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Endo/Repro Exam 1 > 6. Endocrine Pancreas > Flashcards

6. Endocrine Pancreas Flashcards

1
Q

The endocrine cells of the pancreas secrete what?

A

1. Insulin

2. Glucagon

3. Somatostatin

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2
Q

What 3 things does the endocrine pancreas regulate?

A

1. Glucose

2. FA metabolism

3. AA metabolism

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3
Q

How are the endocrine cells of the pancreas arranged?

A

Islets of langerhans.

  • Most of them are beta cells, located mostly in the center and secrete insulin and C peptide.
  • Alpha cells are located in the periphery and secrete glucagon.
  • Delta cells secrete somatostatin. They are dispersed in the islet and send dendrite-like processeses to B cells to assist with regulation.
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4
Q

What are the three ways the cells of the islet of Langerhands communicate with each other and alter each others secretion?

A

1. Gap junctions

2. Blood supply

3. Innervation by adrenergic, cholinergic or peptidergic neurons.

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5
Q

Cells in the islet of Langerhans communicate with one another via _______

A

Gap junctions located in between alpha cells, beta cells or alpha-beta cells.

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6
Q

Describe the blood supply of the endocrine pancreas.

A

The endocrine pancreas receives about 10% of total blood supply.

Blood flows first to the capillaries in the center of the islet and picks up insulin. Then, the blood flows to the peripherphy, bathes the other cells and acts on alpha cells to inhibit the secretion of glucagon.

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7
Q

Venous blood in the pancreas from the ____ cells carries ______ to the ____ and _____ cells.

A

Venous blood in the pancreas from the B cells carries insulin to the alpha and delta cells.

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8
Q

Endocrine cells are arranged in clusters called islets of langerhans. What type of neurons are they innervated. by?

A
  1. Adrenergic -> decrease insulin secetion
  2. Cholinergic -> increase insulin secretion “rest and digest”
  3. Peptidergic neurons.
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9
Q

What are the paracrine mechanisms of hormones in the pancreas?

A

1. Delta cells inhibit alpha cells and beta cells.

2. Beta cells inhibit alpha cells.

3. Apha cells stimulate beta cells.

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10
Q

Insulin is a _________ hormone that is secreted when we eat a meal with _________ or _______.

A
  • ANABOLIC
  • CARBS
  • PROTEINS
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11
Q

What is the main stimulatory factor for insulin secretion?

A

GLUCOSE

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12
Q

Describe the process of insulin synthesis.

A

Insulin is made in beta cells of the pancreas.

    1. Begins as preproinsulin (signal peptide, A and B chains of insulin and C peptide).
    1. Signal peptide is removed and preproinsulin -> proinsulin. At this point, the C peptide is still attached to the insulin and disulfide bridges form in the ER
    1. Packed in secretory vesicles in the Golgi.
    1. During this process, proteases cleave proinsulin-> insulin and C peptide.
    1. Insulin and C peptide are secreted in EQUAL amounts.
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13
Q

What is the importance of C peptide?

A

C peptide is a good measure of insulin because it is secreted in the same amounts and excreted unchanged in our urine.

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14
Q

We have high glucose.

We need to secrete insulin. How do we do this?

A
  1. Glucose is going to bind to GLUT2 R on the pancreatic B cell.
  2. Glucose goes inside and Glu–> G6P via glucokinase.
  3. G6P will undergo glycolysis, TCA cycle and oxidation–> ATP
  4. ATP will close KATP channels
  5. Cell depolarizes
  6. Depolarization opens the VGCa2+ channels and allows Ca2+ influx
  7. Triggers exocytosis of secretory vesicle
  8. insulin and C peptide are released
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15
Q

When do the K+ ATPase channels close in the pancreatic B cell?

A

When ATP increases.

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16
Q

Sulfonylurea drugs are used to help treat Type 2 DM.

What receptors do they act upon?

A

Sulfonylurea drugs will close K+ ATP-dependent channels, thus, increasing insulin secretion.

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17
Q

When does insulin begin to respond to and increase in blood glucose?

A

When our blood glucose reaches 80 mg/dl, insulin will be secreted. When levels glucose levels are at 200 mg/dl, insulin is responding at 100%. Thus, no more will be released.

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18
Q

What modulates the release of insulin?

