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Endo/Repro Exam 2 > Insulin, Glucagon and Somatostatin > Flashcards

Insulin, Glucagon and Somatostatin Flashcards

1
Q

What are the three cells found in the pancreas?

A

Alpha cells
Beta cells
Delta cells

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2
Q

What do alpha cells secrete?

A

Glucagon

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3
Q

What do beta cells secrete?

A

Insulin

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4
Q

What do delta cells secrete?

A

Somatostatin

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5
Q

What is insulin produced as?

A

Pre-proinsulin -> proinsulin -> Insulin + C-peptide

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6
Q

What mineral is required for insulin formation?

A

Zinc (Zn2+)

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7
Q

What two things are released with insulin?

A

Zinc

C-peptide

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8
Q

What is C-peptide?

A

It is the part of the prohormones of insulin that is cleaved and secreted also

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9
Q

What is C-peptide used for?

A

A marker to help determine how much insulin a diabetic’s pancreas is producing

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10
Q

What two things can C-peptide levels help with?

A

Newly diagnosed type I diabetic

Type II diabetic whose insulin production is being boosted by drugs

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11
Q

Half-life of C-peptide compared to insulin?

A

Much longer

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12
Q

What glucose transporter is most abundant in beta cells?

A

GLUT-2

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13
Q

Where is GLUT-1 found?

A

On all cells

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14
Q

What is the importance of GLUT-1?

A

Fastest transporter/works at lowest concentration of glucose and is important at fasting blood glucose levels

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15
Q

Where is GLUT-2 found?

A

Liver
Pancreas
Intestines

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16
Q

What is the importance of GLUT-2?

A

Immediately after a meal when glucose is increased and during gluconeogenesis when intrahepatic glucose is increased

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17
Q

Where is GLUT-4 found?

A

Muscle
Fat
Heart

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18
Q

What is the importance of GLUT-4?

A

After a meal when insulin is released

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19
Q

What two enzymes phosphorylate glucose and where are they found?

A

Hexokinase: extrahepatic cells
Glucokinase: liver only

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20
Q

Glucokinase has a higher Km, what does this mean?

A

It needs more glucose levels in order to work

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21
Q

Glucokinase higher Km importance?

A

It can only sequester glucose in the liver for glyconeogenesis when glucose is higher in concentration so when it is in low concentration the hexokinase in extrahepatic cells can still take in the glucose without the liver stealing it all

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22
Q

What controls the secretion of insulin?

A

The amount of glucose coming in and being converted to ATP

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23
Q

What is the mechanism for insulin release?

A

Glucose enters via GLUT-2 in beta cells-> glucose converted to ATP-> increased ATP/ADP-> ATP sensitize K channel closes-> cell depolarized-> depolarization of cell causes voltage Ca channel opening-> Ca enters the cell-> Ca triggers vesicular release of insulin

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24
Q

Where are sulfonylurea receptors found?

A

Surrounding the ATP sensitive K channel on beta cells

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25
Q

What does sulfonylurea receptor stimulate?

A

Secretion of insulin by closing the ATP sensitive K channel

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26
Q

What do you use sulfonylurea drugs for?

A

Type II diabetes only

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27
Q

What are two sulfonylureas?

A

Glyburide (drug of choice)

Tolbutamide

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28
Q

Two SUR receptors and where they’re found:

A

SUR1: Beta cells
SUR2: all type of muscle cells

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29
Q

What drug inhibits secretion of insulin in cases of hypoglycemia?

A

Diazoxide

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30
Q

What causes a larger secretion of insulin oral or IV glucose?

A

Oral glucose

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31
Q

Why does oral glucose cause a larger increase in insulin?

A

GI hormone release GLP-1 and GIP

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32
Q

What are incretins?

A

GLP-1

GIP

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33
Q

What secretes GLP-1?

A

L cells in small intestine

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34
Q

What does GLP-1 cause?

A

An increase in insulin secretion

35
Q

What is the primary stimulus for GLP-1 release?

A

Free fatty acids and glucose

36
Q

What can GLP-1 be used to treat?

A

Diabetes Type II

37
Q

What is the primary stimulus for GIP release?

A

Free fatty acids
TAGs
Glucose
AA

38
Q

What cells release GIP?

A

K cells in the small intestine

39
Q

What does GIP cause?

A

Insulin secretion

40
Q

What receptor do GIP and GLP-1 work on?

A

GPCR-> adenylate cyclase pathway

41
Q

What two receptors from SNS have an affect on insulin release and what are the effects?

A

Beta-2: augments

Alpha-2: inhibits

42
Q

What do free fatty acids in the blood cause?

A

Stimulate insulin release

43
Q

What receptor do FFA bind to in beta cells?

