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biochemistry iii > LECTURE 9 (Insulin & Glucagon) > Flashcards

LECTURE 9 (Insulin & Glucagon) Flashcards

1
Q

Which 2 parts does the Pancreas consist of?

A

Exocrine & Endocrine

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2
Q

Describe the Endocrine part of the pancreas

A
  • Secretes hormones
  • Made up of “Islets of Langerhans”
  • Include Beta cells, Alpha cells and Delta cells
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3
Q

What are the different cell types in the endocrine part of the pancreas?

A
  • Beta cells = secrete insulin (most abundant) & is centrally located
  • Alpha cells = secrete glucagon
  • Delta cells = secrete somatostatin
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4
Q

What differentiates insulin from glucose?

A

Unlike glucose, insulin does not cross the placenta

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5
Q

What are the properties of Insulin?

A
  • Protein hormone
  • Insulin + C-peptide are increased insulinoma, whereas exogenous insulin lacks C-peptide
  • Insulin structure: alpha chain, beta chain, disulphide bridges & C-peptide
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6
Q

What is C-peptide?

A

“connecting” peptide which has a long half-life and is an indicator of INSULIN PRODUCTION

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7
Q

Describe how insulin in formed

A

1) Synthesised as “PREPROINSULIN” made by ribosomes of the RER and is then cleaved into “PROINSULIN”
2) Proinsulin is transported to the Golgi apparatus and packaged into secretory granules
3) Proinsulin is cleaved -> exocytosis of INSULIN + C-PEPTIDE equally

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8
Q

Describe Insulin secretion by pancreatic B cells

A

Glucose enters B cells -> Increased ATP generated from glucose metabolism closes K+ channels (target of SULFONYLUREAS) and depolarises B cell membrane -> Voltage-gated Ca2+ channels open -> Ca2+ influx and stimulation of insulin exocytosis

[more glucose -> more insulin release]

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9
Q

What is insulin also release in response to apart from glucose?

A

Amino acids

[especially when glucose + amino acids]

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10
Q

Production of insulin is inhibited by ______________

A

Epinephrine

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11
Q

What increases and decreases insulin release?

A
  • Beta-2-receptors = increase insulin release
  • Alpha-2-receptors = decrease insulin release
    [alpha effect is the dominant effect in the pancreas]
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12
Q

What is the result of the Fight or flight response?

A

Increased plasma glucose

Explanation: If you’re feeling stressed, your body releases stress hormones like cortisol and adrenaline. This should give you an energy boost for a ‘fight or flight’ response. But the hormones actually make it harder for insulin to work properly, known as insulin resistance -> decrease use of glucose for insulin release -> increased plasma glucose

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13
Q

Describe GLUT 1

A

Insulin-dependent

FOUND IN:
- Blood
- Blood-brain barrier
- Heart (lesser extent)

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14
Q

Describe GLUT 2

A
  • Insulin-dependent
  • High Km
  • Low affinity

FOUND IN:
- Liver
- Pancreas
- Small intestine

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15
Q

Describe GLUT 3

A
  • Insulin-dependent
  • Low Km
  • High affinity

FOUND IN:
- Brain
- Neurons
- Sperm

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16
Q

Describe GLUT 4

A

Insulin-dependent

FOUND IN:
- Skeletal muscle
- Adipose tissue
- Heart

17
Q

What is the GLUT-2 Transporter?

A
  • Bidirectional glucose transporter
  • Found in the liver, kidney, intestine and beta cells of pancreas
  • Liver & Kidney -> used for gluconeogenesis
  • Beta cells in pancreas -> glucose in/out based on plasma levels (glucose pumped out when low levels and insulin release falls)
18
Q

What is the GLUT-4 Transporter?

A
  • Stored in vesicles in cells, especially muscle and fat
  • Insulin -> PIK3 pathway -> GLUT-4 activation
  • Major mechanism for increased glucose uptake
  • Depends on insulin (no insulin = no GLUT-4)
19
Q

What can increase GLUT-4 expression?