A
    1. Glucagon and GLP-1 binds to a Gs GCPR to stimulate insulin secretion.
    1. ACh binds to a Gq GCPR (muscarinic receptor) to stimulate insulin secretion.
    1. CCK binds to a Gq GCPR to stimulate insulin secretion.
    1. Somatostatin binds to a Gi GCPR and inhibits the release of insulin.
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19
Q

Glucose will stimulate insulin secretion in a _________ manner. Describe this.

A

BIPHASIC MANNER.

1st phase: insulin will be relased rapidly and transiently from our ready pool.

2nd phase: insulin will have to be freed up from our reserve poor.

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20
Q

Upon insulins release from the pancreas, it must go to the liver. How does it do so?

A

Via the portal vein. 80% will then arrive in the liver.

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21
Q

Where do we see a higher amount of insulin: portal vein or systemic circulation?

A

Portal vein.

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22
Q

When giving medications, it is important to consider that insulin is released in a __________ manner. Describe this.

A

Pulsatile manner.

Insulin release from the pancreas oscillates every 3-6 min, changing the concentration of blood insulin from 800 pmol/l to 100 pmol/l.

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23
Q

Describe the insulin receptor.

A

The insulin receptor is a tetramer tha has two α subunits and two β subunits.

  • α subunits lie in the extracellular domain,
  • β subunits span the cell membrane.
  • A disulfide bond connects the two α subunits, and each α subunit is connected to a β subunit by a disulfide bond. The β subunits have intrinsic tyrosine kinase activity.
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24
Q

How do we get rid of the insulin + receptor?

A

It is internalized by its own cell.

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25
Q

How does insulin affect its own receptor?

A

Insulin DOWNREGULATES its own receptor by decreasing rate of synthesis and increasing rate of degradation of its own receptor.

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26
Q

Insulin receptor signaling via the RAS dependent pathway.

A
  1. Insulin binds to insulin receptor, a RTK, which is already dimerized.
  2. Tyrosine residues are autophosphorylated
  3. IRS-1 (insulin receptor substrate-1) binds to phosphorylated receptor tyrosine kinase
  4. Insulin receptor phosphorylates IRS-1 on its tyrosine.
  5. IRS-1 then recruits an adapter protein called GRB-2 (which is assx with SHC), which activates the RAS and MAP kinase pathway.
  6. MAPK will cause growth effects by altering gene transcription
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27
Q

Insulin receptor signaling via the RAS independent pathway.

A
  1. Insulin binds to insulin receptor, a RTK, which is already dimerized.
  2. Tyrosine residues are autophosphorylated
  3. IRS-1 (insulin receptor substrate-1) binds to phosphorylated receptor tyrosine kinase
  4. Insulin receptor phosphorylates IRS-1 on its tyrosine.
  5. IRS-1 then recruits an adapter protein called PI 3-kinase (phosphoionositide-3-kinase).
  6. P1 3-kinase phosphorylated phosphoinositides to make PIP2 and PIP3.
  7. PIP2 and PIP3 act as second messengers and recruit PKB and activate it via phosphorylation.
  8. Causes metabolic effects
    1. Increase GLUT4 (in muscle and adipose tissue) and GLUT2 (liver) movement into the plasma membrane
    2. Activate protein phosphatases.
      9.
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28
Q

How does a cell take up glucose?

A

Facilitated diffusion via GLUT transporters.

  • Insulin also causes glucose uptake by inserting transporters into the membrane. Adipose tissue and skeletal muscle NEED insulin to uptake glucose.
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29
Q

What are the major effects of insulin on MUSCLE?

A
  1. Increase glucose uptake by via GLUT 4 transporters.
  2. Increase glycogenesis: Increase glycogen synthesis by increasing hexokinase (or glucokinase in liver and B cells) and activating glycogen synthase.
  3. Increase glycolysis and carbohydrate oxidation by increasing hexokinase, PFK and pyruvate dehydrogenase.
  4. Decrease gluconeogenesis.
  5. Increase protein synthesis and decrease protein breakdown.
    * Decreases blood AA.
30
Q

Why is exercise important for management of insulin resistance and DB?

A

Muscle contractions activate AMPK (AMP Kinase), resulting in GLUT4 translocation to the plasma membrane.

31
Q

How does insulin affect adipose tissue?

