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FHB - Endocrine & Reproductive > Lecture9 (76): Pancreas > Flashcards

Lecture9 (76): Pancreas Flashcards

1
Q

Brain can only use what as an energy source?

TG can only be made from glucose under what conditions?

What enzyme, produced by the liver but not found in the liver, is needed for ketone body utilization?

A

** Brain can only use glucose or ketone bodies as energy source

  1. Under high caloric intake
    - large accumulation in organs (fatty liver) can cause cell death
  2. THIOPRASE
    - only found in the brain
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2
Q

What does the endocrine pancreas consist of?

(3 major cell types)

Which cells are the majority? What does each cell secrete?

A

Consists of 3 major cell types clustered in groups “islets of Langerhans”

  1. Beta cells : 73 - 75%. Synthesize and secrete INSULIN.
  2. Alpha cells : 18 - 20%. Synthesize and secrete GLUCAGON.

Delta cells : 4 - 6%. Synthesize and secrete SOMATOSTATIN (SS14).

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3
Q

What are the 2 additional cells of the endocrine pancreas that are not as important?

Function?

A

PP - secrete pancreatic polypeptide , inhibit acinar cells via paracrine action

Epsilon cells - Secrete GRHELIN
- stimulate hunger
- GH release
inversely correlated with obesity

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4
Q

What hormone is secreted with insulin?

The pancreas is organized in _____ arrangement surrounded by fine reticular fiber network

About one million in human pancreas

What type of capillaries?

A
  1. Amylin
  2. “cord”
  3. Plentiful fenestrated capillaries
    - let hormones pass through easily
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5
Q

How are alpha and beta cells arranged?

Which are on the outside and which are on the inside?

What can inhibit what? Insulin/glucagon/epinephrine

A

Alpha cells = OUTER edges (make glucagon)

BETA cells = INNER edges (make Insulin)

Insulin can inhibit glucagon, but glucagon cannot inhibit insulin since the blood flows through the center and OUT

EPINEPHRINE can inhibit insulin

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6
Q

Arrangement of Alpha and Beta cells:

Beta cells clustered in core; other cells in _____

_____ effects between alpha and beta cells

A
  1. mantle

Alpha cells surround beta cells in a sandwich formation

  1. Paracrine

INSULIN rich blood flow inside, glucagon alpha cells on outside

BLOOD FLOW is important for feedback mechanisms (test)

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7
Q

What is the half life of insulin?

Insulin and ______ released together

What is the half life of C peptide as compared to insulin? What is it a good indicator of?

A
  1. 6-8minutes VERY SHORT***
  2. C-peptide
  3. C-peptide half-life = 35 min (much longer than insulin)

Good indicator of pancreatic function.

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8
Q

Without the cleavage of what will there be no insulin action?

A

Cleavage of C-peptide critical

exposes end of insulin chain that interacts with the receptor

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9
Q

Insulin Release:

What transporters let in Glucose from outside the BETA cell?

What affinity for glucose does this transporter have?

A

GLUT-2 = LOW affinity for glucose. Only when glucose is high will it transport

-inside the cell: insulin is stored in secretory granules (docked & ready to be released; or waiting to be released later)

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10
Q

What happens to glucose once it enters the BETA cell?

What transporters did it use?

Metabolism of ____ generates ATP.

A
  1. Glucose phosphorylated by glucokinase
  2. GLUT 2 (low affinity –> cannot be easily saturated)
  3. G6P metabolism generates ATP

Glucose will be phosphorylated by glucokinase & TRAPPED

(glucokinase:only activated when glucose is HIGH HIGH)

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11
Q

In Glucose Metabolism:

  1. Increased ATP closes what channels?
  2. What subunits do these channels have?
  3. What drugs can also close this channel?
A
  1. K+ channels
  2. K+ channel has a SUR subunit.

Sulfonyureal subunit - one of the earliest targets for anti-diabetic drugs

when it senses ATP , channel will close and HOLD POTASSIUM IN THE CELL - cause the cell to DEPOLARIZE
dopalarization opens voltage gated calcium
influx of calcium
SIGNAL TO RELEASE INSULIN

  1. Sulfonylurea drugs close the channel
    - bypass glucose steps
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12
Q

What is the main signal for insulin release in the cell?

A

K+ channels sensed increased ATP and close

  • when they close, the cell depolarizes and opens voltage gated Calcium channels
  • influx of CALCIUM into the cell signals the release of INSULIN
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13
Q

What are the 3 other modulatory pathways of Insulin Release. And state their function.

