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Endocrine - MSI Spring > Endocrine Pancreas > Flashcards

Endocrine Pancreas Flashcards

1
Q

What is the major function of the endocrine pancreas?

A

Regulate glucose, fatty acids, and a.a. metabolism

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2
Q

How are endocrine cells of the pancreas arranged in?

A

clusters - islets of langerhans (1-2% of pancreatic mass)

Each Islet contains 2500 cells

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3
Q

What are the islets of Langerhans innervated by?

A

adrenergic, cholinergic, and peptidergic neurons

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4
Q

Describe beta cells of the pancreas

A

60-65% of the islet
secrete insulin and C peptide
Tend to be located in the central core

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5
Q

Describe alpha cells of the pancreas

A

20% of islet
Secrete glucagon
tend to be located near the periphery of the islet

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6
Q

Describe delta cells of the pancreas

A

5% of the islet
Secrete somatostatin
Interspersed between alpha and beta cells
neuronal appearance, send dendrite-like processes to beta cells

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7
Q

What do gap junctions permit in islets of Langerhans?

A

rapid cell-to-cell communication
a-a
b-b
a-b

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8
Q

Describe the blood supply in the islets of Langerhans

A

islets receive about 10% of total pancreatic blood flow
Blood flows first to capillaries in the center and pick up insulin beta cells
Blood flows to periphery of islets, and bathes the other types of cells

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9
Q

What is the main stimulatory factor of insulin secretion

A

Glucose

insulin secreted in response to carbohydrate and/or protein-containing meal

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10
Q

Describe preproinsulin

A

4 peptides (signal peptide, A and B chains of insulin, and connecting peptide: C peptide)

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11
Q

Describe proinsulin

A

no signal peptide
C peptide still attached to insulin
Disulfide bridges form in ER
Packed into secretory vesicles in the Golgi

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12
Q

What happens to proinsulin while being packed into secretory vesicles

A

proteases cleave proinsulin

Insulin and cleaved C peptide packed together

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13
Q

What is C peptide used to test for?

A

Test Beta cell function in type I DM pts receiving insulin injections

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14
Q

What transporter does Glucose use to get into beta cells of the pancreas?

A

GLUT 2

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15
Q

How does Glucose cause Insulin to be secreted?

A

Glucose enters the cell
Glucose –(glucokinase)->G6P
Oxidation leads to ATP increase
ATP increase closes K channels causes the membrane to depolarize and open Ca channels
Increase intracellular Ca causes exocytosis of insulin and C peptide

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16
Q

What do sulfonylurea drugs do?

A

promote the closing of ATP-dependent K channels

This increases insulin secretion; used in the treatment of type II DM

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17
Q

How much C peptide is secreted compared to insulin?

A

in equimolar and is excreted unchanged in urine

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18
Q

Glucose stimulates insulin secretion in a _____ manner

A

biphasic

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19
Q

What type of receptor is the insulin receptor?

A

Tyrosine kinase receptor

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20
Q

Insulin-receptor complex is internalized by its target cell. What downregulates the receptor?

A

Insulin itself

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21
Q

How often is insulin released from the pancreas?

A

release oscillates with a period of 3-6 min

Blood concentration from 800 pmol/l to 100

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22
Q

What Tyrosine kinase pathway activates the metabolic effects of insulin?

A

Ras-independent pathway

IRS->PI3K->PIP3->PKB

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23
Q

What tyrosine kinase pathway activates the growth effects of insulin?

A

The Ras-dependent pathway

IRS->GRB/SOS->RAS/GDP->GTP->MAPK

24
Q

What do endocrine cells of the pancreas secrete?

A

insulin, glucagon, and somatostatin

25
Q

What glucose transporter is inserted into membrane after insulin activation of adipose tissue, resting skeletal m, and other tissues?

A

GLUT 4

26
Q

What are the insulin actions in muscles?

A

Glucose uptake increased via GLUT 4
Increase glycogen synthesis by increasing hexokinase (or glucokinase in liver and b cells), PFK, and pyruvate DH

Increase glycogen synthase

Decrease protein breakdown and gluconeogenesis

27
Q

What are the effects of insulin of TGs and FA metabolism in adipose tissue

A

Inhibits breakdown of TGs by inhibiting hormone sensitive lipase

Promote glucose ->A-glycerol-P+FA’s->TGs

Increase TGs storage and export (VLDLs)

28
Q

Describe the actions of insulin in liver

A

GLUT2 increase
Increase glucokinase, glycogen synthesis, glycolysis (increase acetyl CoA, and FA synthesis)
Decrease gluconeogenesis and glucose-6-phosphatase

Increase TG storage and export
Increase protein synthesis and decrease degradation

29
Q

Describe the actions of insulin in adipose tissue

A

Increase GLUT 4, glycolysis (increase a-glycerol phosphate, acetyl CoA, and FA synthesis)

Increase TGs and lipoprotein lipase for uptake
Decrease HPL to decrease lipolysis

30
Q

Describe insulin actions in muscle

A

Increase GLUT 4, glycogen synthesis, glycolysis, protein synthesis, and TGs

31
Q

What are the effects of insulin on blood levels?

A

Decrease glucose, a.a., F.A., ketoacid, and K

32
Q

What are factors that stimulate insulin secretion?

