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
two types of solute linked carrier/ glucose transporters
GLUT transporters (SLC2 family), sodium-glucose linked transporters (SLC5 family)
26
what does uniporter mean
transports in one direction
27
where is GLUT-1 and GLUT-3 mainly expressed
blood brain barrier
28
where is GLUT-2 expressed
gut, liver, kidney, beta cells
29
describe GLUT-2 transporters
low affinity, high capacity transporter, transport rate dependent on glucose conc, works in both directions in the liver
30
where are GLUT-4 expressed
adipocytes and muscles, intracellular location if low insulin levels, translocate cell membrane under insulin action
31
what are SGLT transporters
secondary active symporter transporters, indirectly require ATP, acts in partnership with GLUT-2
32
where are SGLT transporters expressed
lumen side of intestinal and renal epithelial cells
33
structure of glucagon
single chain peptide hormone
34
where is glucagon synthesised
alpha cells and upper GIT
35
what stimulates glucagon to be released
low blood glucose/amino acids/para/sympathetic nervous system
36
what inhibits the secretion of glucagon
somatostatin, high blood glucose, fatty acids
37
glucagon works via what receptor
glucagon receptor
38
name other regulators of blood glucose levels
incretins, hormones- adrenaline, growth hormone, glucocorticoids
39
what is incretin secreted by
endocrine cells of GIT when digested food reaches duodenum
40
main effect of hormones like adrenaline, growth hormones and glucocorticoids
increase blood glucose
41
what stimulates adrenaline, growth hormones and glucocorticoids
hypoglycaemia (low blood sugar)
42
what is diabetes mellitus
chronic metabolic disorder characterised by high blood glucose concentration (hyperglycaemia)
43
what causes diabetes mellitus
insulin deficiency (type 1), impaired insulin secretion and insulin resistance (type 2)
44
what is glycosuria
glucose in urine
45
what is diuresis
increased urine production
46
symptoms of diabetes melllitus
glycosuria (glucose in urine), diuresis (more pee), dehydration, thirst, fatigue, blurred vision, infections
47
effects of diabetes mellitus
ketoacidosis (diabetic coma), mainly in type 1 patients, production of ketone decreases pH causing nausea/vomiting/breathlessness/loss of consciousness
48
effects of ketoacidosis
production of ketone bodies by liver from fatty acid breakdown decreases pH causing nausea/vomiting/breathlessness/loss of consciousness
49
long term complications of diabetes
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
difference between the cause of type 1 and 2 diabetes
type 1- autoimmune disease type 2- obesity
51
treatment of type 2 diabetes
weight loss, oral drugs, insulin injections
51
auto immunity of type 1 diabetes
progressive destruction of beta cells
52
treatment of type 1 diabetes
insulin injections, islet transplant
53
what causes type 2 diabetes
obesity, elevated fatty acids in plasma cause insulin secretions and down regulation of insulin receptors
54
main side effect of insulin treatments
hypoglycaemia
55
what is human insulin made by
recombinant DNA technology
56
why different formulations of insulin treatments and name them
to achieve different peak of effect and duration of action soluble insulin- rapid/short effect insulin suspension- delayed/prolonged effect
57
other (older) drugs for type 2 diabetes
biguanides- increases glucose uptake in muscles and reduce glucose production in liver, advantages doesnt cause hypoglycaemia sulfonylureas glitazones a-glucosidase inhibitors
58
name a newer drug for type 2 diabetes
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
disadvantage of using sodium glucose cotransporter 2 inhibitors
high risk of ketoacidosis
60
pharmacological targets for developing drugs
glucagon receptor, free fatty acid 1, glycogen synthase kinase 3, transporter proteins, proteases, growth factors etc.