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Flashcards in Biochemistry of Insulin Deck (43):
1

Which cells secrete insulin?

b-cells

2

Which cells secrete glucagon?

alpha cells

3

Which cells secrete somatostatin?

d cells

4

Which cells secrete pancreatic polypeptide?

PP cells

5

Where is insulin made?

RER in b cells of pancreas

6

What is insulin synthesized as?

larger single chain preprohormone called preproinsulin

7

What chains does insulin contain?

2 polypeptide chains, linked by disulphide bonds

8

Why is human insulin now used?

to avoid problem of antibody formation

9

What is the glucose sensor which leads to insulin secretion?

Glucokinase

10

How does glucose enter b cells?

through GLUT2 glucose transporter

11

What phosphorylyses glucose?

glucokinase

12

What does a change in glucose concentration lead to?

dramatic change in glucokinase activity

13

Increased metabolism of glucose leads to what happening to intracellular ATP?

increases

14

What does ATP do to the KATP channel?

inhibits this

15

What does inhibition of KATP lead to?

depolarisation of cell membrane

16

What does depolarisation of cell membrane result in opening of?

calcium channels

17

How does an increases in calcium concentration in the cells cause insulin release?

leads to fusion of secretory vesicles

18

What is release of insulin in terms of phases?

biphasic

19

Why are there two phases of insulin?

5% of insulin granules immediately ready for release
Reserve pool must undergo preparatory reactions to become mobilised and available for release

20

Which proteins do KATP channels consist of?

KIR6.1 (inward rectifier subunit, pore)
SUR1 (sulphonylurea receptor, regulatory)

21

What type of structure is the KATP channel

octomeric

22

Are both proteins (KIR6.1 and SUR1) required for a functional channel to form?

YES BOTH

23

Which class of drugs directly inhibits KATP?

sulphonylureas eg glibenclamide, tolbutamide

24

What is KATP stimulated by?

diazoxide

25

What does diazoxide do to insulin secretion?

inhibits

26

What causes MODY?

mutations - genetic defect in b cell function

27

What type of diabetes is MODY?

familial version of Type II

28

What do HNF transcription factors and MODY play a key role in?

pancreas foetal development and neogenesis
regulate beta cell differentiation and function

29

What allows for differentiation between type 1 diabetes and MODY?

robust genetic screening - means MODY can be treated with sulphonylurea rather than insulin

30

loss of insulin secreting beta cells?

type 1 diabetes

31

defective glucose sensing in the pancreas and/or loss of insulin secretion?

MODY

32

Initially hyperglycaemia, with hyperinsulinaemia, so primary problem is reduced sensitivity in tissues?

Type 2 diabetes

33

What type of receptor are insulin receptrs?

receptor kinases

34

What provides for a reversible method for altering protein function?

protein phosphorylation

35

What can proteins get phosphorylated onto?

any hydroxyl group, introduces large negative charge into protein structure

36

What is the insulin receptor?

a dimeric tyrosine kinase

37

Name a rare autosomal recessive genetic trait with mutations in the gene for insulin receptor causing growth retardation, decreased muscle mat, no subcutaneous fat and elfin facial appearance?

leprechaunism/Donohue syndrome

38

Which autosoma recessive trait causes severe insulin resistance, hyper glycaemia, developmental abnormalities and acanthosis nicrigans?

rabson mendenhall syndrome

39

Where are ketone bodies formed?

liver mitochondria

40

What organs are ketone bodies important molecules of energy for?

heart muscle
renal cortex

41

What does fatty acid oxidation yield?

acetyl CoA

42

What can accumulation of ketone bodies lead to?

acidosis

43

What type of diabetes is ketoacidosis associated with?

type 1