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Endocrinology 1 > Endocrine Pancreas > Flashcards

Endocrine Pancreas Flashcards

1
Q

What do pancreatic endocrine cells secrete?

what does the endocrine pancreas regulate?

A

Insulin, glucagon, somatostatin

plasma glucose levels, metabolism of fatty acid, and a.a. metabolism

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2
Q

where are endocrine cells arranged?

what are the main cell types and where is their presence in this structure?

what does each of these cells make?

A

in islets of langerhans

B cells (mostly found in the center) –> insulin + C peptide (product of cleavage of insulin)

A cells (periphery)–> Glucagon

D cells (periphery but interdispersed) –> somatostatin

(F cells too) –> pancreatic polypeptide

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3
Q

innervation of islets of langerhans? (2)

what does each do?

A

adrenergic (alpha adrenergic –> lowering insulin)

cholinergic (stimulation of insulin),

peptidergic neurons.

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4
Q

of the different cells, What is in the most amount of the langerhans? next biggest? least amount?

where are they located inside these islets

why is delta cells interdespersed?

A

B, A, D

B in the center, A on periphery.. but D are interspersed in the islet (D cells are regulating secretion of the islet to decrease B and A cell secretion)

regulating the secretion of insulin and glucagon in the islet.

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5
Q

glucagon vs insulin and antagonism?

A

glucagon, even though it is the opposite effect of insulin, glucagon isn’t an antagonist of insulin secretion… but insulin is an antagonist of glucagon

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6
Q

What kind of junctions are you going to see in the islet of langerhans?

what are the different options of gap junctions?

A

Gap junctions –> allowing rapid cell-to-cell communication

a-a-, b-b, a-b.

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7
Q

Blood supply of the islet of langerhands/

A

venous blood from one cell is bathing the other it so the predominant secretion product from the islet is going to be from insulin that’s going to be bathing the islet (because there is mostly beta cells in the islets)

blood flows to the periphery and out from there.

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8
Q

Delta does what to beta and alpha?

A

can inhibit alpha cells and beta cells through somatostatin.

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9
Q

Alpha on Beta?

Beta on Alpha?

A

can stimulate insulin (but not inhibit)

can inhibit, NOT stimulate

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10
Q

what kind of hormone is insulin?

what do they respond to?

what is the main stimulatory factor?

A

anabolic hormone.

responding to carbohydrates and or protein containing meal

insulin is predominately responding to glucose since its regulating plasma glucose.

increase in glucose, insulin is secreted

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11
Q

What is the structure of insulin? include which one is longer than the other.

A 
A chain (shorter)
B chain (longer)
C peptide (gone)
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12
Q

what kind of hormone is insulin?

A

peptide.

disulfide bridges

cleavage is from

Preproinsulin –> (removing the signal peptide (C peptide)) to Proinsulin –>

(cleavage of proinsulin –> Insulin

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13
Q

Why do we care about C peptide? (2 reasons).. why not just look at insulin?

When would it be important?

A

it’s a good estimator of insulin release.

the cleavage of Proinsulin generates C peptide and insulin, which is a ONE TO ONE RATIO, so it’s a linear relationship to understanding the amount of insulin processed.

the amount of insulin produced by the pancreas is not what’s actually in circulation because the liver is taking it and processing it, but C PEPTIDE IS NOT PROCESSED SO ITS AN IMMEDIATE MEASUREMENT OF SYNTHESIS.

in diabetes.. it’ll tell you that the Beta cell integrity of the pancreas is good or not.

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14
Q

How does the synthesis of insulin occur? (biochem identical)

what cell

what responds to it?

A

B cell in the pancreas is responding to glucose through Glut 2.

glucose is going through glycolysis and we have oxidation and it creates ATP.

ATP modulates the ATP dependent potassium channel. this modulates the conductance of potassium

this causes a depolarization, causing ca to come in.

once calcium comes in it increases the exocytosis of Insulin and C peptide.

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15
Q

What are the portions of the ATP dependent K channel?

A

sulfonylurea receptor (SUR)

inward rectifier K+ channel

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16
Q

What does the sulfonylurea receptor do clinically?

