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Endocrine > biochem of glucose + insulin > Flashcards

biochem of glucose + insulin Flashcards

1
Q

what type of hormone is insulin?

A

-peptide hormone

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2
Q

what level is fasting blood sugar in a diabetic?

A

> 7mM

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3
Q

what level is fasting blood sugar in a healthy patient?

A

4-6mM

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4
Q

what level is fasting blood sugar in a prediabetic?

A

6-7mM

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5
Q

what level is fasting blood sugar in hypoglycaemia?

A

<4mM

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6
Q

what do beta cells in the pancreatic islet secrete?

A

insulin

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7
Q

what do alpha cells in the pancreatic islet secrete?

A

glucagon

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8
Q

what do delta cells in the pancreatic islet secrete?

A

somatostatin

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9
Q

what do PP cells in the pancreatic islet secrete?

A

pancreatic polypeptide

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10
Q

how is insulin secreted into plasma from the pancreatic islet?

A
  • preproinsulin is synthesised in rough endoplasmic reticulum of pancreatic beta cells
  • preproinsulin is cleaved to form insulin
  • connecting C peptide is also cleaved
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10
Q

how is insulin secreted into plasma from the pancreatic islet?

A
  • preproinsulin is synthesised in rough endoplasmic reticulum of pancreatic beta cells
  • preproinsulin is cleaved to form insulin
  • connecting C peptide is also cleaved
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11
Q

why would C peptide be measured?

A

-to see how much insulin body has actually produced as when insulin is injected C peptide is not produced

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12
Q

what is insulin lispro?

A

short acting insuli

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13
Q

what advantage does short acting insulin give?

A

it reduces chances of hypoglycaemia

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14
Q

when is short acting insulin normally administered?

A

within 15 minutes of beginning of meal

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15
Q

what is short acting insulin usually given with for type 1 diabetes?

A

-must be used with longer acting insulin for type 1 diabetes unless used for continuous infusion

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16
Q

whats an example of long acting insulin?

A

insulin glargine

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17
Q

when is long acting insulin usually administered?

A

-as a single dose at bedtime

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18
Q

what does the primary structure of pro insulin contain?

A
  • A chain
  • B chain
  • C peptide
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19
Q

what do the A chain and B chain of the primary structure of pro insulin contain and why?

A

-disulphide bridges between cystene residues which help provide the tertiary structure of the 3D structure

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20
Q

what allows C peptide to be cleaved in proinsulin?

A

Ca+ dependant endopeptidases (PC2 and PC3)

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21
Q

how does glucose enter beta cells for glycolysis?

A
  • through GLUT2 glucose transporter by diffusion (as glucose rises in blood a concentration gradient will be created and glucose will enter beta cells)
  • glucose is then phosphorylated into glucokinase and glycolysis can occur to produce ATP
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22
Q

how is insulin secreted from beta cells?

A
  • glycolysis causes generation of ATP
  • generation of ATP closes ATP sensitive potassium channel
  • this depolarises beta cell membrane
  • depolarisation of beta cell membrane allows voltage gated calcium channels to open
  • influx in Ca2+ allows the insulin secretory granules to fuse with the cell membrane and release insulin into plasma
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23
Q

what is the role of glucokinase?

A

it is responsible for turning glucose into glucose-6-phosphate

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24
Q

what occurs to glucose phosphorylation as glucose levels change from 4.5mmol/l to 5.5mmol/l?

A

a massive change in glucose phosphorylation (so a massive increase in glucokinase)

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25
Q

what molecule would dictate the level of glucose that would be present in the plasma: hexokinase or glucokinase?

A

glucokinase- as it’s Km for glucose lies in the physiological range of concentrations

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26
Q

what is Vmax?

A

-maximal rate of reaction at unlimited substrate concentration

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27
Q

what is Km?

A

50% of Vmax

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28
Q

what does increase in ATP in beta cell do to ATP potasium channel?

A

it inhibits it

29
Q

what does inhibition of ATP potassium channel in beta cells lead to?

A

-depolarisation of membrane

30
Q

what does depolarisation of beta cell membrane lead to?

A

opens the voltage-gated calcium channel causing an influx of calcium

31
Q

what does an increase in internal Ca2+ in the beta cell lead to?

A

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

32
Q

what glucose level is insulin produced at?

A

above 5mM

33
Q

how many times is insulin usually secreted in healthy individuals?

A

-its biphasic (in two phases)

34
Q

what is the first phase for insulin secretion for?

A
  • this is when glucose is initially decreased in blood

- it is a sharp peak of insulin secretion which helps prevent rapid hypoglycaemia

35
Q

how is the second phase of insulin secretion different to the 1st?

A

-the 2nd phase is more tuned to the insulin requirement related to glucose intake (amount and duration) and tends to be lower and longer

36
Q

what is the first pool of insulin granules called?

