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endocrine > biochemistry > Flashcards

biochemistry Flashcards

1
Q

what glucose level is hypoglycemia

A

<4mM

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2
Q

what blood sugar level is considered high (risk of diabetes)

A

6-7mM

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3
Q

what blood sugar is considered very high (diabetes)

A

> 7mM

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4
Q

what do beta cells secrete

A

insulin

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5
Q

what do alpha cells secrete

A

glucagon

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6
Q

what do gamma cells secrete

A

somatostatin

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7
Q

what do PP cells secrete

A

pancreatic polypeptide

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8
Q

where is preporoinsulin synthesised

A

in the RER of pancreatic beta bells

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9
Q

what happens after preproinsulin

A

cleaved to form proinsulin and a signal peptide which is then cleaved to form C peptide and insulin

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10
Q

three chains of proinsulin

A

C peptide
A chain
B chain

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11
Q

what is pure insulin then made up of

A

A chain and B chain

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12
Q

5 types of synthetic insulin preparations

A
  • ultra fast/ultra short acting
  • short acting
  • intermediate acting
  • long acting
  • ultra long acting
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13
Q

what is the name of the ultra fast insulin

A

lispro

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14
Q

when is lispro used

A

15 minutes of beginning a meal

-must be used in combination with long acting ones

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15
Q

what is the most commonly used long-acting insulin

A

glargine

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16
Q

when is glargine used

A

single bedtime dose

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17
Q

what does glucose enter the beta cells through

A

the GLUT2 glucose transporter

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18
Q

what is glucose phosphorylated by

A

glucokinase

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19
Q

at what mmol/L of glucose does glucokinase start being more active

A

7

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20
Q

what does an increased metabolism of glucose lead to in terms of ATP

A

leads to an increase in intracellular ATP concentration

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21
Q

how many ATP is produced per glucose

A

36

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22
Q

what does ATP then inhibit (in the secretion of insulin)

A

the ATP-sensitive K+ channel Katp

23
Q

what does inhibition of Katp lead to

A

depolarisation of the cell membrane

24
Q

what does depolarisation fo the cell membrane lead to in insulin secretion

A

opening of voltage-gated Ca2+ channels

25
Q

what does an increase in calcium concentration lead to

A

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

26
Q

what happens in T1DM to the beta cells

A

they are mostly lost

27
Q

what does the first phase of insulin secretion prevent

A

a sharp increase in blood glucose

28
Q

what does the second phase of insulin secretion look like

A

broader and shorter

29
Q

why are there two phases

A
  • 5% are immediately ready for release (RRP)

- reserve pool must undergo preparatory reactions to be ready to be released

30
Q

why in poorly controlled T2DM does insulin secretion weaken and flatten

A
  • downregulation of the sensing process
  • limited glucokinase activity
  • mitochondrial exhaustion
  • reduced ATP production
31
Q

what is wrong in type 1 diabetes

A

destruction of pancreatic beta cells

32
Q

what is wrong in type 2 diabetes

A

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

33
Q

later stages of type 2 diabetes, what can go wrong?

A

-decline in beta cell function

34
Q

what is associated with gestational diabetes

A

women with declining beta cell formation and high risk of future T2DM
develops during pregnancy

35
Q

what is maturity onset diabetes of the young (MODY)?

A

monogenic disease with common clinical features to both type 1 and 2
-beta cell dysfunction but not autoimmune destruction

36
Q

what is neonatal diabetes

A

rare form of monogenic diabetes which is mainly caused by mutations in the glucose sensing mechanism

37
Q

what are the two proteins in the Katp channel

A

Kir6

SUR1

38
Q

what can mutations in Kir6.2 lead to

A

neonatal diabetes

-as unable to secrete insulin

39
Q

what mutations can cause congenital hyperinsulinism

A

Kir6.2 and SUR1

40
Q

where do the mutations in MODY mostly happen

A

in glucokinase

-also several transcription factors (5)

41
Q

in which transcription factors are most of the MODY mutations

A

HNF 1 and 3

42
Q

what defines type 1 diabetes

A

loss of insulin secreting beta cells

43
Q

what defines MODY

A

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

44
Q

what defines type 2 diabetes

A

initially hyperglycemia with hyperinsulinemia so primary problem is reduced insulin sensitivity in tissues

45
Q

what does insulin regulate

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
  • glycogen synthesis in liver and muscle
  • gene expression
  • turns off lipolysis and gluconeogenesis in liver
46
Q

how can obesity cause insulin resistance

A

due to excess fat deposition in liver, muscle and pancreas, reducing insulin signalling in those tissues, combined with a deficit in adipose functionality

47
Q

symptoms of diabetic ketoacidosis

A
  • vomiting
  • dehydration
  • increased heart rate
  • distinctive smell on breath
48
Q

where are ketone bodies formed

A

liver mitochondria

49
Q

how does insulin usually reduce the risk of ketone body overload

A

by inhibiting lipolysis

50
Q

when is DKA a risk in T1DM

A

if insulin supplementation is missed and hyerglycemia ensues

51
Q

what results in fatty acid oxidation in relation to insulin

A

having no insulin reduces the amount of glucose being taken up by tissues from blood and reduces glycolysis making the body switch to fatty acid oxidation

52
Q

what causes ketones to be produced as a result of fat utilisation

A
  • fat utilisation outstrips glucose utilisation
  • no glycolysis
  • pyruvate/oxaloacetate is limited
  • acetly CoA is diverted to ketones
53
Q

what can cause ketosis

A
  • starvation

- diabetes

endocrine (40 decks)

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