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Endocrine > Biochemistry of Glucose and Insulin > Flashcards

Biochemistry of Glucose and Insulin Flashcards

1
Q

What are the different cell types present in the pancreatic islets?

A

Beta cells = 60-80%, secrete insulin
Alpha cells = 10=20%, secrete glucagon
Delta cells = about 5%, secrete somatostatin
PP cells = <1%, secrete pancreatic polypeptide

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2
Q

What is the prehormone form of insulin?

A

Preproinsulin = cleaved from single large chain to produce insulin

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3
Q

Where is preproinsulin formed?

A

In the RER of pancreatic beta cells

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4
Q

What is the structure of insulin?

A

Two polypeptide chains linked by disulphide bonds

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5
Q

What is connecting (C) protein?

A

Byproduct of cleavage = has no known physiologic function

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6
Q

What are some insulin preparations?

A 
Short acting = regular insulin
Intermediate acting = NPH
Long acting = ultralente
Ultra fast/ultra short acting = lispro
Ultra-long acting = glargine
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7
Q

What are some features of lispro?

A

Lysine (B28) and proline (B29), monomeric, not antigenic, most rapidly acting insulin preparation, injected within 15 mins of beginning a meal

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8
Q

How is lispro used to treat type 1 diabetics?

A

Used in combination with longer acting preparations unless being used for continuous infusion

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9
Q

What is glargine?

A

Recombinant insulin analogue that precipitates in the neural environment of subcutaneous tissue

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10
Q

How is glargine used?

A

Is peakless so has prolonged action

Administered as a single bedtime dose

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11
Q

How does glucose enter beta cells?

A

Through GLUT 2 transporters

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12
Q

What phosphorylates glucose once it is in the cell?

A

Glucokinase

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13
Q

What can a change of glucose concentration do to glucokinase?

A

Causes dramatic change in glucokinase activity

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14
Q

Where does the Km of glucokinase for glucose lie?

A

in the physiological range of concentration

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15
Q

What does the increased metabolism of glucose cause?

A

An increase in intracellular ATP concentration

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16
Q

What does ATP inhibit?

A

The ATP sensitive K+ channel (KATP) = inhibition of KATP leads to depolarisation of the cell membrane

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17
Q

What does the depolarisation of the cell membrane cause?

A

Opening of voltage gated Ca2+ channels = rise in internal Ca2+ concentration causes fusion of secretory vesicles within the cell membrane and release of insulin

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18
Q

Why can insulin be used as a marker for beta cells?

A

Beta cells are the only cells in the body that make and secrete insulin

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19
Q

When should beta cells make and secret insulin?

A

When blood glucose rises above 5mM

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20
Q

What happens to the beta cells of type 1 diabetics?

A

They are mostly lost

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21
Q

Why do beta cells lose the ability to sense changes in glucose in some forms of diabetes?

A

Due to hyperglycaemia taking glucose concentration outwith the Km of glucokinase

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22
Q

What kind of process in insulin release?

A

Biphasic process

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23
Q

What is the readily releasable pool in relation to insulin release?

A

5% of insulin granules are immediately available for release

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24
Q

What must happen to the reserve pool of insulin granules before they can be used?

A

It must undergo reactions to become mobilised and available for release

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25
Q

What happens to insulin secretion in poorly controlled type 2 diabetics?

A

It weakens and flattens = likely due to downregulation of the sensory process

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26
Q

What are the two proteins that make up the KATP channel?

A

Inward rectifier subunit (KIR) = pore subunit (Kir6)

Sulphonylurea receptor = regulatory subunit (SUR1)

27
Q

What structure do KATP channels exist as?

A

Octameric structures

28
Q

What can inhibit KATP?

A

Intracellular ATP inhibits KATP to elicit depolarisation

KATP is directly inhibited by sulphonylurea drug class

29
Q

What can stimulate KATP to inhibit insulin secretion?

A

Diazoxide

30
Q

What are SURs used for the therapy of?

A

Second line therapy for type 2 diabetics

31
Q

What patients is SURs therapy most effective in?

A

Patients who have trouble injecting insulin

Patients who have improved their glucose control and lessened the stress on the islet

32
Q

What can Kir6 mutations cause?

A

Neonatal diabetes = due to constitutively activated KATP channels or an increase in KATP numbers

33
Q

What can be used to treat neonatal diabetes?