A

some drugs bind to this (sulfonylurea drugs = Totbutamine, glyburide)

it’ll close the ATP dependent channel so we have a way to secrete insulin ( and c peptide in equimolar levels ) through a depolarization

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17
Q

What is to note about insulin and C peptide release?

A

they’re secreted in equimolar amount with insulin.

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18
Q

What’s insulin’s response to plasma glucose under 80?

what about when we eat or have an intravenous dose of glucose?

A

When the plasma levels are controlled from 40-80, minimal insulin is going to respond.

as we eat or get an intravenous dose, insulin needs to bring the glucose back to normal.. so above 80 it’ll start working.

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19
Q

What is going to inhibit the release of insulin?

how does it do this?

A

somatostatin –> inhibits adenylyl cyclase (and therefore no cAMP) through Gi

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20
Q

what is Acetylcholine going to go through and what is its effect on insulin?

A

ACh is going to bind to a muscarinic receptor, which is associated with a Gq receptor–> acts on Phospholipase C and increases IP3 to increase Ca2+ leading increasing synthesis –> increasing insulin secretion

also increases DAG –> acts through Protein Kinase C to increase insulin secretion as well

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21
Q

What is GLP1 and glucagon going to do on insulin release?

A

they’re going through Gs to increasing insulin release.

increasing adenyl cyclase increasing cAMP –> increase protein kinase A –> increase insulin release

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22
Q

What does CCK do for insulin?

A

increase insulin release similarly to acetylcholine.. (through gq)

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23
Q

what is the pattern of insulin secretion?

what is causing the first phase?

what about phase 2?

A

biphasic

phase 1) super fast. this is for the most part is preformed vesicles released from the membrane.

phase 2) this is newly synthesized insulin.

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24
Q

What’s the pathway of insulin?

what are you going to see at the portal vein vs systemic? (note amount and changing of levels)

A

insulin from the pancreas –> portal system to the liver.. so it’s important for clearance.

the concentration of the portal vein vs systemic circulation is a big difference.

the portal vein sees a higher amount of insulin than what’s seen at the systemic circulation.

the insulin is also going to have bursts of insulin.. it’s not tonic. that pattern is still kept in systemic circulation.

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25
Q

What is the clearance of insulin in the liver?

A

(80% ish is taken up) the hepatocyte takes insulin and insulin receptor and pinocytosis it and destroy it to clear the insulin.

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26
Q

Explain the insulin receptor?

explain the subunits too, make sure to know that!

A

the RTK has 2 beta subunits going into the cell membrane and two alpha subunits that are binding insulin.

the beta has the tyrosine kinase on it.

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27
Q

Explain the insulin receptor?

A

the RTK has 2 beta subunits going into the cell membrane and two alpha subunits that are binding insulin.

the beta has the tyrosine kinase on it.

28
Q

What does IRS 1-4 attach to (left arm of biochem + more RAS Pathway))? –> what is it important for?

what about for the (right arm)

A

SHC which is associated with GRB –> activates the RAS pathway

this leads to the activation of MAPK for growth effects and other signaling processes within the intracellular areas.

it is dependent on PI3K –> leads to the formation of PIP3 –> important for activation for PKB/AKT signaling –> for the most part metabolic effects

29
Q

what does PKB/AKT help signal (2 major ones)

A

Activation of protein phosphatases

Glut 4 and Glut12 translocation to cell membrane

30
Q

Glut 4 is found where?

glut 2 is found where?

A

uptake of glucose in muscle and adipose tissue

Liver and pancreas

31
Q

How does peripheral uptake of glucose happen because of insulin?

A

insulin facilitates the uptake through insertion of glut4 into the membrane.. this effects the adipose tissue, resting skeletal muscle.

32
Q

Insulin effects:

glucose uptake?

glycogen?

what about metabolism of proteins and carbs??

A

1) increase glucose uptake through increased glut4 transporters
2) increased glycogen synthesis (modulating enzymes to favor this)..
3) increased glycolysis and carbohydrate oxidation (burning out carbohydrate and syntehsizing lipids and amino acids( hexokinase in liver, glucokinase in the B cells.)
4) decrease GNG
5) increase protein synthesis
6) decrease protein breakdown

33
Q

what happens during exercise

A

muscle contraction.. so this leads to glucose uptake and glucose utilization.