A
    1. Uptakes TAGS via lipoprotein lipase
    1. Increases glucose uptake into cells -> a-glycerol-P, which is used to make TAGS.
    1. Take up FA to make TAGS.
    1. Inhibits [hormone sensitive lipase], which break down TAGS–> FA.
32
Q

How does insulin affect blood levels of:

  1. Glucose
  2. FA
  3. Ketoacids
  4. Amino acids
A

Decreases ALL

33
Q

Summary of insulin action on adipose tissue, straited muscle and liver.

A
  1. Adipose tissue: increase glucose uptake, increase lipogenesis, decrease lipolysis
  2. Striated muscle: increase glucose uptake, glycogenesis, increase protein synthesis.
  3. Liver: Increase glycogenesis, lipogenesis and decreases gluconeogenesis.
34
Q

**** IMPORTANT****

How does insulin affect plasma K+ concentration?

A

Increase K+ uptake into the cells, causing a decrease in blood [K+].

35
Q

Increase in K+ cause cause arrythmias.

Thus, how can we treat this in the ER?

A

Give the patient insulin and glucose. Glucose is given because so we do not reduce levels of glucose.

36
Q

What 10 things cause insulin secretion?

A
  • 1. high glucose
  • 2. high AA
  • 3. high FA and ketoacids
  • 4. Glucagon
  • 5. ACh
  • 6. High K+
  • 7. CCK
  • 8. GIP (glucose-dependent insulinotropic peptide)
  • 9. Sulfonylyrea drugs
  • 10. Obesity.
37
Q

What 5 things inhibit insulin secretion?

A

DEAFS

  • Decrease blood glucose
  • Exercise
  • Alpha-adrenergic AGO
  • Fasting
  • Somatosatin
38
Q

What is type 1 DM?

A
  • Destruction of B cells that causes a decrease in insulin secretion. It is often caused by autoimmune disease.
  • We do not see sx until about 80% of B cells are dead.
39
Q

What is the precipitating event for Type 1 DM?

A

Overt immunologic abnormalities.

40
Q

What do we see if someone has type 1 DM?

A
  1. Increase blood glucose: decrease uptake, decrease utilization, increase gluconeogenesis.
  2. Increase blood FA and ketoacid; FA are converted to ketoacids but we do not utilize it. Result: DKA (diabetic ketoacidosis) and metabolic acidosis.
  3. Increase blood AA.

4. Hyperkalemia

5. Osmotic diuresis.

41
Q

Type 1 DM can cause hyperkalemia.

How?

A
  • K+ moves out of the cell, reducing intracellular concentration. Insulin does not effect Na+/K Pump.
  • Even though plasma levels are above normal, total body K+ is normal d/t poluria and dehydration.
42
Q

Type 1 DM can cause osmotic diuresis.

How?

A
  1. Increase in blood glucose -> increases filtered load, causing us to filter more than we can reabsorb. It acts as an osmotic solute in the pee, preventing water and electrolyte absorbtion. Leads to
    1. –> Polyuria and thirst: increase excretion of Na+/K even though urine concentration of electrolytes is low.
43
Q

In diabetic individuals, the first thing to disappear is what?

A

First phase or our acute insulin response.

44
Q

What is the GOAL of insulin replacement treatment of type 1 DM?

A

Recreate normal physiology (basal and bolus insulin)/

45
Q

What is the downsides of insulin replacement therapy?

A
  1. Painful and time consuming.
  2. Lag of time between administration of insulin and glucose measurement.
  3. Absorbtion of insulin is slow after subcutaneous injection
  4. Poor blood glucose control. We will have periods of hyperglycemia.
46
Q

What is type 2 DM?

A

Type 2 DM is often assx with obesity. It is caused by downregulation of insulin receptors and insulin resistance. Insulin is secreted normally from B cells, but it cannot activate insulin receptors.

47
Q

Type 2 DM is associated with reactive _________, followed by relative _________-.

A
  • Type 2 DM is associated with reactive hyperinsulinemia, followed by relative hypoinsulinemia.
48
Q

What are 3 causes for obesity-induced insulin resistance?

A
  1. GLUT4- receptors no longer respond to insulin and take up glucose
  2. Insulin can no longer inhibit HSL or increase LPL
  3. Insulin can not stop liver from making glucose
49
Q

Obese people have ____ levels of C peptide and ____ levels of insulin.

A

HIGH.

HIGH.

50
Q

What can cause type 2 DM, insulin resistance?

