0:00 hello and welcome to the next portion of
0:02 the endocrine physiology chapter going
0:04 over the endocrine pancreas of
0:06 costanzo's physiology textbook if you
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0:18 so jumping into the endocrine pancreas
0:21 remember this is different to our
0:23 exocrine pancreas which secretes
0:25 enzymes into our gi system to then break
0:27 down
0:28 our food products the endocrine pancreas
0:31 secretes hormones into the bloodstream
0:33 to mainly regulate our glucose
0:35 concentrations
0:37 so we have these areas called the islets
0:39 of langerhans
0:41 which contain the endocrine pancreas
0:43 cells
0:44 predominantly we have alpha cells beta
0:46 cells
0:47 some delta cells and then some other
0:49 cells intermixed
0:50 but the alpha cells secrete glucagon
0:53 they the cells secrete
0:54 insulin and then delta cells release
0:57 somatostatin
0:58 the other cells that aren't really
1:00 depicted in here at least pancreatic
1:01 polypeptide but there is less known
1:03 about this
1:04 actual hormone so we won't be covering
1:06 that in this chapter
1:07 so since we have this organization of
1:10 the cells and these eyelets of
1:11 langerhans
1:12 they actually have some cells to cell
1:14 communication either by gap junctions
1:17 which is just the electrical
1:18 communication between the cells or due
1:21 to the blood supply that comes in
1:23 once one cell has received its blood
1:25 supply that venous blood from that cell
1:28 actually disperses to the other cells so
1:30 they are able to communicate with one
1:32 another
1:33 and then there's also adrenergic
1:34 cholinergic and peptidogenic
1:36 neurons as well that innervate these
1:38 cells so we're going to go through
1:40 each of those major hormones insulin is
1:42 a big one
1:43 because clearly it causes a pretty
1:45 significant clinical disease and
1:46 diabetes
1:48 so starting with the synthesis and the
1:49 structure of insulin
1:51 it gets synthesized into first pre pro
1:53 insulin
1:54 from the mrna within the cell it is then
1:57 cleaved early into
1:59 pro insulin before getting shuttled away
2:01 until the endoplasmic reticulum where it
2:03 is modified to be folded
2:05 into a folded form of insulin and then
2:07 finally packaged up
2:09 into some secretory granules in the
2:11 golgi apparatus ready to be released as
2:14 actual insulin now insulin gets
2:16 regulated predominantly from
2:18 glucose but it can be thought of as a
2:21 hormone
2:22 of abundance so any abundance of
2:24 nutrients
2:25 insulin is going to be secreted to try
2:27 and store that energy in the body for
2:29 use in the future so although increased
2:32 glucose concentrations are by far the
2:35 most important stimulatory factor
2:37 increased amino acids or fatty acids
2:39 will also stimulate insulin release
2:41 in addition to glucagon which we'll talk
2:43 about in a second
2:44 cortisol which has a insulin resistant
2:47 factor
2:48 that will actually increase the
2:49 secretion of insulin just because
2:51 cortisol is going to increase our
2:52 glucose and then also increase our
2:54 insulin as well
2:55 glucose-dependent and selenotropic
2:57 peptide
2:58 gip this is a hormone that's released
3:01 from the gi system when we eat food and
3:03 this
3:04 causes an increased release of insulin
3:06 due to oral glucose
3:08 versus if we give glucose intravenously
3:11 it's all because gip comes in and
3:13 further stimulates insulin release
3:15 potassium causes the release of insulin
3:18 potassium is in our diet and this is
3:20 important because insulin helps
3:21 potassium get shuttled away into cells
3:24 so when we eat
3:25 insulin gets released to move those
3:26 potassium from the diet
3:28 into our cells vagal stimulation and
3:30 some drugs will do it so
3:32 sulfonylurea drugs increase the
3:34 secretion of insulin and these are some
3:36 treatments
3:37 for type 2 diabetes we'll get into
3:39 diabetes in a second here
3:40 and then clearly obesity there will be
3:42 abundant nutrients
3:43 with obesity so that will stimulate
3:46 increased insulin secretion
3:47 the inhibitory factors of insulin
3:49 secretion include low glucose which is
3:52 understandable fasting and exercise
3:54 because we no longer have an abundance
3:56 for nutrients we actually want to start
3:58 using those stores of energy so insulin
4:00 is going to be bad in this situation so
4:02 we inhibit the secretion there
4:04 somatostatin remember our stopping
4:06 hormone is going to stop
4:08 our insulin secretion and then some
4:10 drugs as well so getting into how
4:12 insulin gets secreted first of all the
4:14 stimuli
4:15 mainly is glucose so we're going to
4:16 focus on glucose here it enters the cell
4:19 via the glute 2 transporter which is