Activation of AMP-kinase results in glut4 translocation

muscle contractions stimulate this process

34
Q

What two things are needed to up regulate the Glut-4 vesicle signaling to the membrane in the insulin pathway?

A

CBL protein + the AKT pathway

35
Q

What stimulates AMPK? what does it do?

why do we care?

A

AMPK is helping translocate GLUT4 to the plasma membrane

muscle contractions stimulate this.

Highlights the importance of exercise of management of insulin resistance and diabetes.

36
Q

What players are insulin stimulating to form triglycerides?

what is it inhibiting?

A

uptake of triglycerides via lipoprotein lipase

increase of glucose uptake.

decreasing hormone sensitive lipase (which usually breaks down triglycerides)

overall goal is to form triglycerides, NOT BREAK THEM DOWN

37
Q

What are the levels of glucose, fatty acids, ketoacids, amino acids with insulin in the system? like what is it going to do?

A

all decreased!

38
Q

What does insulin do to adipose tissue?

A

lipogenesis.. creates lipids!

depressing lipolysis.. decrease breakdown!

increase glucose uptake

39
Q

what does insulin do to striated muscle?

A

increasing glucose uptake

glycogen synthesis

protein synthesis

40
Q

what does insulin do on the liver?

A

lowers GNG

increases glycogen synthesis

increase lipogenesis

41
Q

what does insulin have on K+ uptake?

so diabetes?

why is it important?

what’s the treatment for hyperkalemia

A

insulin is going to be important for the intake of potassium from extracellular to intracellular.

diabetes = no insulin, so someone might have hyperkalemia

in hyperkalemia, we’ll have cardiac function being compromised…

we give them insulin with glucose.. we give them glucose because we don’t want to lower the glucose more.

42
Q

What are the different stimulatory factors for insulin secretion… to try to regulate glucose? (10)

don’t memorize, just make sure each makes sense.

A

increased glucose

increased AAs

increased FA and ketoacids

glucagon

Cortisol

GIP

Vagal stimulation;Ach

K+

Sulfonylurea drugs

Obesity

43
Q

what inhibits insulin secretion (5)

A

low blood glucose

fasting

exercise (you want the system to have enough glucose to give to your muscle)

somatostatin

alpha adrenergic agonists

44
Q

Explain Type 1 Diabetes Mellitus.

what does it result in?

when do you have symptoms?

A

Destruction of Beta cells, often as a result of autoimmune disease.

LACK OF INSULIN

not until 80% of the Beta cells are destroyed… takes YEARS

45
Q

In people with Type 1 diabetes, what happens with

blood glucose: what about glucose uptake, glucose utilization, GNG?

A

increase blood glucose: lower, lower, higher

production

46
Q

In people with Type 1 diabetes, what happens with

blood fatty acids and ketoacids?

F.A synthesis?
Triglyceride synthesis? triglyceride breakdown? circulating free F.A? Conversion of F.A to ketoacids?
ketoacid utilization by tissues?

A

higher (more breakdown since we don’t have insulin modulating it)

lower
lower
higher
higher
higher
lower --> results in DKA
47
Q

type 1 diabetes and potassium?

what does it effect then?

what about diuresis?

what does this lead to?

A

hyperkalemia –> shift of K+ from in the cell to out of the cell (remember insulin helps bring it in)

this then effects the Na/K ATP pump

higher blood glucose results in increased filtered load of glucose, exceeding reabsorptive capacity of the proximal tubule. water and electrolyte reabsorption is prevented..

so you get polyuria –> losing Na/K even though urine concentration of electrolytes is low

super thirsty

48
Q

in type 1 DM, what phase of insulin is effected most?

patients with what have this affected?

A

the first phase is affected most.

patients with high amount of plasma glucose are missing the acute insulin phase!

