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ESA2 > MEH - The Endocrine Pancreas > Flashcards

MEH - The Endocrine Pancreas Flashcards

1
Q

What two functions does the panccreas have?

A

Exocrine (lipase amylase/alkaline secretions etc) and Endocrine (insulin glucagon)

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2
Q

What part of the pancreas produces hormones? How much of the pancreas does this take up?

A

Islets of langerhans

1%

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3
Q

What are islets of langerhans made up of?

A

75% beta cells - insulin
20% alpha cells - glucagon
some others

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4
Q

How are alpha/beta cells suited to hormone production (5)?

A
  • Rough ER for protein synthesis (peptide hormones)
  • Many vesicles (granules) to store hormone in ready for secretion when needed (15,000)
  • Well defined golgi (post translational modification)
  • Many mitochondria
  • Tubules/microfilaments for transporting
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5
Q

What is the structure of insulin?

A

2 polypeptide chains (alpha and beta) linked by disulphide bonds (2 for stability, 1 to create a coil), and a C-peptide that detaches

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6
Q

What foods do insulin and glucagon regulate the metabolism of?

A

Carbs
Fat
Protein (Only insulin)

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7
Q

What are the target tissues for insulin?

A

Liver, skeletal muscle, adipose

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8
Q

What are the target tissues for glucagon?

A

Liver and adipose

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9
Q

Why is plasma glucose kept within a tight range?

A

1) Brain sensitive to changes in blood glucose - glucose is an osmolite so can lead to cerebral swelling/shrinking among other things - bad

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10
Q

Normal glucose range? How about immediately after a meal? What is the renal threshold for glucose? What happens after this?

A

3.3-6mmol/L (UHL)
7-8mmol/L
10mmol/L - after this glycosuria - gets excreted as kidney reaches max reabsorption rate

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11
Q

Which organ uses glucose at the fastest rate?

A

Brain

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12
Q

What happens to the renal threshold for glucose in pregnancy and age?

A

Age the threshold goes up

Pregnancy the threshold goes down

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13
Q

Are insulin and glucagon water-soluble? How are they carried in the blood?

A

Water soluble and don’t need carrier proteins

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14
Q

What is the half-life of insulin and glucagon?

A

Short - 5mins

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15
Q

What kind of receptors recognise insulin and glucagon? How does the hormone become inactivated?

A

Insulin - Tyrosine kinase - on cell surface receptor - that goes on to phosphorylate things when insulin bound. Insulin+receptor can be internalised and this will inactivate

Glucagon - GPCR

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16
Q

Name some enzymes that insulin activates/inhibits in carb/fat metabolism

A

Insulin activates glycogen synthesise PFK and pyruvate dehydrogenase, and inactivates and hormone-sensitive lipase.

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17
Q

How is pre-pro-insulin modified to mature insulin?

A

Pre pro insulin enters ER –> becomes pro insulin (signal peptide cleaved off)
Pro insulin folds to ensure correct disulphide bonds are formed
Pro insulin goes to golgi to be packaged into vesicles
In the vesicles the C peptide is cleaved off
= mature insulin + C peptide

18
Q

How can C peptide be used in monitoring of insulin dependent diabetic patients?

A

As it is released in the vesicles with insulin in equimolar amounts can be used to compare to insulin to see whether there is any endogenous insulin being secreted.

19
Q

What is insulin stored as in the vesicle?

A

crystalline zinc- insulin complex hexer

6 insulin around 2 zinc molecules

20
Q

How can insulin have both immediate and long term effects on target cells?

A

Immediate anabolic effects due to its action on already formed proteins e.g. enzymes.

