Insulin, Glucagon and Somatostatin Flashcards Preview

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

Flashcards in Insulin, Glucagon and Somatostatin Deck (83):
1

What are the three cells found in the pancreas?

Alpha cells
Beta cells
Delta cells

2

What do alpha cells secrete?

Glucagon

3

What do beta cells secrete?

Insulin

4

What do delta cells secrete?

Somatostatin

5

What is insulin produced as?

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

6

What mineral is required for insulin formation?

Zinc (Zn2+)

7

What two things are released with insulin?

Zinc
C-peptide

8

What is C-peptide?

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

9

What is C-peptide used for?

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

10

What two things can C-peptide levels help with?

Newly diagnosed type I diabetic
Type II diabetic whose insulin production is being boosted by drugs

11

Half-life of C-peptide compared to insulin?

Much longer

12

What glucose transporter is most abundant in beta cells?

GLUT-2

13

Where is GLUT-1 found?

On all cells

14

What is the importance of GLUT-1?

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

15

Where is GLUT-2 found?

Liver
Pancreas
Intestines

16

What is the importance of GLUT-2?

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

17

Where is GLUT-4 found?

Muscle
Fat
Heart

18

What is the importance of GLUT-4?

After a meal when insulin is released

19

What two enzymes phosphorylate glucose and where are they found?

Hexokinase: extrahepatic cells
Glucokinase: liver only

20

Glucokinase has a higher Km, what does this mean?

It needs more glucose levels in order to work

21

Glucokinase higher Km importance?

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

22

What controls the secretion of insulin?

The amount of glucose coming in and being converted to ATP

23

What is the mechanism for insulin release?

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

24

Where are sulfonylurea receptors found?

Surrounding the ATP sensitive K channel on beta cells

25

What does sulfonylurea receptor stimulate?

Secretion of insulin by closing the ATP sensitive K channel

26

What do you use sulfonylurea drugs for?

Type II diabetes only

27

What are two sulfonylureas?

Glyburide (drug of choice)
Tolbutamide

28

Two SUR receptors and where they're found:

SUR1: Beta cells
SUR2: all type of muscle cells

29

What drug inhibits secretion of insulin in cases of hypoglycemia?

Diazoxide

30

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

Oral glucose

31

Why does oral glucose cause a larger increase in insulin?

GI hormone release GLP-1 and GIP

32

What are incretins?

GLP-1
GIP

33

What secretes GLP-1?

L cells in small intestine

34

What does GLP-1 cause?

An increase in insulin secretion

35

What is the primary stimulus for GLP-1 release?

Free fatty acids and glucose

36

What can GLP-1 be used to treat?

Diabetes Type II

37

What is the primary stimulus for GIP release?

Free fatty acids
TAGs
Glucose
AA

38

What cells release GIP?

K cells in the small intestine

39

What does GIP cause?

Insulin secretion

40

What receptor do GIP and GLP-1 work on?

GPCR-> adenylate cyclase pathway

41

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

Beta-2: augments
Alpha-2: inhibits

42

What do free fatty acids in the blood cause?

Stimulate insulin release

43

What receptor do FFA bind to in beta cells?

GRPAD/FFA1/GPR40
all three the same

44

What does GRPAD being bound cause intracellularly?

Gq receptor so PLC-> IP3-> Calcium intracellularly

45

What do the alpha and beta subunits of insulin have?

Disulfide bonds

46

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

Tyrosine kinase receptors

47

What three things can the IRS tyrosine kinase receptors phosphorylate?

SHC
SH2

48

The SH2 domain on what two molecules gets phosphorylated?

GRB2
PI3K

49

What is the sequence of events once GRB2 is phosphorylated?

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

50

What occurs when SHC is phosphorylated?

It activates SOS

51

What occurs when PI3K is phosphorylated?

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

52

What are the overall affects of GRB2 and PI3K?

GRB2: transcription of genes
PI3K: activity of enzymes

53

What does PDK also activate?

mTOR

54

What does mTOR do?

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

55

What does PKB do?

Recruits GLUT-4
Activates glycogen synthase kinase

56

What is a peptide released with insulin?

Amylin

57

What does amylin do?

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

58

What affect does amylin have on the stomach?

It slows gastric emptying and promotes satiety

59

What is the overall affect of amylin?

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

60

What can occur with proamylin?

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

61

What would proamylin become too concentrated in vesicles?

In times of high demands

62

What GLUT is on alpha cells?

GLUT-1 not GLUT-2

63

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

It transports glucose when it is at all concentrations

64

What is the mechanism of glucagon release from alpha cells?

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

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

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

66

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

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

67

What are three things that inhibit glucagon secretion?

Insulin
Zinc 2+
Somatostatin

68

What type of receptor does glucagon bind to?

GPCR-> AC-> cAMP

69

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

SS-14
SS-28

70

What SS does the stomach and intestinal tract secrete?

SS-28

71

What SS does the nervous system secrete?

SS-14

72

Sole form of SS secreted from pancreas?

SS-14

73

Which SS inhibits growth hormone?

SS-28

74

Which SS inhibits glucagon release?

SS-14

75

What cells in the stomach release SS?

D cells

76

What cells in the pancreas release SS?

Delta cells

77

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

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

78

Actions of SS on the anterior pituitary?

Inhibit release of:
GH
TSH
PRL

79

Action of SS on pancreas?

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

80

Affect of SS on the stomach?

Decrease rate of gastric emptying, motility, blood flow

81

What is a somatostatinoma?

Tumor that produces somatostatin

82

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

Pancreas: decreased insulin so diabetes
GI tract: CCK suppression and decreased GB contraction so gallstones

83

What would a SS deficiency cause?

Excess GH secretion