4:22 facilitated transfusion
4:24 going to occur when we have
4:25 hyperglycemia you know we have a high
4:28 glucose concentration outside the cell
4:30 it then gets facilitated diffusion into
4:32 the salvia glut2
4:33 it gets oxidized essentially through
4:35 glycolysis
4:36 to produce some atp to produce some
4:38 energy molecules
4:40 these energy molecules actually
4:42 ironically close the potassium channels
4:45 on the cell by closing the potassium
4:47 channels
4:48 we stop the loss of a positive ion out
4:51 of the cell
4:52 so this actually depolarizes the cell
4:54 because remember
4:56 if we wanted to repolarize a cell then
4:58 we increase the movement of potassium
5:01 out of the cell
5:01 by stopping potassium moving out of the
5:04 cell we depolarize it so that
5:06 depolarization causes an
5:08 increase in calcium influx into the cell
5:11 high intracellular calcium then results
5:14 in exocytosis of our insulin into our
5:16 bloodstream
5:18 so that is how insulin gets stimulated
5:20 to be released because of
5:22 high glucose concentrations in our blood
5:24 now that is a similar method for if we
5:27 have increased amino acids or fatty
5:28 acids etc
5:30 so once insulin is in our bloodstream it
5:33 will go to our cells and work via the
5:35 intrinsic tyrosine
5:37 kinase receptors remember these
5:39 receptors are the ones with
5:41 actual kinase enzymes as attached to the
5:44 receptor
5:45 so by the insulin binding it we get a
5:47 conformational change so then the
5:49 tyrosine kinase enzyme
5:51 will now phosphorylate proteins and
5:53 enzymes within the cell
5:54 ultimately that will produce the effects
5:56 that we'll talk about a little bit later
5:58 in the video
5:58 now once that tyrosine kinase receptor
6:01 has been bound to insulin it actually
6:03 gets
6:03 internalized and degradated by
6:05 intracellular proteases
6:07 so insulin actually down regulates its
6:10 own receptor
6:11 so now it's going to be less sensitive
6:13 to the presence of insulin
6:15 now this is becomes a problem when we
6:17 have constantly high insulin levels
6:20 such as with diabetes mellitus
6:22 specifically
6:23 type 2 which happens with obesity
6:26 because usually
6:27 with obesity you have such an abundant
6:29 nutrients within your bloodstream you
6:31 typically are always hyperglycemic
6:34 then that's going to constantly cause
6:36 the secretion of insulin
6:37 the receptors get down regulated so now
6:39 you no longer respond to insulin
6:42 and you effectively have no useful
6:44 insulin in your body and that is when
6:46 you get diabetes mellitus
6:48 now the actions of insulin is next now
6:51 once again
6:52 this is a hormone of abundance so it's
6:54 going to function to try and shut all
6:56 away
6:56 all of our nutrients inside our body for
6:59 use at a later date
7:00 so it's able to decrease our blood
7:02 glucose concentration by
7:04 increasing the glucose transport into
7:06 cells using
7:08 the glute for transporters and increases
7:10 the production of those transporters
7:12 it promotes the formation of glycogen in
7:14 the liver and muscle remember glycogen
7:17 is just a big polymer of glucose that
7:19 stores that glucose away
7:21 it also inhibits the breakdown of
7:23 glycogen and also inhibits the formation
7:26 of new glucose via gluconeogenesis
7:29 which creates glucose basically from
7:31 amino acids
7:32 it reduces the blood fatty acid and
7:35 ketoacid concentration and stimulates
7:37 all that fat in the bloodstream to
7:39 actually get deposited
7:40 in your fatty tissue and inhibits your
7:42 lipolysis
7:44 it decreases your amino acid
7:45 concentration by increasing the uptake
7:48 by tissues and
7:49 increasing your protein synthesis and
7:51 also
7:52 promotes the uptake of potassium into
7:54 your cells remember we talked about that
7:56 you have high potassium in your diet so
7:58 insulin at the same time getting
8:00 secreted but the glucose is going to
8:01 help shuttle away all that extra
8:03 potassium into your cells
8:05 so if you have an abnormality in your
8:06 insulin you essentially end up with
8:08 diabetes mellitus
8:10 diabetes mellitus just means sugary
8:12 urine and the reason behind the sugary
8:14 urine
8:14 is because you have high blood glucose
8:17 concentrations
8:18 now that's either because of type 1
8:20 diabetes mellitus which means you are
8:22 not producing enough insulin
8:24 and that usually occurs due to an
8:26 autoimmune destruction
8:28 of your beta cells so you no longer
8:30 produce insulin
8:31 or type 2 diabetes which is insulin
8:34 resistance
8:35 and that may occur due to a constant
8:37 hyperglycemia state
8:38 this is the one that's typically
8:40 associated with obesity
8:41 due to just having so much glucose in
