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GINME > Week 4: Endocrine pancreas > Flashcards

Week 4: Endocrine pancreas Flashcards

1
Q

Exocrine pancreatic cells

A

Acinar cells (digestive enzymes)

Duct cells (HCO3-)

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2
Q

Endocrine pancreatic cells

A

Islets of langerhans

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3
Q

Identify structures and functions

A
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4
Q

Identify histology of islets of Langerhans histology cartoon

A
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5
Q

Insulin function

A

tells cells to take up glucose (such as skeletal muscle through GLUT 4)

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6
Q

Insulin counter hormone

A

Glucagon

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7
Q

Insulin secreted by

A

β cells of the pancreas

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8
Q

What is the normal fasting range of glucose?

A

70-110 mg/dL

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9
Q

What secretes somatostatin?

A

D cells of the pancreas

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10
Q

What secretes glucagon?

A

α-cells of the pancreas

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11
Q

Explain what is happening here

A
  • fasting level of glucose goes up after a meal to around 130 or 140 mg/dL and it slowly declines back to basal levels due to glucose going into cells where it is utilized or stored.
  • Insulin is secreted by β cells of the pancreas in response to the rise in glucose levels in the blood after a meal
  • Insulin never drops to 0 it always is there even in the fasting state
  • Glucagon is high during the fasting state and it spikes but then goes way down to basal levels after a meal
  • After fasting for a while glucagon levels will rise to fed state levels
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12
Q

Insulin and glucose are?

A

counter-hormones secreted by the pancreas

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13
Q

What happens when blood glucose level is high to the pancreatic hormones

A
  • after a meal the β cells of the pancreas respond to high glucose levels and secrete insulin
  • α- cells respond to the high glucose levels and stop secreting glucagon
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14
Q

what is in the center of the islet of langerhans?

A

β-cells

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15
Q

Describe the blood supply of the islet of Langerhans

A

there is a central artery so the β-cells respond first because they are in the center of the islet

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16
Q

How is pancreatic secretion regulated

A
  • paracrine regulation
  • Insulin inhibits secretion of glucagon from the α cells
  • This all has to do with the architecture of the islet of Langerhans
  • So the β cells actually control insulin and glucagon levels
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17
Q

Describe what happens in the fasting state

A

low blood glucose slows insulin secretion which stops inhibiting glucagon so the α cells can start secreting glucagon again

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18
Q

Catabolic state hormone

A

Glucagon

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19
Q

Anabolic state hormone

A

Insulin

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20
Q

Identify the mechanism of insulin synthesis

A
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21
Q

Describe the synthesis of insulin

A
  • mRNA from Preproinsulin gene
  • Synthesis of preproinsulin (excision of the signal peptide and a disulfide bond is formed)
  • Transport of proinsulin to the Golgi where it is cleaved into insulin and is packaged into vesicles
  • Mature insulin is ready for signaling in storage vesicles
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22
Q

Describe the molecular structure of insulin

A
  • 2 disulfide bonds
  • cleavage of the proform of proinsulin (2 endoproteases) releases the mature insulin which is the A chain and the B chain which is held together by a disulfide bond
  • The disulfide-linked A and B chain is the mature form of insulin
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23
Q

How do β cells sense glucose?

A
  • in the β cell, GLUT 2 glucose transporter facing the blood
  • Glucose enters
  • oxidized through glycolysis, TCA cycle and electron transport
  • Creating a high ATP>/>ADP ratio
  • ATP dependent K+ channel (normally allows the passage of K+ outside the cell) When ATP binds to the channel, it is inhibited from transporting so a + charge builds in the β cell
  • There is a voltage-gated Ca2+ channel which responds to the difference in charge and lets Ca2+ into the cell
  • The Ca2+ activates transport of insulin storage vesicles to the membrane to let insulin into the blood
24
Q

What are Sulfonylurea drugs?

