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Endocrine lectures > Biochemistry-insulin production > Flashcards

Biochemistry-insulin production Flashcards

1
Q

what type of hormone is insulin?

A

Peptide Hormone

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2
Q

what does loss of glucose homeostasis lead to?

A

Hyperglycaemia

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3
Q

what is the blood sugar threshold for diabetes

A

> 7mM at fasting level

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4
Q

what is a healthy blood sugar level

A

4-6mM

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5
Q

In the pancreatic islet, what do beta cells secrete?

A

insulin

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6
Q

in the pancreatic islet, what do gamma cells secrete?

A

somatostatin

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7
Q

in the pancreatic islet, what do PP cells secrete?

A

secrete pancreatic polypeptide

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8
Q

what is insulin initially synthesized as?

A

preproinsulin (before being cleaved into insulin)

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9
Q

what do pancreatic alpha cells secrete

A

glucagon

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10
Q

can the brain make its own glucose?

A

No

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11
Q

what are the risks of hypoglycemia?

A

Danger of coma

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12
Q

what is the pre diabetic blood sugar range?

A

6-7mM

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13
Q

does insulin increase or decrease blood sugar levels?

A

decrease

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14
Q

what is the proportion of cells in the pancreatic islet?

A

Alpha: 10-20%
beta: 60-80%
gamma: about 5%
PP cells: <1%

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15
Q

what is the formation of insulin?

A

2 polypeptide chains linked by disulphide bonds

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16
Q

proinsulin is made up of?

A

3 chains (ABC)

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17
Q

which chains does active insulin have?

A

A chain and B chain

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18
Q

which synthetic insulin is ultra short acting?

A

lispro

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19
Q

which synthetic insulin is short acting

A

Regular

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20
Q

which synthetic insulin is intermediate acting?

A

NPH

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21
Q

which synthetic insulin is long acting?

A

ultralente

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22
Q

which synthetic insulin is ultra long acting

A

glargine

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23
Q

lispro features

A

– monomeric
– not antigenic
– the most rapidly acting insulin
– Injected within 15 minutes of beginning a meal
– short duration of action- must be used in
combination with longer-acting preparation for Type
1 diabetes unless used for continuous infusion

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24
Q

glargine features

A

Recombinant insulin analog that precipitates in the neutral environment of
subcutaneous tissue
– Peakless- prolonged action
– Administered as single bedtime dose

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25
Q

is there a suitable synthetic alternative to the beta cell?

A

No

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26
Q

through what receptor does glucose enter beta cells

A

GLUT 2

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27
Q

what phosphorylates glucose?

A

glucokinase

28
Q

what does increased metabolism of glucose lead to?

A

an increase in intracellular ATP conc

29
Q

what is glucokinase

A

the blood glucose sensor

30
Q

how many ATP are produced per glucose?

A

36

31
Q

what does ATP do?

A

inhibits the ATP sensitive K+ channel

32
Q

what does inhibition of KATP lead to?

A

depolarisation of membrane

33
Q

what does depolarisation of the cell membrane lead to?

A

opening of voltage gated Ca2+ channels

34
Q

what does an increase in internal Ca+ conc lead to?

A

fusion of secretory vesicles with the cell membrane and release of insulin

35
Q

how does the secretion of insulin work?

A
  • Beta cell is only cell in body that makes and secretes
    insulin (insulin used as marker of beta cell).
  • It should only do this in response to blood glucose rising
    above 5 mM.
  • In T1DM the beta cells are mostly lost.
  • In other forms of diabetes the beta cells lose the ability to sense changes in glucose
36
Q

why are there 2 phases of insulin release?

A

About 5% of insulin granules are instantly ready of release
Reserve pool must undergo preparatory reactions to become mobilised and available for release
* In poorly controlled T2DM insulin secretion weakens and flattens.

37
Q

how does pharmacological regulation of insulin secretion work?

A

sulphonylurea drugs mimic the action of ATP to depolarise beta cells.
Incretins induce a glucose-dependent insulin release

38
Q

what is Type 1 diabetes caused by?

A

autoimmune destruction of the pancreatic beta cells.