A

GRPAD/FFA1/GPR40

all three the same

44
Q

What does GRPAD being bound cause intracellularly?

A

Gq receptor so PLC-> IP3-> Calcium intracellularly

45
Q

What do the alpha and beta subunits of insulin have?

A

Disulfide bonds

46
Q

What type of receptor are the IRS (insulin receptors)?

A

Tyrosine kinase receptors

47
Q

What three things can the IRS tyrosine kinase receptors phosphorylate?

A

SHC

SH2

48
Q

The SH2 domain on what two molecules gets phosphorylated?

A

GRB2

PI3K

49
Q

What is the sequence of events once GRB2 is phosphorylated?

A

GRB2 -> SOS-> Ras-> Raf-1 (kinase)-> phosphorylates MEK (kinase)-> MAPK-> nucleus for transcription

50
Q

What occurs when SHC is phosphorylated?

A

It activates SOS

51
Q

What occurs when PI3K is phosphorylated?

A

Activates PDK-> phosphorylates PKB-> recruits GLUT-4 to the cell membrane

52
Q

What are the overall affects of GRB2 and PI3K?

A

GRB2: transcription of genes
PI3K: activity of enzymes

53
Q

What does PDK also activate?

A

mTOR

54
Q

What does mTOR do?

A

Increases protein synthesis and decreases proteolysis (insulin as a growth factor)

55
Q

What does PKB do?

A

Recruits GLUT-4

Activates glycogen synthase kinase

56
Q

What is a peptide released with insulin?

A

Amylin

57
Q

What does amylin do?

A

Reduces the secretion from all three pancreatic cell types acting as a safety mechanism

58
Q

What affect does amylin have on the stomach?

A

It slows gastric emptying and promotes satiety

59
Q

What is the overall affect of amylin?

A

Slow the appearance of glucose in the blood after eating and therefore reduces food intake

60
Q

What can occur with proamylin?

A

It is concentrated in vesicles so it can lead to apoptosis leading to Type II diabetes

61
Q

What would proamylin become too concentrated in vesicles?

A

In times of high demands

62
Q

What GLUT is on alpha cells?

A

GLUT-1 not GLUT-2

63
Q

What is the importance of GLUT-1 on alpha cells and not GLUT-2?

A

It transports glucose when it is at all concentrations

64
Q

What is the mechanism of glucagon release from alpha cells?

A

Glucose is coming in at all levels-> low amounts of ATP-> slight closing of the ATP sensitive K channel-> slight depolarization-> unique T-type Ca channel open to depolarize membrane just a little-> Na channels respond and depolarize membrane enough to open L/N- Ca channels-> glucagon released

65
Q

What are special channels only found in alpha cells needed from glucagon release?

A

T-type Ca channels
L and N-type Ca channels
Na channels

66
Q

Why don’t alpha cells release glucagon all the time if glucose is always present?

A

Because once beta cells do get stimulated they secrete insulin which inhibits secretion from alpha cells

67
Q

What are three things that inhibit glucagon secretion?

A

Insulin
Zinc 2+
Somatostatin

68
Q

What type of receptor does glucagon bind to?

A

GPCR-> AC-> cAMP

69
Q

What are the two active forms of somatostatin (SS)?

A

SS-14

SS-28

70
Q

What SS does the stomach and intestinal tract secrete?

A

SS-28

71
Q

What SS does the nervous system secrete?

A

SS-14

72
Q

Sole form of SS secreted from pancreas?

A

SS-14

73
Q

Which SS inhibits growth hormone?

A

SS-28

74
Q

Which SS inhibits glucagon release?

A

SS-14

75
Q

What cells in the stomach release SS?

A

D cells

76
Q

What cells in the pancreas release SS?

A

Delta cells

77
Q

Where are each of the 5 SS receptors (SSTR) located?

A 
SSTR1: stomach and jejunum
SSTR2: cerebrum and kidney
SSTR3: brain and pancreatic islet
SSTR4: fetal and adult brain and lung
SSTR5: pancreatic islets
78
Q

Actions of SS on the anterior pituitary?

A

Inhibit release of:
GH
TSH
PRL

79
Q

Action of SS on pancreas?

A

Inhibits release of:
Insulin and glucagon
CCK release
Secretin and HCO3

80
Q

Affect of SS on the stomach?

A

Decrease rate of gastric emptying, motility, blood flow

81
Q

What is a somatostatinoma?

A

Tumor that produces somatostatin

82
Q

What would a somatostatinoma cause from affects on pancreas and GI tract respectively?

A

Pancreas: decreased insulin so diabetes

GI tract: CCK suppression and decreased GB contraction so gallstones

83
Q

What would a SS deficiency cause?

A

Excess GH secretion

Endo/Repro Exam 2 (18 decks)

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