A
  1. FFAs, Amino Acids ——- can increase ATP
  2. Incretins (GLP-1) potentiate insulin release – still needs glucose!
  3. Catecholamines inhibit release via alpha-adrenergic receptors
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14
Q

Protein alone will not stimulate much insulin.

Why?

A

In general  protein alone will not stimulate much insulin

which is why the ATKINS diet works (skew the ratio of insulin:glucagon, glucagon will be much higher on a protein only diet)

  • GLUCAGON will be much higher
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15
Q

How do incretins work (GLP-1)?

What type of receptors?

What do they potentiate the release of?

Do they cause insulin release on their own?

What type of diets do they respond to?

A

Incretins (GLP-1):

act on G protein through cAMP

  • potentiate the CALCIUM RELEASE
  • do not cause enough intracellular calcium to release insulin alone
    but respond to HIGH CARB HIGH FAT diets
    work to INCREASE INSULIN than you normally would secrete
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16
Q

What inhibits insulin directly at the beta cell?

Through what type of receptors specifically?

A

Catecholamines
- INHIBIT INSULIN DIRECTLY AT BETA CELL

-through alpha-adrenergic
need to keep more glucose mobilized in blood (during stress/exercise)

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17
Q

Why is insulin release in response to glucose biphasic?

What is the 1st phase? 2nd phase?

A

5% of vesicles are available for immediate release - docked at membrane

95% are “stored” or reflect newly synthesized insulin

1st phase = insulin docked at membrane and ready

2nd phase = glucose still elevated as body is digesting food

18
Q

What type of receptors are insulin?

Where does insulin bind the receptor? (subunit)

Which unit is then autophosphorylated?

A
  1. Receptor tyrosine kinase
    (intrinsic catalytic activity)
  2. alpha subunit = for insulin
  3. Beta subunit is autophosphorylated
19
Q

Insulin Action:

Glucose does not enter cell without _____.

Autophosphorylation of receptor recruits _____.

What do these activate?

A
  1. insulin
  2. IRSs (insulin receptor substrates).
  3. IRSs activate intracellular signaling cascades
20
Q

What is the result of IRSs activating intracellular signaling cascades?

A

RESULT: GLUT-4 inserted in membrane
– glucose can enter cell

  • GLUT 4 can become defective and result in insulin insensitivity (relies on insulin for glucose uptake)
21
Q

Through what pathways is insulin action occurring to facilitate the following:

  1. Metabolic effects
  2. mitogenic
A
  1. Metabolic effects
    - PKB and TC-10 pathways.
  2. Mitogenic effects
    - MAPK pathways
22
Q

Which transporter is the only one that is insulin dependent?

Which is a fructose transporter?

Which 2 transporters are used by the brain and neurons?

Where are GLUT 2 receptors found?(4) When are these used?

A
  1. GLUT 4
  2. GLUT 5
  3. GLUT 1 and 3

Pancreatic beta cells, liver, intestine, kidney

  • only used when glucose is HIGH
23
Q

What is the primary action of insulin in the liver?

A
  1. promotes glycogen and TG production;
  2. reduces glucose production/output
  3. Inhibits glucose-6 phosphatase
  4. Stimulates glucokinase synthesis
24
Q

What is the primary action of insulin in the muscle?

In fat?

A
  1. Muscle – promotes glycogen and TG production,
    - protein synthesis (insulin inhibit proteolysis along with GH)
  2. Fat – promotes TG production,
    - release of FFAs from chylomicrons,
    - glycolysis
    - inhibits lipolysis
25
Q

________ – important clinical use
Synthesized from the same prohormone as glucagon

What are they stimulated by?

Are they similar to glucagon, since there are synthesized from it?

A

Incretins (GLP-1 and GLP-2)
- GLP potentiates the affect of INSULIN

Intestinal GLP stimulated by carbohydrates

-GLP ARE NOT SIMILAR TO GLUCAGON (only called glucagon like peptide since synthesized from same preproglucagon)

26
Q

What is the Major counterregulatory hormone to insulin?

Released in response to (low/high) blood glucose levels

What type of meals stimulate its release?

A
  1. Glucagon
  2. LOW
  3. AAs stimulate release
    (protein meals)
27
Q

How do catecholamines affect glucagon?

A

Catecholamines stimulate release (exercise)

28
Q

What is the primary action of glucagon?

2 main targets? Are there receptors on skeletal muscle?

A

ENERGY MOBILIZATION

Main targets:

  1. liver
  2. adipose tissue.

No glucagon receptors in skeletal muscle

Opposite effects of insulin

29
Q

Why is ketoacidosis rare in Type 2 diabetes?

