insulin/diabetes Flashcards

1
Q

what is insulin produced by

A

islet of langerhans in pancreas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are islet of Langerhans

A

cluster of endocrine cells scattered throughout the pancreas

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is insulin

A

small protein, peptide hormone, two peptide chains, stored as granules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

structure of insulin

A

2 peptide chains

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what synthesises insulin

A

beta cells as proinsulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

when is insulin released

A

as response to high blood glucose levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

other stimuli of insulin:

A

amino acids, fatty acids, parasympathetic nervous system, peptide hormones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is insulin stored as

A

hexamers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is a hexamer

A

3 dimers associating to form a hexamer stabilised by 2 zinc ions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is a dimer

A

2 insulin molecules bonded by hydrogen bonds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what do hexamers precipitate to form and the effects of it

A

precipitates to form crystals, increases stability and protects against proteases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is the process of insulin release

A

glucose enters beta cells
glucose metabolised
increase ATP/ADP intracellular ratio
K+ channels close
cell membrane depolarisation
voltage dependent Ca2+ channels open
Ca2+ influx
exocytosis of stored insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is type 1 diabetes

A

no release of insulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is type 2 diabetes

A

early stages not enough is produced, later stages no response from cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is insulin inhibited by

A

low blood glucose and somatostatin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is somatostatin

A

peptide hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is somatostatin produced by

A

delta cells, hypothalamus, GIT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

functions of insulin

A

promotes cell proliferation/tissue growth/development, promotes cell uptake of K+ and Ca2+, promotes uptake and storage of glucose/amino acids/fats after meals for fuel conservation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

anabolic action of insulin

A

mainly on liver, muscle and adipocytes via insulin receptors to decrease glucose levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is anabolic action

A

mechanism of bonding smaller units together to make a bigger structure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is an insulin receptor

A

tyrosine kinase receptor, preformed dimer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what are the relay proteins for insulin receptor called

A

IRS, insulin receptor substrate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

how does glucose enter cells

A

transporters

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what are glucose transporters

A

solute linked carriers of membrane transport

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

two types of solute linked carrier/ glucose transporters

A

GLUT transporters (SLC2 family), sodium-glucose linked transporters (SLC5 family)

26
Q

what does uniporter mean

A

transports in one direction

27
Q

where is GLUT-1 and GLUT-3 mainly expressed

A

blood brain barrier

28
Q

where is GLUT-2 expressed

A

gut, liver, kidney, beta cells

29
Q

describe GLUT-2 transporters

A

low affinity, high capacity transporter, transport rate dependent on glucose conc, works in both directions in the liver

30
Q

where are GLUT-4 expressed

A

adipocytes and muscles, intracellular location if low insulin levels, translocate cell membrane under insulin action

31
Q

what are SGLT transporters

A

secondary active symporter transporters, indirectly require ATP, acts in partnership with GLUT-2

32
Q

where are SGLT transporters expressed

A

lumen side of intestinal and renal epithelial cells

33
Q

structure of glucagon

A

single chain peptide hormone

34
Q

where is glucagon synthesised

A

alpha cells and upper GIT

35
Q

what stimulates glucagon to be released

A

low blood glucose/amino acids/para/sympathetic nervous system

36
Q

what inhibits the secretion of glucagon

A

somatostatin, high blood glucose, fatty acids

37
Q

glucagon works via what receptor

A

glucagon receptor

38
Q

name other regulators of blood glucose levels

A

incretins, hormones- adrenaline, growth hormone, glucocorticoids

39
Q

what is incretin secreted by

A

endocrine cells of GIT when digested food reaches duodenum

40
Q

main effect of hormones like adrenaline, growth hormones and glucocorticoids

A

increase blood glucose

41
Q

what stimulates adrenaline, growth hormones and glucocorticoids

A

hypoglycaemia (low blood sugar)

42
Q

what is diabetes mellitus

A

chronic metabolic disorder characterised by high blood glucose concentration (hyperglycaemia)

43
Q

what causes diabetes mellitus

A

insulin deficiency (type 1), impaired insulin secretion and insulin resistance (type 2)

44
Q

what is glycosuria

A

glucose in urine

45
Q

what is diuresis

A

increased urine production

46
Q

symptoms of diabetes melllitus

A

glycosuria (glucose in urine), diuresis (more pee), dehydration, thirst, fatigue, blurred vision, infections

47
Q

effects of diabetes mellitus

A

ketoacidosis (diabetic coma), mainly in type 1 patients, production of ketone decreases pH causing nausea/vomiting/breathlessness/loss of consciousness

48
Q

effects of ketoacidosis

A

production of ketone bodies by liver from fatty acid breakdown decreases pH causing nausea/vomiting/breathlessness/loss of consciousness

49
Q

long term complications of diabetes

A

deterioration of blood vessel and nerves, damaged blood vessels in eyes lead to losing sight, higher risk of heart attack and stroke, nerve damage in lower limbs lead to cramps/numbness/loss of sensation, wounds take longer to heal, tissue dies, amputation

50
Q

difference between the cause of type 1 and 2 diabetes

A

type 1- autoimmune disease
type 2- obesity

51
Q

treatment of type 2 diabetes

A

weight loss, oral drugs, insulin injections

51
Q

auto immunity of type 1 diabetes

A

progressive destruction of beta cells

52
Q

treatment of type 1 diabetes

A

insulin injections, islet transplant

53
Q

what causes type 2 diabetes

A

obesity, elevated fatty acids in plasma cause insulin secretions and down regulation of insulin receptors

54
Q

main side effect of insulin treatments

A

hypoglycaemia

55
Q

what is human insulin made by

A

recombinant DNA technology

56
Q

why different formulations of insulin treatments and name them

A

to achieve different peak of effect and duration of action

soluble insulin- rapid/short effect
insulin suspension- delayed/prolonged effect

57
Q

other (older) drugs for type 2 diabetes

A

biguanides- increases glucose uptake in muscles and reduce glucose production in liver, advantages doesnt cause hypoglycaemia

sulfonylureas

glitazones

a-glucosidase inhibitors

58
Q

name a newer drug for type 2 diabetes

A

sodium glucose co-transporter 2 inhibitors- inhibits SGLT2 in renal proximal tubule, decrease glucose reabsorption, increases urine excretion, high risk of ketoacidosis

gdipeptidylpeptidase-4 inhibitors- inactivate enzyme that degrades GLP1, increase insulin secretion

59
Q

disadvantage of using sodium glucose cotransporter 2 inhibitors

A

high risk of ketoacidosis

60
Q

pharmacological targets for developing drugs

A

glucagon receptor, free fatty acid 1, glycogen synthase kinase 3, transporter proteins, proteases, growth factors etc.