49
Q

what are you trying to do when doing replacement therapy?

drawbacks of insulin replacement therapy back in the day? (3)

A

Insulin is trying to recreate normal physiology..both basal and bolus insulin need to be accounted for when trying to replacement therapy of insulin.

trying to control the insulin release is tough especially if the patient isn’t following the diet.

there is some lagging of the insulin once it’s delivered –> so you have periods of hyperglycemia

painful and time consuming

50
Q

What happens during type 2 DM in the adipose tissue?

what happens to insulin resistance at different phases of the disease? (beginning, starting to develop glucose tolerance, full onset of the disease)

A

insulin resistance…

we have changes in the adipose tissue (inflammation, changes in FFAs, adipokine changes) that lead to insulin resistance.

at the beginning we can observe normal insulin secretion and control.

when individuals start developing glucose tolerance, the beta cells are compensating by increasing insulin secretion

with time, the system can’t keep going so it secretes less insulin. the cells get tired (B cell failure)

51
Q

What are the three causes for obesity-causing insulin resistance?

A

decreased glut-4 uptake of glucose in response to insulin. so exercise can help you with this part because of AMPK!!

lower ability of insulin to repress hepatic glucose production

inability of insulin to repress (HSL - hormone sensitive lipase) or increase lipoprotein lipase (LPL) on adipose tissue

52
Q

C peptide and Type 2 DM?

A

for C peptide, obese people have increased levels of C peptides compared to normal individual.

53
Q

Type 2 DM and ketoacidosis?

type 2 and non obese people?

A

not as prone as compared to type 1. this is due to a very small amount of insulin being secreted

still common but just due to. deficit in pancreas function

54
Q

what is the treatment for Type 2 DM?

A

sulfonylurea drugs

incretin analog of GLP

55
Q

Glucose tolerance test and incretin effect?

A

administering glucose orally triggers insulin and it brings it back to normal! but when you intravenous injection it’s much different. the whole difference is the incretin effect (happens because of GIP?)

when you have diabetes, you’ll have a lower incretin effect.

healthy patients have a huge difference.

56
Q

What stuff works on hyperglycemic action (increasing glucose in the system)?

hypoglycemic action (lowering glucose in the system)

A

glucagon, epinephrine, cortisol, growth hormone.

insulin

57
Q

What is glucagon start off before its cleaved?

what happens if it’s cleaved in alpha cells?

Intestinal L cells?

A

Prohormone that is cleaved to generate glucagon

alpha it’s cleaved to GRPP, glucagon, and proglucagon fragments

beta it’s cleaved to “glicentin, GLP-1, IP-2, GLP-2”

58
Q

in low glucose what happens in Beta cells? Alpha cells?

A

glucagon activation is dependent on the alpha cells.. through G alpha –> more cAMP to the secretion of glucagon.

Beta cells are not secreting insulin at that point.

59
Q

what’s in common of insulin and glucagon both being active?

what 4 other things are good for stimulating glucagon secretion?

A

AA’s

  1. CCK
  2. B adrenergic
  3. fasting
  4. ACh
60
Q

high glucose, what cells work? what is being inhibited?

what is inhibiting each?

A

B cells active producing insulin

A cells are being inhibited by B cells

Somatostatin is going to inhibit A cells as well

61
Q

How do we go from preproinsulin to insulin?

what about C-peptide?

A

preproinsulin –> proinsulin through removing a signal peptide, but we still have “Connecting Peptide” or “C Peptide” attached.

then from proinsulin –> Insulin is done during the packaging in vesicles.. C peptide is still with it until it goes to circulation where both are released!

62
Q

what 5 things happen because of the insulin receptor substrates (IRS)?

A

glucose transport

protein synth

fat synth

glycogen synth

growth and gene expression

63
Q

Other than AKT pathway helping to insert Glut4 into the membrane of skeletal muscle and adipose, what else is up regulating that from the binding of insulin to the RTK?

A

CBL

64
Q

What does insulin do to repress lipid breakdown?

A

usually inhibits Hormone Sensitive Lipase (HSL)

65
Q

What’s going to be happening during signaling of those with T2D?

A

less signaling of the RTK, so imparting signaling that can have growth functions being altered.

66
Q

What is the effect of glucagon on blood glucose, fatty acids, and ketoacids?

A

increase all

67
Q

glucagon on Lipolysis? GNG? Glycogenolysis? ketoacid formation?

A

increases all

Endocrinology 1 (14 decks)

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