A

Exercise

20
Q

Describe the pathway for Insulin-dependent glucose uptake

A
  • Insulin receptor is a tyrosine kinase receptor
  • Receptor is a tetramer: 2 alpha + 2 beta units joined by disulphide bonds
  • Insulin binding -> activation of tyrosine kinase domains -> autophosphorylation -> binds substrates (eg Insulin receptor substrates) which mediates downstream effects (PIK3 PATHWAY & RAS/MAP KINASE PATHWAY)
21
Q

What are the effects of insulin?

A
  • Glucose uptake (skeletal muscle + adipose tissue)
  • Glycogen synthesis -> activates glycogen synthase + inhibits glycogen phosphorylase
  • Inhibits gluconeogenesis -> increases fructose 2,6 bisphosphate level
  • Fatty acid synthesis -> activates acetyl-CoA carboxylase + inhibits hormone-sensitive lipase
  • Protein synthesis -> stimulates the entry of amino acids into cells, important for muscle growth (key side effect of insulin therapy -> weight gain)
  • Na+ retention -> increases Na+ resorption in the nephron
  • Lowers K+
  • Inhibits glucagon release
22
Q

Why is insulin and glucose used in treatment of hyperkalemia?

A

Insulin lowers K+ -> enhanced activity of Na/K-ATPase pump in skeletal muscle

23
Q

What is Glucagon?

A
  • Protein hormone
  • Structure: single polypeptide chain
  • Synthesised by alpha cells
  • Opposes actions of insulin
  • Main stimulus for release: low plasma glucose
24
Q

What are the effects of Glucagon?

A
  • Increases liver glycogen breakdown (raises blood glucose level)
  • Increases gluconeogenesis
  • Increases amino acid uptake in liver (insulin increases uptake in muscles) -> more carbon skeletons for glucose via gluconeogenesis -> plasma amino acid levels fall
  • Activated lipolysis (via hormone-sensitive lipase)
25
Q

If glucagon doesn’t cause muscle glycogen breakdown, what does?

A

Ca2+ levels and exercise

Explanation: muscle glycogen breakdown depends on Ca2+ levels and exercise

26
Q

What are the properties of Glucagon receptor?

A
  • Found mostly in liver and in other tissues but with lower density than liver
  • Not found in skeletal muscle
  • G-protein receptor -> Activates adenylyl cyclase -> Increases cAMP levels -> activates protein kinase A (PKA)
27
Q

What are the clinical uses of glucagon?

A
  • Hypoglycaemia
  • Beta-blocker overdose
28
Q

How is Glucagon used in Hypoglycaemia?

A

If you find an unconscious patient with hypoglycaemia
- 1st line treatment: IV dextrose
- 2nd line treatment: Intramuscular glucagon (if IV access cannot be established)

29
Q

What is Insulinoma?

A

A rare pancreatic islet-cell tumour that mainly occurs in adults (around 50 years)

KEY FEATURES
- Fasting hypoglycaemia (insulin levels remain elevated when fasting)
- Sympathetic activation from low glucose causes palpitations, diaphoresis + tremor

MANIFESTATIONS:
- confusion + odd behaviour

29
Q

How is Glucagon used in Beta-blocker overdose?

A

Beta blocker overdose = bradycardia + hypotension

Acts at a different site in contrast to beta-adrenergic agents -> activates adenylyl cyclase -> raises cAMP -> increases myocyte calcium -> increases myocyte chronotropy (heart rate) & inotropy (muscle contraction)

30
Q

What will you see alongside fasting insulin level?

A

Elevated C-peptide and proinsulin

31
Q

What are the differential diagnosis for fasting hypoglycaemia?

A
  • Exogenous insulin
  • Oral hypoglycaemic used in diabetes (SULFONYLUREAS -> increased insulin)
  • Insulinoma
32
Q

What is Glucagonoma?

A

A glucagonoma is a pancreatic alpha-cell tumor that secretes glucagon, causing hyperglycemia and a characteristic rash

CAUSES:
- Excess glucagon secretion -> elevated blood glucose (looks like diabetes)
- Rare to develop diabetic ketoacidosis

MANIFESTATIONS:
- Weight loss (liver gluconeogenesis consumes proteins and amino acids)
- Necrolytic migratory erythema (red blistering rash)
[sites = genitals, buttocks and groin]
- Key clinical scenario: new onset diabetes and rash

33
Q
A

biochemistry iii (12 decks)

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