscles.
So then the skeleton muscle starts to break down producing
AA which can then feed into pathways to produce energy.
Early starvation:
Adipose tissues releases FA and goes to liver.
Liver sends glucose it produces to the brain.
Skeleton muscles starts to use triglycerides to save that
glucose which is been produced by the liver to the brain.
As we lose that lipid and glycogen sotre, liver starts
producing ketone bodies so brain can use them.
You can see the muscles start to break down.
We need the energy to supply the necessary tissues of the
brain.
AA are sent to the loiver wher they can feed into different
pathway. They can feed into the trchloroacidic cycle.
In the end generates energy.
So we have this reorganization tissues stop using glucose and
start using FA if they can.
In late starvation we have the breakdown of proteins from
muscles which therefore allows those tissues to use AA to
produce energy. And ketone bodies are produced by liver is
released into circulation and can be used by the brain In late
starvation response.
BIO270 Page 24