A 
increase [glucose], [a.a.], [F.A] and [Ketoacid] 
Glucagon
Cortisol
GIP
Vagal: ACh
K
Sulfonylurea drugs
obesity
33
Q

What are factors inhibiting insulin secretion ?

A

decrease blood [glucose], fasting, exercise, somatostatin, alpha-adrenergic agonists, diazoxide

34
Q

Describe the pathophysiology of insulin in T1DM?

A

inadequate insulin secretion
Destruction of beta cells - usually autoimmune
Symptoms not there until 80% of beta cells are destroyed

35
Q

Describe what happens in DMT1 to glucose levels

A

inadequate insulin secretion causes increase in blood glucose concentration

  • decrease uptake of glucose
  • decrease glucose utilization
  • increase gluconeogenesis
36
Q

Describe what happens in DMT1 to FA and Ketoacid levels

A

Increase blood FA and Ketoacid concentrations

  • decrease FA synthesis
  • Decrease TG synthesis
  • Increase TG breakdown
  • Increase level of circulating free FA
  • Conversion of FA to ketoacids and decrease ketoacid usage by tissues = DKA
37
Q

Describe what happens in DMT1 to a.a. levels

A

Increase

  • increase protein breakdown
  • decrease protein synthesis
  • increase catabolism of a.a. : loss of LBM
  • increase ureagenesis
38
Q

Describe what happens in DMT1 with osmotic diuresis

A

Increase blood [glucose] results in increase filtered load of glucose, exceeds capacity of proximal tubule
Water and electrolyte reabsorption prevented
Polyuria: increase excretion of Na and K
Thirst

39
Q

Describe what happens in DMT1 to K levels?

A

Shift K out of cell causing hyperkalemia

  • intracellular concentration low
  • lack of insulin effect on Na/K - ATP pump
  • plasma levels above normal but total body K usually below normal due to polyuria and dehydration
40
Q

What is the Tx for T1DM?

A

insulin replacement: recreate normal physiology (basal and bolus insulin)

41
Q

What are the drawbacks of insulin replacement therapy?

A

painful and time consuming
lag btwn glucose measurement and insulin dosing
delayed absorption of insulin following subcutaneous injection
poor blood glucose control: periods of hyperglycemia

42
Q

What is the pathophysiology of insulin in TIIDM?

A

insulin resistance
- vast majority of diabetes is type II
Pts make insulin but not enough to overcome insulin resistance
normal or elevated insulin concentration initially; relative insulin deficiency (reactive hyperinsulinemia followed by relative hypoinsulinemia)

43
Q

What are the 3 causes for obesity-induced insulin resistance?

A

Decrease GLUT-4 uptake of glucose in response to insulin release

Decreased ability of insulin to repress hepatic glucose production

Inability of insulin to repress hormone-sensitive lipase or increase LPL in adipose tissue

44
Q

In DMTII there is a (Hyper/Hypo) glucagonemia

A

hyper

45
Q

What are the Tx of DMTII?

A
  • Caloric restriction and weight reduction
  • insulin secretagogues: sulfonylurea drugs and incretin analog of GLP-1 (exenatide); injection needed
  • slow absorption of Carbs: alpha-glucosidase inhibitors and amylin analogs
  • insulin sensitizers: biguanide drugs: upregulate insulin receptors on target tissues
46
Q

Describe glucagon

A

single straight-chain polypeptide with 29 a.a.
Member of a family of peptide that includes GI hormones secretin and GIP
Synthesized as preproglucagon
Stored in dense granules until alpha cells are stimulated

47
Q

What is the major stimulatory factor of glucagon secretion? What else also stimulates glucagon secretion?

A 
Decrease in blood glucose concentration 
Increase in a.a. (arginine and alanine) 
Fasting
CCK
B-adrenergic agonists
ACh
48
Q

What inhibits the synthesis and secretion of glucagon?

A

Insulin

Somatostatin
Increase in F.A. and ketoacid concentration

49
Q

What is the process of release of glucagon from alpha-cells?

A 
Mitochondria increases the amount of ATP 
Inhibits K-ATPase pump
Membrane depolarizes
Na channels open
VDCC channels open allowing Ca influx
Granules released
50
Q

Where are the major actions of glucagon?

A

in the liver

51
Q

What are the actions of glucagon in the liver?

A

Increase glucogenolysis and inhibits glycogen formation

Increase gluconeogenesis by decreasing production of F2,6-BP via cAMP/PKA pathway

52
Q

What is the effect of glucagon on blood levels?

A

increased glucose, FA, and ketoacid levels

Glucagon increases lipolysis and inhibits FA synthesis - shunts substrates towards gluconeogenesis

FA->ketoacids

53
Q

In insulin resistance, the ability of insulin to suppress _____ in adipose tissue and ______ secretion by alpha cells in the islet results in ___________ gluconeogenesis

A

lipolysis
glucagon
increase

54
Q

What are the incretin hormones?

A

intestine derived hormones
GLP-1, GIP
Short T1/2
Secreted in response to GI glucose and fat

55
Q

What do incretin hormones do?

A

stimulate insulin secretion (glucose dependent)
inhibit glucagon secretion
slow gastric emptying

56
Q

What transporter does the liver use?

A

GLUT 2

Endocrine - MSI Spring (15 decks)

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