Long term effects due to its ability to stimulate synthesis of new proteins and to stimulate DNA replication (Insulin is friends with growth hormone)

21
Q

10 Major actions of insulin on carb, lipid and protein metabolism?

A

Increase glucose transport into adipose tissue & skeletal muscle.
 Increase glycogenesis and decrease glycogenolysis in liver &
muscle.
 Decrease gluconeogenesis in liver.
 Increase glycolysis in liver & adipose tissue.
 Decrease lipolysis in adipose tissue.
 Increase lipogenesis and esterification of fatty acids in liver & adipose tissue.
 Decrease ketogenesis in liver.
 Increase lipoprotein lipase activity in the capillary bed of tissues
such as adipose tissue.
 Increase amino acid uptake and protein synthesis in liver, muscle & adipose tissue.
 Decrease proteolysis in liver, skeletal muscle & heart muscle.

22
Q

Is there a big store of insulin in the pancreas?

A

Yes daily secretion is just 15% of that stored per day

23
Q

What three groups of substances have an effect on insulin secretion?

A

Hormones - cortisol inhibits
Metabolites - glucose, AA, FAs
Neurotransmitters - NA inhibits

24
Q

Does glucagon have disulphide bonds? How is it synthesised/secreted roughly?

A

No

Pre pro glucagon –> then post translational modification to glucagon

25
Q

4 main actions of glucagon? Which organ does it have its main effect?

A

 Increase glycogenolysis and decrease glycogenesis in liver.
 Increase gluconeogenesis in liver.
 Increase ketogenesis in liver.
 Increase lipolysis in adipose tissue.

Main effect liver.

26
Q

What is the receptor for glucagon and how does it work?

A

GPCR - G alpha S —> cAMP —> PKA phosphorylates important enzymes in target cells

Glucagon recognises low glucose in alpha-cells

27
Q

Can insulin inhibit glucagon?

A

Yes

28
Q

What are the kATP channels? How are the kATP channels regulated by metabolism?

A

K channels gated by ATP/ADP and control insulin secretion

Inhibited by ATP (high energy signal) - ATP is high due to glucose being high so ATP is made. K channels shut means membrane is depolarised –> Ca channels open —> cause insulin vesicles to fuse with membrane and release insulin

Low glucose –> glucagon –> low ATP –> disinhibition of kATP channel —> K out of beta cell = hyperpolarises cell –> no Ca in so no insulin released

29
Q

How does insulin lead to uptake and metabolism of glucose?

A

Stimulates GLUT4 transporter to translocate to cell membrane of target cell so glucose can go from plasma to cell

30
Q

Which metabolite when increased alone (e.g. just this in diet) stimulates both insulin and glucagon

A

Amino Acids - maybe survival mechanism

31
Q

What takes longer lipogenesis or gluconeogenesis?

A

Lipogenesis

32
Q

Is glucose uptake to muscle and adipose fast or slow?

A

Fast

33
Q

Is protein synthesis fast/slow/intermediate?

A

Intermediate

34
Q

What level of blood sugar indicates diabetes?

A

Random >11mmol/L

Fasting >7mmol/L

35
Q

What two reasons for Type 1 diabetes are there?

A

Its autoimmune

1) Destruction of pancreatic beta cells
2) secretory response of beta cell is abnormally slow or small

= insulin deficiency

36
Q

How can a gain of function kATP mutation lead to decreased insulin secretion?

A

As less sensitive to ATP so not inhibited at high levels of glucose so insulin not released. (not autoimmune more population/mutation problem)

37
Q

How can type 2 diabetes occur? Which is the most common?

A

Normal insulin
Peripheral resistance

1) Defective insulin receptor mechanism - change in receptor number or affinity
2) Defective post receptor events
3) Excessive or inappropriate glucagon secretion

Insulin resistance is most common 92% of people with type 2 diabetes

38
Q

What can lead to type 2 diabetes (3)?

A

Genetics

Environment - Sedentary lifestyle/obestiy

39
Q

What happens in young (before 12 years) insulin resistance onset?

A

Initially: beta cells compensate by increasing insulin production

Then: beta cells unable to maintain increased insulin –> impaired glucose tolerance

Then: beta cell dysfunction leads to relative insulin deficiency –> overt type 2 diabetes

40
Q

What is the role of C peptide?

A

Protective role against vascular damage in patients with diabetes. Research into whether C peptide should added to insulin therapy due to its protective functions

ESA2 (37 decks)

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