A
  1. Post-receptor signaling – ultimately results in decreased glucose transporter number and mobilization
  2. Increased hepatic glucose productions
  3. Hyperglucagonemia
51
Q

Are those with type 2 more or less prone to ketoacidosis than type 1?

A

Less.

52
Q

Can non-obese pts get type 2 DM?

A

Yes. it can occur d/t decrease in insulin release by. the pancreas and insulin resistance.

53
Q

How can we tx type 2 DM?

A
    1. Reduce calories and lose weight
    1. Sulfonylyrea drugs
    1. Incretin analog of GLP (exenatide); an injection.
    1. Slow absorbtion of carbs via a-glucosidase inhibitors and amylin analogs.
    1. Insulin sensitizers that upregulate the receptors on target. tissue
  • (biguanidine)
54
Q

What is the incretin effect?

A

When normal subjects are given oral vs. IV glucose, they see a high release of insulin when given oral glucose because it activates incretins (GLP-1 and GIP), which causes insulin release.

55
Q

What is seen ind diabetic patients who receive oral glucose?

A

Diabetic pts have glucose levels that. are set higher than normal.

When given oral glucose, phase 1 is absent and there is a small rise in insulin.

56
Q

What happens when normal subjects are given IV glucose?

A

Effects are quick and you can see the 1 and 2 phases of insulin release because incretins are not released.

57
Q

What are incretin hormones?

A

Intestine derived hormones (GLP-1, GIP, Short T1/2) that are secreted in response to GI glucose and fat.

They will cause insulin secretion, inhibit glucagon secretion and slow gastric emptying.

58
Q

What does the incretin effect look like in patients who have type 2 DB?

A

Reduced incretin effect

59
Q

Compare and contrast.

Age of onset for type 1 and type 2 DB.

Ketosis onset

Pathophysiology

Assx conditions

A

Type 1

  • Peak in early childhool and adolesnce
  • Likely.
  • Autoimmune
  • Autoimmune thyroid, celiac and addisons

Type 2

  • After puberty
  • uncommon but can happen
  • insulin-resistance
  • obsetity, lipid abnormalities, PCOS, NFLAD
60
Q

What increases plasma glucose?

A

GGEC

  1. Glucagon
  2. GH
  3. EPI
  4. Cortisol
61
Q

When we eat food, how does this effect insulin, glucagon and glucose?

A

Rises in glucose–> insulin secretion.

Glucagon secretion decreases!

62
Q

How do we get glucose from mmol/L -> mg/dL?

A

*18

63
Q

What is glucagon?

  • A straight polypeptide with ___ AA
  • Family with ____ and ____.
  • Made as ______.
  • Stored in pancreatic alpha cells.
A
  • A straight polypeptide with 29 AA
  • Family with secretin and GIP.
  • Made as preproglucagon.
  • Stored in pancreatic alpha cells.
64
Q

What are the effects of glucagon of blood levels of

-glucose

-FA

-ketoacids?

A

INCREASE ALL

65
Q

What causes secretion of glucagon?

A
  • 1. MAIN: LOW BLOOD GLUCOSE.
    1. Increased AA (arginine and alanine)
    1. Fasting
    1. ACh
    1. B adrenergic receptors
    1. CCK

LIFABC

66
Q

What causes in increase in BOTH insulin and glucagon?

A

1. increased AA

2. CCK

3. B adrenergic R

4 ACh.

67
Q

Our plasma glucose tells us the balance between what?

A

Hypoglycemic action of insulin and hyperglycemic action of anti-insulin hormones.

68
Q

What inhibits glucagon secretion and synthesis?

A

1. Insulin

2. Somatostatin.

3. Increased FA

4. Ketoacid concentration.

69
Q

Major actions of glucagon by the liver?

A

Increase blood glucose by

    1. Increase glucogenolysis and inhibit glycogenesis.
    1. Increase gluconeogenesis by decreasing producting of F26P
    1. Substrates all directed to form glucose.
70
Q

Effects of glucagon on adipose tissue

A
  • Increase lipolysis
  • Inhibit FA synthesis and thus, shunting substrates towards gluconeogenesis.
  • high FA in blood will cause high. ketoacid
71
Q

What inhibits glucagon secretion?

A
  1. Insulin
  2. Somatostatin
  3. Increase FA and ketoacids.
72
Q
A

Endo/Repro Exam 1 (14 decks)

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