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Endocrine > Endocine Pancreas > Flashcards

Endocine Pancreas Flashcards

1
Q

Where is insulin synthesis end

A

RER of pancreatic β-cells

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2
Q

What is the initial insulin form made in the RER

A

preproinsulin

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3
Q

How is pro insulin made from preproinsulin

A

The removal of prrproinsulin’s signalling peptide during insertion into the endoplasmic reticulum generates proinsulin

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4
Q

What is pro-insulin composed of

A

A chain, B chain & connecting C peptide

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5
Q

How is insulin different compared to proinsulin and how is this clinically relevant

A

Proinsulin forms insulin by losing the C peptide
C peptide & insulin are secretion together
& so c peptide can be used to measure endogenous insulin production

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6
Q

Describe the structure of insulin

A

2 polypeptides (A & B) linked by a disulphide bond

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7
Q

What are the effects of insulin in the body

A

General
- DNA synthesis
- Protein synthesis
- Growth responses
- Increased lipogenesis, decreased lipolysis
- Increased glycogen formation, decreased gluconeogenesis
I.e. increased glucose storage & decreased glucose release

Muscle
- Increased amino acid uptake
- Increased glucose uptake
- Increased glycogen synthesis

Adipose
- Increased glucose uptake
- Increased lipogenesis (lipid synthesis)

Liver
- Increased glycogen synthesis
- Increased lipogenesis

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8
Q

At what level should pancreatic beta cells start producing insulin to decrease glucose

A

5 mmol/l

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9
Q

What receptor transports glucose into beta cells

A

GLUT2

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10
Q

What happens to glucose once it enters beta cells

A

Glucose is phosphorylated by glucokinase

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11
Q

What is the role of glucokinase in the secretion of insulin

A

It acts as a glucose sensor - a change of glucose concentration leads to a dramatic change in glucokinase activity & hence glucose phosphorylation

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12
Q

What is the effect of increased glucose metabolism/ phosphorylation in the beta cells

A

Increase in intracellular ATP

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13
Q

What is the effect of increased ATP in the beta cells that eventually results in the secretion of insulin

A

Inhibition of ATP-sensitive K+ channel KATP =>
Depolarisation =>
opening of voltage gated Ca2+ channels =>
Increased intracellular ca2+ concentration =>
Fusion of secretory vesicles with the cell membrane =>
Insulin release

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14
Q

Summarise the steps that lead to the release of insulin from pancreatic beta cells

A

Glucose enters beta cells through CLUT2 =>
Glucose is phosphorylated by glucokinase =>
Inhibition of ATP-sensitive K+ channel KATP =>
Depolarisation =>
opening of voltage gated Ca2+ channels =>
Increased intracellular ca2+ concentration =>
Fusion of secretory vesicles with the cell membrane =>
Insulin release

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15
Q

Describe the pattern of release of insulin

A

Low basal rate (accounts for ~5%)
Post-prandial insulin release in biphasic pattern (~95%)

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16
Q

Describe the post-prandial release of insulin

A
  • Is biphasic
  • 5% insulin granules available & released immediately (1st)
  • This prevents sharp increase in blood glucose
  • Preparation & release of reserve insulin occurs in response to signalling (2nd)
  • This means the second phase is more tuned to the insulin requirement/ blood glucose levels
17
Q

What is the importance of the first phase of post-par dial insulin release

A

Prevents sharp increase in blood glucose

18
Q

What is the importance of the second phase of post-par dial insulin release

A

It is controlled by signalling processes (GLUT2 glucose transport in beta cells) that are related to the amount of glucose exposure.
This allows a more tuned response related to the insulin requirement

19
Q

Describe the three main cell types of the islets of langerhans. state what they secrete & where they are located within the islet of langerhans

A

Beta cells - Secrete insulin, located near the blood vessel
Alpha cells - Secreted glucagon, located near the blood vessel
Delta cells - Secrete somatostatin, location on periphery

Two other, less common cell types
- PP cells - secrete pancreatic polypeptide, periphery
- ε cells - secrete ghrelin

20
Q

Thinking about the cell types in the islets of langerhans, name the hormones produced & what there main roles are

A
  • Insulin - lowers blood glucose, increases glucose storage
  • Glucagon - raises blood glucose, breaks down storage
  • Somatostatin - inhibits insulin & glucagon secretion (prevents fluctuation) & reduces gastric secretions
  • Ghrelin - increases appetite
  • Pancreatic polypeptide - regulates pancreatic secretions & food intake
21
Q

What are the islets of langerhans

A

Clumps of cells that form the endocrine part of the pancreas

22
Q

Summarise glucose homeostasis

A

Hypoglycaemia/lipidaemia =>
Increased glucagon, decreased insulin =>
Gluconeogenesis & lipolysis

*above pathway can also be stimulated by raised adrenaline (in response to fasting or exercise)

Hyperglycaemia/lipidaemia =>
Increased insulin, decreased glucagon =>
Glucose storage (lipogenesis, glycogen formation)

  • above pathway can also occur in response to eating
23
Q

Describe the relationship between insulin sensitivity & release in a normal vs T2 diabetic patient

A

Increased insulin sensitivity => decreased insulin secretion
Decreased insulin sensitivity => increased insulin secretion
& vice versa

This compensatory mechanism does not occur in T2DM

24
Q

What changes occur in a T2DM & pre diabetic patients between cells

A

the number of secretory granules per β-cell is reduced - degranulation

25
Q

How is the pattern of insulin secretion different in a patient with T2DM & why is this

A

They no longer have a biphasic pattern (due to degranulation)

26
Q

What happens in the alpha cells in response to low glucose

A
  • Glucose uptake and metabolism low
  • decrease in ATP & KATP channels closure
  • membrane depolarisation
  • voltage gated calcium channels open & calcium influx
  • Glucagon exocytosis triggered
27
Q

What organ does glucagon target & what effect does it have

A

Liver - increased hepatic gluconeogenesis

28
Q

How are alpha cells affected by T2DM

A

Excessive glucagon secretion in the fed state in T2DM
This contributes to hyperglycaemia

29
Q

What is the type of regulation involved in the suppression of insulin & glucagon secretion by somatostatin

A

Paracrine regulation

30
Q

What is the incretin effect

A

Greater increase in insulin production in response to oral glucose than in response to IV glucose due to the release of GLP-1 by GI L-cells following eating

31
Q

What is the main hormone of the incretin effect, what cell type secretes it and when is it secreted

A

GLP-1 hormone
Secreted by GI L-cells
Secreted following eating

32
Q

What is the effect of GLP-1 on beta & alpha cells & satiety

A
  • Beta cells - Increases glucose-induced insulin release by β-cells, promotes beta cell proliferation
  • Alpha cells - Suppress glucagon secretion at depolarising glucose concentrations
  • Satiety - Increases feeling of fullness & slows gastric emptying
33
Q

What is the type of receptor of GLP-1

A
  • G protein-coupled receptor (second messenger cAMP)
34
Q

What enzyme breaks GLP1 down

A

DDP4

Endocrine (22 decks)

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