A

They target β cells ATP dependent K+ channels and act like ATP

It mimics the glucose-sensing system of the β cells to get insulin into the circulation

25
Q

What is the primary organ responsible for reducing plasma glucose levels

A

Skeletal muscle

26
Q

Describe insulin action on skeletal muscle

A
  • insulin binds to Tyrosine kinase receptor on skeletal muscle membranes and activates it, the tyrosine kinase portion autophosphorylates the Tyrosine kinase receptor cytoplasmic portion of the dimer which phosphorylates the other side
  • The Activated insulin receptor phosphorylates and activates IRS-1 which activates the AKT pathway
  • AKT pathway translocates the cytoplasmic GLUT 4 vesicles to the membrane to allow glucose into the skeletal muscle cells
  • Plasma Glucose can now enter through GLUT 4
27
Q

What is the main defect in insulin resistance?

A

Insulin receptor can be activated but the activation of IRS-1 is broken

28
Q

How do skeletal muscles respond to the fasting state

A

the ligan insulin is no longer present so the tyrosine kinase insulin receptor is no longer activated which no longer activated IRS-1 which no longer activates the AKT pathway and so skeletal muscle endocytoses the GLUT 4 transportes back into cytoplasmic receptors

If this did not happen blood glucose levels would continue to drop and could cause death

29
Q

GLUT 4 affinity

A

High affinity

30
Q

Describe GLUT 2 vs GLUT 4 kinetics

A

The differing affinity and transport activity of the various GLUT transporters allow for targeted transport of glucose

GLUT 1, GLUT 3, and GLUT 4 are high-affinity glucose transporters

GLUT 2 will only work when there are high levels of glucose because of its low affinity

31
Q

1/2 Vmax =

32
Q

GLUT 1 expression and function

33
Q

GLUT 2 expression and function

34
Q

GLUT 3 expression and function

35
Q

GLUT 4 expression and function

36
Q

GLUT 5 expression and function

37
Q

Glucagon molecular structure

38
Q

What is the fructose transporter

39
Q

What are the insulin-responsive glucose transporters

A

GLUT 4 is the only insulin-responsive glucose transporter

40
Q

Describe the glucagon signaling pathway

A

Glucagon binds to its receptor which is a heterotrimeric gαs protein receptor

activates adenylate cyclase and increases cAMP and activates PKA which phosphorylates a bunch of regulators and effectors (lots of enzymes) an enormous shift in metabolic pathways

41
Q

What kind of hormone is insulin?

A

peptide hormone

42
Q

What kind of hormone is glucagon?

A

Peptide hormone

43
Q

Insulin effects on Fatty acid uptake and release in adipose

A

Stimulates the synthesis of triglycerides (TG) from free fatty acids (FFA)

Inhibits the release of FFA from TG

44
Q

Glucagon effects on Fatty acid uptake and release in adipose

A

stimulates release of FFA from TG

45
Q

Insulin effects on the liver

A

increases glucose uptake and synthesis of glycogen

46
Q

Glucagon effects on the liver glycogen

A

stimulates glycogenolysis and glucose release

47
Q

Insulin effects on gluconeogenesis in the liver

A

inhibits and saves amino acids

48
Q

Glucagon effects on gluconeogenesis in the liver

A
  • Stimulates gluconeogenesis
  • glucose is synthesized and release
49
Q

Insulin effects on glucose uptake in skeletal muscle

A

stimulates glucose uptake by locating GLUT 4 to the membrane

50
Q

Glucagon effects on glucose uptake in skeletal muscle

A

no receptors so there is no effect

51
Q

Insulin effects on skeletal muscle glycogen

A

stimulates glycogenesis

52
Q

Glucagon effects on skeletal muscle glycogen

A

no receptor so no effects

53
Q

Insulin effects on amino acid uptake

A

stimulates uptake to increase protein synthesis

54
Q

Glucagon effects on amino acid uptake

A

no receptor so no effect

55
Q

Insulin effects on the brain

A

reduces hunger

56
Q

Glucagon effects on the brain

GINME (63 decks)

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