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Endocrine > Insulin production, secretion and action > Flashcards

Insulin production, secretion and action Flashcards

1
Q

What do all the cells of pancreatic islets secrete?

A

Beta - insulin
Alpha - glucagon
Delta - somatostatin
PP - pancreatic polypeptide

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2
Q

How is insulin synthesized?

A

In the RER of pancreatic beta cells as preproinsuln where it is then cleaved to insulin releasing C peptide

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3
Q

What is the name of the ultrafast insulin?

A

Lispro

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4
Q

When is lispro used?

A

Within 15 mins of a meal

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5
Q

What is the name of the ultra long acting insulin?

A

Glargine - peakless prolonged action

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6
Q

When is glargine used?

A

As a single bedtime use

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7
Q

How does glucose enter beta cells?

A

Via GLUT2 receptors

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8
Q

What happens when glucose enters the pancreatic cells?

A

It is phosphorlyates by glucokinase to glucose-6-phosphate

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9
Q

What is the Km for glucokinase?

A

Around 5mmol/L

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10
Q

How many ATP are produced per glucose molecule?

A

36

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11
Q

What is the action of ATP in the secretion of insulin?

A

Inhibits kATP which leads to depolarisation of the cell membrane

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12
Q

What occurs when the cell membrane of beta islet cells depolarises?

A

Opening of voltage gated calcium channels which leads to fusion of clacium with secretory vesicles releasing insulin

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13
Q

When will beta cells release insulin?

A

In blood glucose levels over 5 mM

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14
Q

Why is the release of insulin biphasic?

A

Only 5% of insulin granules are readily avaliable for release to prevent all the stores of insulin being depeted

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15
Q

What is the action of sulphonylurea?

A

Mimics the action of ATP to depolarise beta cells

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16
Q

What are the 2 subunits of the kATP channel?

A

An inward rectifier subunit - Kir6

A sulphonylurea receptor which is regulatory - SUR1

17
Q

What is the action of diazoxide?

A

Stimulates kATP receptors inihibiting insulin secretion

18
Q

What does a mutation in Kir6.2 lead to?

A

Neonatal diabetes due to an increase in kATP receptors

19
Q

What is MODY?

A

Monogenic diabetes with a genetic defect in beta cell function usually in the function of gluokinase or the development of the cell

20
Q

What is MODY2?

A

Glucokinase activity impaired leading to a glucose sensing defect where the blood glucose threshold for insulin secretion is too high

21
Q

What is MODY 1 and 3?

A

Mutation in HNF transcription factors which play a key role in pancreatic foetal development and neogenesis

22
Q

Why is it important to distinguish between MODY and type 1 DM?

A

MODY can be treated with sulphonylurea (tablets) instead of insulin (injections)

23
Q

What will insulin turn on biologically?

A 
Amino acid uptake in muscle
DNA and protein synthesis
Growth response
Glucose uptake in muscle and adipose tissue
Liogenesis in adipose tissue and liver
Glycogen synthesis in liver and muscle
24
Q

What will insulin turn off biologically?

A

Lipolysis

Gluconegenesis in liver

25
Q

What class of receptor is the insulin receptor?

A

Receptor tyrosine kinase

26
Q

What will binding of insulin to its receptor cause?

A

Insulin will bind to the alpha subunit and cause the beta subunits to dimerise and to autophosphorylate thus activating the catalytic activity of the receptor

27
Q

What pathway will regulate the metabolic pathway?

A

PKB pathway

28
Q

What pathway will regulate the gene expression properties of insulin?

A

Ras

MAP kinase pathway

29
Q

What is leprechaunism?

A

Rare autosomal recessive genetic disease resultin in severe insulin resistance due to mutations in the gene for the insulin receptor

30
Q

What developmental abnormalities are present in leprechaunism?

A

Elfin facial appearance
Growth retardation
Absence of subcutis fat, decreased muscle mass

31
Q

What is rabson mendenahll syndrome?

A

A rare autosomal recessive genetic disease that results in severe insulin resistance, hyperglycaemia and compensatory hyperinsuliemia

32
Q

What wil rabdon mendenhall syndrome present with?

A

Developmental abnormalities
Acanthosis nigricans
Fasting hypoglycaemia
DKA

33
Q

What are the symptoms of DKA?

A

Vomiting
Dehydration
Increased HR
Distinctive pear drop smell on breath

34
Q

Where are ketone bodies formed?

A

In the liver mitochrondria from acetyl-CoA from beta oxidation of fats

35
Q

What are ketone bodies needed for?

A

Energy metabolism for heart muscle and renal cortex where they are converted back to acetyl co-A to enter the TCA cycle

36
Q

How does DKA come about?

A

There is a lack of glucose and therefore a lack of oxaloacetate and therefore oxaloacetate is used for gluconeogenesis
When glucose is not avaliable, fatty acida are oxidised but this produces excess acetyl-coA
Excess acetyl coA is converted to ketone bodies and the accumulation leads to acidosis

Endocrine (35 decks)

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