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Endocrine > Biochemistry > Flashcards

Biochemistry Flashcards

1
Q

What cells release glucagon?

A

alpha cells

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2
Q

What are the 4 types of endocrine cell in the pancreas?

A

beta cells; alpha cells; PP cells; delta cells

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3
Q

What do the delta cells release?

A

somatostatin

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4
Q

What do the PP cells release?

A

pancreatic polypeptide

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5
Q

What is synthesised at the RER in beta cells?

A

preproinsulin

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6
Q

What are the 3 parts of the preproinsulin?

A

two polypeptide chains and a connecting peptide

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7
Q

what type of bonds link the two polypeptide chains?

A

disulfide bonds

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8
Q

What is the most rapidly acting insulin?

A

insulin lispro

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9
Q

What insulin is administered as a single bedtime dose?

A

insulin glargine

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10
Q

What is the graph of action for insulin glargine like?

A

a peakless prolonged action

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11
Q

What transporter does glucose enter the beta cells by?

A

GLUT2 transporters

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12
Q

What happens to glucose when it enters the cell?

A

it is phosphorylated by glucokinase and then undergoes oxidative phosphorylation

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13
Q

How many ATP are produced per glucose?

A

36

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14
Q

What is the function of ATP in the beta cell?

A

ATP inhibits the ATP-sensitivie K+ channel Katp

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15
Q

What does inhibition of the Katp channel lead to?

A

depolarisation of the cell membrane

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16
Q

What does depolarisation of the cell membrane result in?

A

opening of the voltage-gated caclium channels

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17
Q

What does the intracellular calcium do?

A

leads to fusion of secretory vesicles with the cell membrane adn release of insulin

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18
Q

Why is the release of insulin biphasic?

A

only 5% of insulin granules are immediately available for release, reserve pool must undergo preparation to become mobilised, if blood sugar is not stabilised by inital release

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19
Q

What are the 2 proteins taht form the Katp channel?

A

the pore subunit- Kir6 and the regulatory subunit-SUR1

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20
Q

Which part of the Katp channel does the ATP bind to?

A

Kir6 part

21
Q

What class of drugs can bind to the SUR1 and inhibit the channel?

A

sulphonylurea

22
Q

What drug stimulates the Katp channel?

A

diazoxide

23
Q

What effect does diazoxide have?

A

inhibits insulin secretion as the membrane is not depolarised by keeping the K inside

24
Q

What would Kir6 mutations that result in activated Katp channels or increase in Katp numbers result in?

A

neonatal diabetes (insulin wouldnt get released as no depolarisation)

25
Q

What is MODY?

A

monogenic diabtes with genetic defect in beta cell function

26
Q

What is the difference between type 1 diabetes and MODY?

A

type 1 is a loss of insulin secreting beta cells and MODY is a defective glucose sensing in the pancreas and/or loss of insulin secretion

27
Q

What is type 2 diabetes?

A

intially hyperglcaemia with hyperinsulinamia then there is reduced insulin sensitivity in tissues

28
Q

What are the biological effects of insulin?

A

amino acid uptake in muscle; DNA synthesis; protein synthesis; growth responses; glucose uptake in muscle and adipose tissue; lipogenesis in adipose tissue and liver. turns off lipolysis and gluconeogenesis

29
Q

Is insulin an anabolic or catabolic hormone?

A

anabolic

30
Q

On what group do proteins get phosphorylated?

A

hydroxyl group

31
Q

What amino acids are able to be phosphorylated?

A

serine; threonine; tyrosine

32
Q

Why does adding phosphate change the structure of the protein?

A

introduces a large negative charge into the protein structure

33
Q

What is the insulin receptor made up of?

A

a dimeric tyrosine kinase- two extracellular alpha subunits with insulin binding domains and two transmembrane beta subunits

34
Q

What bond links the alpha and beta subunits?

A

disulfide bonds

35
Q

What does binding of the insulin to the receptor cause?

A

causes them to phosphorylate themselves (autophosphrylation thus actiavting the catalytic activity of the recetpor

36
Q

What does the phosphorylated receptor then do?

A

phosphorylates the insulin receptor substrates

37
Q

What do the phosphorylated IRS-1 proteins activate?

A

the Ras/MAPK pathway and gene expression; PI3K,PKB and glycogen synthesis

38
Q

What does PKB do?

A

causes the translocation of GLUT4 receptors and glucose to enter the cell

39
Q

What is the key mediator of insulin sensitivity?

A

adipose functionality

40
Q

Wh is it believed that adipose functionality is the key mediatory of insulin sensitivity?

A

because seever insulin resistance occurs with obesity as well as with complete absence of adipose tissue

41
Q

What is leprechaunism-donohue syndrome?

A

a rare autosomal recessive gene in the insulin receptor leads to severe insulin resistance

42
Q

What are the developmental abnormalities associated with leprechaunism-donohue syndrome?

A

elfin facial appearance; growth retardation; absence of subcutaneous fat, decreased muscle mass

43
Q

What is rabson medenhall syndrome?

A

rare autosomal recessive genetic trait that causes severe insulin resistance hyperglycaemia and compensatory hyperinsulinaemia

44
Q

Where are ketone bodies formed?

A

in liver mitochondria

45
Q

What are ketone bodies derived from?

A

from acetyl-CoA from beta oxidation

46
Q

What are ketone bodies used for in the body?

A

important molecules of energy metabolism for heart muscle and renal cortex

47
Q

What causes the acidosis in ketone production?

A

they form acid in the blood and the high glucose excretion causes dehydration which exacerbates acidosis

48
Q

Why don’t you get ketoacidosis in type 2 diabetes?

A

high concentrations of insulin in type 2 diabetes inhibits hormone-sensitive lipase

Endocrine (27 decks)

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