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HUBS2207 > L18 Insulin and Type 1 Diabetes > Flashcards

L18 Insulin and Type 1 Diabetes Flashcards

1
Q

What is insulin?
What does it promote?
What does it inhibit?

A
  • Insulin is a peptide hormone involved in blood glucose regulation
  • It promotes glucose uptake from the bloodstream into adipose tissue and skeletal muscle
  • It inhibits hepatic glucose production
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2
Q

What does insulin stimulate?

A

Cell growth and differentiation - increased synthesis of glycogen, proteins and triglycerides

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3
Q

Where and why is insulin synthesised?

A

Synthesised by pancreatic beta cells in response to elevated blood glucose concentrations

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4
Q

What is considered normal BGL?

A

3.6-5.8mM

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5
Q

At what BGL are beta islet cells most sensitive?

A

5.5-6.0mM

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6
Q

Does glucose enter beta islet cells actively or passively?

A

Passively

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7
Q

What is insulin called when it is first synthesised?

A

Preproinsulin

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8
Q

What is the composition of preproinsulin?

A

A single polypeptide containing signal peptide, A-chain, C peptide and B-chain

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9
Q

How is insulin synthesised?

A
  • Initially as preproinsulin
  • Signal
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10
Q

How is insulin synthesised? (4 steps)

A
  • Initially as preproinsulin
  • Signal peptide cleaved in the ER making proinsulin
  • C peptide cleaved in Golgi complex
  • A-chain and B-chain linked to form mature insulin
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11
Q

What type of bond links A- chain and B-chain in mature insulin?

A

Two disulphide bonds

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12
Q

How is insulin secreted? (5 complex steps)

A
  1. Glucose enters beta cell through GLUT2 and is phosphorylated to G-6-P
  2. G-6-P enters the citric acid cycle, increasing the production of ATP
  3. High intracellular ATP closes K+ channels, depolarising the cell membrane
  4. Voltage-gated Ca++ open and Ca++ enters the cell
  5. Ca++ increase causes exocytosis of insulin storage vesicles
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13
Q

What type of receptor is insulin receptor?

A

Type of tyrosine kinase receptor

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14
Q

What is activated when insulin binds to the insulin receptor? (2)

A
  • Phosphorylation of insulin receptor substrate (IRS)
  • Activation of PI3K signalling pathway and activation of GLUT4
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15
Q

Where are GLUT1 transporters found? (5)

A
  • Brain
  • Kidney
  • Colon
  • Placenta
  • Erythrocyte
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16
Q

Where are GLUT2 transporters found? (4)

A
  • Liver
  • Pancreatic beta cells
  • Small intestine
  • Kidneys
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17
Q

Where are GLUT3 transporters found? (3)

A
  • Brain
  • Kidney
  • Placenta
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18
Q

Where are GLUT4 transporters found? (3)

A
  • Heart
  • Skeletal muscle
  • Adipose tissue
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19
Q

Where are GLUT5 transporters found? (1)

A
  • Small intestine
20
Q

What glucose transporter is insulin independent?

A

GLUT2

21
Q

What glucose transporter is insulin dependant?

A

GLUT4

22
Q

GLUT2 transporters have a ___ capacity for glucose but a ___ affinity

A

GLUT2 transporters have a high capacity for glucose but a low affinity

23
Q

What does insulin and GLUT4 do in adipose tissue and how?

A
  • Insulin stimulates glucose uptake and its storage as fat (TGs)
  • Glycolysis to pyruvate to acetyl CoA
24
Q

What does insulin and GLUT4 do in skeletal muscle tissue?

A
  • Insulin stimulates glucose uptake and use, or storage as glycogen
25
Q

How does insulin stimulate glycogen synthesis in skeletal muscle?

A

Activation of glycogen synthase

26
Q

How dues insulin inhibit glycogen breakdown?