A

RRP- readily releasable pool

37
Q

what % of insulin granules are in the readily releasable pool?

A

5%

38
Q

how are the insulin from the second pool of granules released?

A

the second pool must undergo mobilisation

39
Q

which pool of insulin granules does the first phase tend to use?

A

the RRP ( readily releasable pool)

40
Q

what causes type 1 diabetes?

A

-an autoimmune destruction of the pancreatic beta cells

41
Q

how does type 2 diabetes present to begin with compared to later on?

A

to begin with= usually presents with hyperinsulinemia as beta cells try to compensate for the hyperglycaemia caused by insulin resistance

later= often presents with decline in beta cell function, presumably due to prolonged over stimulation following years of hyperglycaemia

42
Q

how is gestational diabetes treated?

A
  • lifestyle advice

- sometimes metformin to improve insulin sensitivity

43
Q

True or False

The diagnostic criteria for gestational diabetes is lower than other forms of diabetes?

A

True

44
Q

what is MODY (maturity onset diabetes of young)?

A

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

45
Q

what is neonatal diabetes?

A

-a rare form of monogenic diabetes much of which is caused by mutations in the glucose sensing machanism (eg in ATP sensitive K channel)

46
Q

what does the ATP sensitive K channel made up of?

A

consists of two proteins with 4 subunits:

  • an inward rectifier subunit (Kir) (has 4 subunits)
  • a sulphonylurea receptor (SUR) (has 4 subunits)
47
Q

what is the pore inward rectifier subunit (Kir) called?

A

Kir6

48
Q

what is the regulatory subunit of the sulphonylurae receptor called?

A

SUR1

49
Q

what does a mutation in Kir6.2 cause?

A

-neonatal diabetes

50
Q

what does the sulphonylurea class of drugs do to KATP?

A

directly inhibit KATP

51
Q

what are examples of sulphonylurea class drugs?

A
  • tolbutamide

- glibenclamide

52
Q

what affect does diazoxide have on KATP?

A

dizoxide stimulates KATP with inhibits insulin secretion

53
Q

why is there higher blood glucose in MODY ?

A
  • the glucokinase activity is impaired
  • glucose threshold required to secrete insulin is increased meaning more glucose is needed before some insulin can be produces
54
Q

what mutation is usually in MODY?

A

mutation in HNF transcription factor 1 and 3

55
Q

what is leprechaunism/ Donohue syndrome?

A
  • rare autosomal recessive genetic trait

- mutation in the gene for insulin receptor causing severe insulin resistance

56
Q

how may leprechaunism present?

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

these are all due to defects in insulin binding or insulin receptor signalling

57
Q

what is Robson Mendenhall syndrome?

A
  • rare autosomal recessive genetic trait

- causes severe insulin resistance, hyperglycaemia and compensatory hyperinsulinemia

58
Q

how does Robson Mendenhall syndrome tend to present?

A
  • ancanthosis nigricans (hyperpigmentation)
  • have severe insulin resistence, hyperglycaemia and compensatory hyperinsulinemia
  • fasting hypoglycaemia (due to hyperinsuliaemie)
  • prone to diabetic ketoacidosis
59
Q

what is one of the most damaging complications of severe insulin resistence?

A

Diabetic ketoacidosis

60
Q

what are the symptoms of diabetic ketoacidosis?

A
  • vomiting
  • dehydration
  • increased heart rate
  • distinctive smell on breath (acetone smell)
61
Q

where are the ketone bodies derived from?

A

-formed in liver mitochondria

derived from acetyl-CoA which is from beta oxidation of fats

62
Q

how do ketone bodies leave the liver?

A

they diffuse into blood stream and to peripheral tissues

63
Q

what are ketone bodies important molecules for?

A
  • ketone bodies are important molecules of energy for heart muscle and renal cortex
  • they are converted back to acetyl-CoA which enters the TCA cycle
64
Q

what is insulins role in lypolysis?

A

insulin normally inhibits lipolysis (breakdown of fat) reducing risk of ketone body overload

65
Q

is diabetic ketoacidosis more common in type 1 or type 2 diabetes?

A

type 1!!!!

66
Q

why is diabetic ketoacidosis more common in type 1 diabetes?

A

as in type 1 diabetes the patient may forget to take their insulin supplementation and hyperglycaemia continues where as in type 2 diabetes there is still some inhibition of lypolysis byt can occur as insulin resistence and deficiency increases alongside increase in glucagon

67
Q

what stimulates the secretion of somatostatin from delta cells?

A

-Growth hormone

68
Q

what is the role of somatostatin?

A

-regulates secretion of insulin, glucagon nad growth hormone

69
Q

what is the role of pancreatic polypeptide?

A

-regulates pancreatic endocrine and exocrine functions

Endocrine (53 decks)

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