______ WILL INHIBIT KETOGENESIS

A

Type 2 diabetes = ALOT of glucose

TP2D KETOACIDOSIS IS RARE IN TYPE 2

  • as long as insulin is present = no ketogenesis!!!
    2. INSULIN
30
Q

What does it mean that both insulin and glucagon target many of the same enzymes? How does this occur?

A
  1. insulin dephosphorylates and turns the enzyme into a kinase
    - push it towards glycolysis
  2. Glucagon can PHOSPHORYLATE the enzyme
    - turn it into a PHOSPHATASE = gluconeogenesis
31
Q

Where is somatostatin produced?

What type of meals stimulate it?

What inhibits it?

What does somatostatin SUPPRESS?

A
  1. Produced by delta cells in pancreatic islets
  2. Stimulated by high fat, high carb meals.
  3. Inhibited by insulin (due to blood flow)
  4. Suppresses insulin release - used in clinic for management of insulin-producing tumors
32
Q

Where is amylin released? With what?

What is it “synergistic” with?

It is increased or decreased in obesity & hypertension?

How does it contribute to beta cell destruction? In what condition?

A
  1. Amylin –
    Released with insulin from vesicles in beta cells
  2. Synergistic with insulin in regulation of blood glucose
  3. Circulating amylin increased in obesity, hypertension
  4. Possibly contributes to beta cell destruction by forming amyloid

obese patients have HIGH AMYLIN
- forms amyloid proteins - deposits can build up in the vessels/heart/ pancreas AND DESTROY BETA CELLS

-theory: beta cells start to die because of excess amyloid (overwhelms ER and it begins to misfold the proteins)

33
Q

Somatostatin 14
blocks _____ release

Is this effect significant? What is it used for clinically?

A

insulin

  • released during a high fat/high carb diet

does not inhibit directly  released into the blood
normally not a huge affect under physiologic conditions
ONLY SIGNIFICANT EXPERIMENTALLY

USED CLINICALLY FOR INSULIN PRODUCING TUMORS!!!!!!

34
Q

Where is ghrelin produced?

What does it stimulate at the level of the hypothalamus?

Which cells?

What does it have paracrine action on?

What is its affect on insulin release?? How?

A

Ghrelin
28 AA peptide

  1. Most circulating ghrelin produced in stomach
  2. Stimulates food intake at level of hypothalamus
    Stimulates GH release (get body ready for food)
  3. Produced in newly described epsilon cells of islets
  4. Paracrine action on beta cells:
  5. Inhibits insulin release via Gαi activation (opens) of K+ channels
    Decreases intracellular Ca++; decreases insulin release

DECREASES INTRACELLULAR CALCIUM

35
Q

_____ correlation between circulating ghrelin and obesity

What is Ghrelin’s affect on insulin release?? How?

A

inverse

  1. Inhibits insulin release via Gαi activation (opens) of K+ channels
    Decreases intracellular Ca++; decreases insulin release

DECREASES INTRACELLULAR CALCIUM

36
Q

Glucagon is the primary hormone stimulating gluconeogenesis and lipolysis.

What two hormones have permissive effects on gluconeogenesis and lipolysis?

Why is this the delayed response?

A
  1. Growth Hormone
  2. Cortisol

Delayed response (6 hours) – defense against prolonged hypoglycemia (starvation)

  • kick in after glucagon
37
Q

What hormones do the following:

  1. Like glucagon, raise plasma glucose levels
  2. Increased during exercise and stress
  3. Inhibits insulin release directly at beta cell, stimulates glucagon in alpha cell
  4. Increases hepatic glucose output
  5. Decreases glucose uptake in skeletal muscle/adipose tissue
A

Catecholamines - EPINEPHRINE

38
Q

What is released during a mixed meal:

  1. Carbs
  2. Fat
  3. Protein

WHAT ABOUT A PROTEIN ONLY MEAL?

A
  1. Carbs - insulin
  2. Fat - insulin
  3. Protein - Glucagon, some insulin

GLUCAGON ONLY

39
Q

When insulin is present:

AA from protein stimulate _____ which stimulates ____ in the liver.

A
  1. GH

2. IGF-I (liver).

40
Q

_____ stimulates glucose uptake in muscle, proliferation of visceral organ tissues; inhibits proteolysis.

What opposes insulin lipogenesis?

What determines the net amount of fat after eating a meal??

A

IGF-I

  1. GH!!!
    - ratio of Gh and INSULIN determines the net amount of fat after eating the meal (since insulin stimulates lipogenesis)

FHB - Endocrine & Reproductive (17 decks)

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