A

Inactivation of glycogen phosphorylase

27
Q

What effects does insulin have on protein? (3)

A
  • Stimulates amino acid uptake
  • Increases net protein synthesis
  • Inhibits protein catabolism
28
Q

What effects does insulin have on fats? (1) What enzyme is affected in particular? (1)

A
  • Insulin prevents inappropriate mobilisation of stored fat
  • Insulin inhibits lipolysis by suppressing Hormone Sensitive Lipase (HSL)
29
Q

What is Hormone Sensitive Lipase and what does it do?

A

HSL is an enzyme that catalyses hydrolysis of stored TGs therefore a key factor in lipid metabolism

30
Q

What are ketone bodies? Where are they produced and when?

A

Metabolites derived from fatty acids, produced in the liver during energy restriction

31
Q

What are three examples of ketone bodies?

A
  • Acetoacetate
  • B-hydroxybutyrate
  • Acetone
32
Q

When is it considered ‘normal’ for ketone bodies to be present

A

During prolonged fasting

33
Q

What hormone promotes ketone bodies?

A

Glucagon

34
Q

Explain ketogenesis (4)

A
  • Stimulation of lipolysis - breakdown of TGs
  • FFAs and glycerol enter the blood stream and are taken up by the liver
  • Liver makes ketone bodies from acetyl CoA
  • Once made they re-enter the bloodstream and used for energy production
35
Q

What is ketogenesis?

A

A metabolic pathway that produces ketone bodies as an alternate energy source for the body

36
Q

What pancreatic cells secrete glucagon?

A

Alpha cells

37
Q

What effects does glucagon have on the body? (3)

A
  • Increased breakdown of glycogen to glucose
  • Increased breakdown of fats to fatty acids
  • Increased synthesis and release of glucose
38
Q

What are some characteristics of T1DM? (6)

A
  • ~10% total diabetic cases
  • Insulin dependant
  • Common in children and adolescents
  • Beta cells of pancreatic islets gradually destroyed causing an absolute insulin deficiency
  • Autoimmune (genetic + environmental)
  • Dependant on insulin administration
  • Severe symptoms if untreated - DKA
39
Q

What are some characteristics of T2DM? (7)

A
  • ~85% diabetic cases
  • Insulin resistant, non insulin dependant (NIDDM)
  • Decreased insulin sensitivity and impaired insulin signalling
  • Generally middle to old age and overweight
  • Milder initial symptoms than T1DM
  • Responsive to dietary changes, weight loss and hypoglycaemics
  • Can develop into T1DM if left untreated over a long time
40
Q

What causes T1DM? (4)

A
  • Genetics
  • Exposure to certain viruses
  • Body’s own immune system attacking Beta pancreatic cells
  • No insulin to let glucose into cells
41
Q

What happens when there is no insulin? (3 steps)

A
  • Body thinks it is starving due to no peripheral nutrient uptake
  • Gluconeogenesis occurs
  • System flooded with glucose and FFA
42
Q

What tissues are most affected by insulin deficiency and why?

A

Adipose and muscle tissue as they have GLUT4 mediated glucose uptake which is insulin dependant

43
Q

What are some symptoms of diabetes? (10)

A
  • Polydipsia
  • Polyphagia
  • Lethargy
  • Blurred vision
  • Acetone breath
  • Weight loss
  • GI upset
  • Kussmaul breathing
  • Polyuria
  • Glycosuria
44
Q

What affects does hyperglycaemia have on the kidneys? (2)

A
  • Glucose in filtrate causes osmotic diuresis = polyuria
  • Increased urine output = dehydration
45
Q

How much glucose is normally reabsorbed in the proximal convoluted tubules of the kidneys?

A

100%

46
Q

What is ‘Hyperglycaemic Hyperosmolar State’?
What is it caused by in diabetics?

A

Very high blood glucose levels - blood becomes hyperosmolar with a high viscosity
Caused due to kidneys overwhelmed by excessive glucose

47
Q

What does insulin deficiency do in muscle? (2)

A
  • Increases protein degradation
  • Release of amino acids to be used for gluconeogenesis and ketogenesis

HUBS2207 (7 decks)

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