A

Some patients may have beta cells responsive to SURs (e.g tolbutamide) = can recover euglycaemia fairly quickly

34
Q

What can some Kir6 or SUR1 mutations cause?

A

Congenital hyperinsulinaemia = caused by trafficking or inhibiting mutations

35
Q

What can be used to treat congenital hyperinsulinaemia?

A

Diazoxide = can help inhibit secretions if channels are still getting to the membrane

36
Q

What is maturity-onset diabetes of the young (MODY)?

A

Monogenic diabetes with genetic defects in beta cell function = familial form of early-onset type 2 diabetes, primary defects in insulin secretion

37
Q

What type of MODY does mutations in glucokinase cause?

A

MODY 2 = glucokinase activity is impaired, defect in sensing glucose, blood glucose threshold for insulin secretion is increased

38
Q

What type of MODY does mutations in HNF transcription factors cause?

A

MODY 1 and 3

39
Q

What do HNF transcription factors do?

A

Play key role in pancreas foetal development and neogenesis, also regulate beta cell differentiation and function

40
Q

Why is there robust genetic screening to differentiate MODY from type 1 diabetes?

A

Allows treatment of MODY with sulphonylurea instead of glucose

41
Q

What causes type 1 diabetes?

A

Loss of insulin secreting beta cells

42
Q

What causes type 2 diabetes?

A

Reduced insulin sensitivity

43
Q

What does insulin cause in the body when activated?

A

Amino acid uptake in muscle, DNA/protein synthesis, growth receptors, glucose uptake in muscles/adipose tissue, lipogenesis in adipose tissue/liver, glycogen synthesis in liver/muscle

44
Q

What does insulin cause in the body when inactivated?

A

Lipolysis, gluconeogenesis in the liver

45
Q

How does insulin signalling occur?

A

Via a cascade

46
Q

What is the insulin receptor?

A

Receptor tyrosine kinases

47
Q

What does binding of insulin to alpha subunits cause?

A

Causes beta subunits to dimerise and to phosphorylate themselves, thus activating the catalytic activity of the receptor

48
Q

What is severe insulin resistance associated with?

A

Obesity (type 2 diabetes) and complete loss of adipose tissues

49
Q

What causes monogenic severe insulin resistance?

A

Mutations in key signalling pathways

50
Q

What is leprechaunism (Donohue syndrome)?

A

Rare autosomal recessive genetic trait = mutations in gene for insulin receptor cause severe insulin resistance

51
Q

What are some features of leprechaunism (Donohue syndrome)?

A

Elfin facial appearance, growth retardation, absence of subcutaneous tissue and decreased muscle mass

52
Q

What is Robson Mendenhall syndrome?

A

Rare autosomal recessive genetic trait = severe cases are linked to mutations in the insulin receptor that reduce sensitivity

53
Q

What are some features of Robson Mendenhall syndrome?

A

Severe insulin resistance, hyperglycaemia, compensatory hyperinsulinaemia, developmental abnormalities, acanthosis nigricans, fasting hypoglycaemia, diabetic ketoacidosis

54
Q

What are the symptoms of diabetic ketoacidosis?

A

Vomiting, dehydration, increased heart rate, smell on breath

55
Q

Where are ketone bodies formed?

A

In the liver = derived from acetyl-CoA from the beta oxidation of fats

56
Q

Where do ketone bodies spread to?

A

Diffuse into bloodstream and to peripheral tissues = important molecules of energy metabolism for the heart muscle and renal cortex

57
Q

What do low levels of insulin do in the body?

A

Inhibit lipolysis and prevent ketone body overload

58
Q

When can diabetic ketoacidosis occur?

A

In type 1 = if insulin supplementation is missed

In type 2 = more uncommon, occurs as insulin resistance and deficiency increases

59
Q

When is acetyl-CoA diverted to ketones?

A

If the supply of oxaloacetate is limited

60
Q

When is oxaloacetate consumed for gluconeogenesis?

A

When ketosis is occurring in glucose limiting states (starvation and diabetes)

61
Q

What is oxidised when there is no glucose to breakdown to produce energy?

A

Fatty acids = causes excess acetyl-CoA which is then converted to ketone bodies

62
Q

What causes dehydration in diabetic ketoacidosis?

A

High glucose excretion = dehydration exacerbates acidosis and can lead to coma or death

63
Q

How is diabetic ketoacidosis treated?

A

Insulin and dehydration

Endocrine (42 decks)

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