39
Q

a definitive T1 diabetes diagnosis need what?

A

evidence of the presence of specific autoantibodies, combined with declining C-peptide production.

40
Q

how does T2 diabetes usually present?

A

hyperinsulinemia, as the beta cells try to compensate for the hyperglycemia caused by insulin resistance.

41
Q

diagnostic criteria in gestational diabetes?

A

lower than for other forms of diabetes (FBG>5.5) as this comes with significant risk of increased weight of offspring at birth.

42
Q

how is gestational diabetes treated?

A

lifestyle advice and sometimes metformin to improve insulin sensitivity

43
Q

is gestational diabetes associated with a high risk for T2 diabetes?

A

yes

44
Q

what is maturity onset diabetes of the young

A

monogenic disease with common clinical features to both type 1 and type 2 diabetes. Beta cell dysfunction but not autoimmune destruction.

45
Q

which proteins does KATP channel consist of?

A

An inward rectifier subunit (KIR) - pore subunit – Kir6
* A sulphonylurea receptor - regulatory subunit - SUR1

  • Both are required to
    form a functional
    channel
46
Q

what mutation can lead to neonatal diabetes?

A

Kir6.2 mutations
this is due to constitutively activated KATP channels or an increase in KATP numbers
usually responds to SURs

47
Q

what does a Kir6.2 or SUR1 mutations lead to?

A

congenital hyperinsulin

48
Q

when does insulin resistance occur?

A

through reduced insulin sensing and/or signalling.

49
Q

why does insulin resistance happen?

A

most commonly associated with obesity, however near complete absence of adipose also results in insulin resistance. Therefore normal adipose functionality should be considered a key mediator of insulin sensitivity, rather than simply thinking of excess fat as a antagonist of insulin action

50
Q

what is the best way to combat insulin resistance?

A

weight loss

51
Q

Type 2 diabetes is usually monogenic-true or false?

A

false
polygenic

52
Q

why does monogenic severe insulin resistance occur?

A

due to mutation in key signalling pathways

53
Q

What is leprechaunism- Donohue Syndrome?

A

Rare autosomal recessive genetic trait
* Mutations in the gene for the insulin receptor
* Severe insulin resistance
* Developmental abnormalities
– elfin facial appearance
– growth retardation
– absence of subcutaneous fat, decreased muscle mass
* Caused by defects in insulin binding or insulin receptor signalling

54
Q

what is Rabson Mendenhall syndrome?

A

Rare autosomal recessive genetic trait
* Severe insulin resistance, hyperglycemia and
compensatory hyperinsulinemia
* Developmental abnormalities
* Acanthosis nigricans (hyperpigmentation)
* Fasting hypoglycaemia (due to hyperinsulinemia)
* Diabetic ketoacidosis
* Severe cases linked to mutations in the insulin receptor that reduce sensitivity

55
Q

what are the symptoms of diabetic ketoacidosis

A

Vomiting
Dehydration
Increased heart rate
Distinctive smell on breath (acetone smell)

56
Q

where are ketone bodies formed?

A

Formed in liver mitochondria
– derived from acetyl-CoA, which is from b oxidation of fats

57
Q

what are they converted back to in energy metabolism?

A

acetyl-CoA

58
Q

what does low levels of insulin inhibit?

A

inhibit lipolysis and prevent ketone body overload

59
Q

In T1 diabetes, what causes DKA?

A

insulin supplementation is
missed

60
Q

is DKA rarer in T1 or T2?

A

T2

61
Q

how does DKA occur in T2?

A

insulin resistance and deficiency increases, alongside increase in glucagon

62
Q

what does fatty acid oxidation yield?

A

acetyl-CoA which enters the TCA cycle if fat and carbohydrate degradation are balanced

63
Q

what happens if supply of Pyruvate/oxaloacetate is limited?

A

Acetyl CoA is diverted to ketones.

64
Q

what is oxaloacetate consumed for?

A

gluconeogenesis

65
Q

what does high glucose excretion cause?

A

dehydration, exacerbates acidosis
Coma, death

Endocrine lectures (32 decks)

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