8:43 the bloodstream there are some
8:45 other causes for insulin resistance but
8:48 let's get into too much detail for this
8:50 particular chapter so with diabetes
8:52 since we have
8:53 ineffective insulin either due to a low
8:55 concentration
8:56 or low receptor numbers we are going to
8:59 have
9:00 increased glucose within our bloodstream
9:02 that's unable to get into our cells
9:04 so that increased glucose in our
9:06 bloodstream is going to make us pee more
9:08 because that's going to be
9:09 over the threshold for our kidneys being
9:11 able to reabsorb it so you end up with
9:13 more glucose and your urine which has an
9:15 osmotic effect to drag water with it so
9:18 you become polyuric
9:19 subsequently polydipsic as well you'll
9:22 also end up being hyperkalemic because
9:24 your potassium can't get into your cells
9:26 you start to break down your proteins
9:28 because you don't have that stimulus to
9:30 get your amino acids into your cells and
9:32 start to
9:33 produce your proteins you also increase
9:36 the amount of fatty acid and keto acids
9:38 in your bloodstream because you have
9:39 reduced
9:40 that hormone that tells that fatty acids
9:43 to get into your
9:44 fat cells and store away so that can
9:46 result in an issue actually called
9:48 diabetic ketoacidosis which is more of
9:50 an
9:50 emergency because you have so many of
9:53 these acids in your bloodstream you get
9:54 this metabolic acidosis that you have to
9:56 treat
9:57 emergently now the treatment for type 1
9:59 diabetes
10:00 is obviously going to be giving insulin
10:03 if you're able to give insulin
10:04 you essentially solve the problem of not
10:06 being able to produce it
10:08 when it comes to type 2 diabetes that's
10:11 slightly different that is non-insulin
10:13 dependent the problem is not
10:15 essentially related to insulin quantity
10:18 is related to the fact that your insulin
10:20 receptors have been down regulated
10:22 so the best way to treat this is trying
10:24 to reduce your blood glucose
10:26 concentrations
10:27 from diet restriction weight reduction
10:30 and then also some drugs that help
10:32 to try to promote some insulin secretion
10:34 but also
10:35 increase our sensitivity of insulin at
10:37 our target cells
10:39 so type 2 diabetes slightly different
10:41 where there's more of an environmental
10:43 component
10:43 into the treatment now glucagon is the
10:46 complete
10:47 opposite of insulin so it is the hormone
10:49 of starvation
10:51 and that is really to remember from our
10:52 alpha cells and it's trying to maintain
10:55 normal glucose concentrations so it's
10:58 going to be secreted for the opposite
11:00 reasons of insulin whenever we have low
11:02 sugar
11:03 within our bloodstream so low glucose
11:05 concentrations
11:06 it will also interestingly be stimulated
11:09 if we ingest
11:09 protein but this will be reduced if we
11:12 have
11:13 glucose simultaneously being secreted so
11:16 if we have high glucose high amino acids
11:18 we won't have an increased glucagon
11:20 because that'll be an issue
11:22 because that'll try to increase the
11:23 glucose even further so essentially
11:25 glucagon
11:26 is trying to increase or maintain normal
11:29 glucose concentrations
11:30 when we are hypoglycemic so it's able to
11:33 break down glycogen
11:35 via glycogenolysis it's also able to
11:38 reproduce
11:38 new glucose via gluconeogenesis from our
11:42 amino acids it's also able to increase
11:44 the breakdown
11:45 of our fat tissue via lipolysis to
11:48 increase the amount of available energy
11:49 and then also help to produce more
11:51 glucose
11:52 so everything is centered around
11:54 increasing our glucose
11:56 concentrations and then the last hormone
11:58 that we'll talk about
11:59 is somatostatin remember this is the
12:01 stopping hormone we talked about this
12:02 with growth hormone we talked about this
12:04 with our gastrointestinal hormones here
12:07 it's
12:07 once again showing its face but this
12:09 time being secreted from the delta cells
12:11 of the pancreas to actually reduce the
12:14 stimulation for secretion
12:16 for glucagon and insulin it's having
12:18 this protective effect so we don't get
12:20 an
12:20 overwhelming response of insulin or
12:22 glucagon whenever they get secreted
12:24 so it's kind of dampening their response
12:27 to a stimuli so this is all that we're
12:29 going to cover for today
12:30 going over the pancreas join us for the
12:33 next video we're going to go over the
12:34 regulation of calcium and phosphorus to
12:36 finish up this chapter
12:38 once again if you haven't subscribed
12:39 please consider doing so as it does help
12:41 the channel out
12:42 see you next time
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