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BM 210: Introduction to Biochemistry > Block D Part 4: Hormonal Control of Metabolic Pathways > Flashcards

Block D Part 4: Hormonal Control of Metabolic Pathways Flashcards

1
Q

What 5 things have an absolute requirement for glucose in order to get energy?

A

Brain
Nerves
Erythrocytes (red blood cells)
Testes
Kidney medulla
(Lecture 4, Slide 4)

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2
Q

How are blood sugar levels kept constant?

A

By a range of homeostatic (to maintain stability and balance) mechanisms
(Lecture 4, Slide 5)

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3
Q

What 2 things is glucose stored as when the body has an excess of it?

A

Glycogen (liver and muscles)
Triglycerides (Triacylglycerides) (adipose)
(Lecture 4, Slide 5)

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4
Q

What is hyperglycaemia?

A

High blood glucose
(Lecture 4, Slide 5)

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5
Q

What is hypoglycaemia?

A

Low blood glucose
(Lecture 4, Slide 5)

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6
Q

What are the 4 levels that metabolic pathways are organised at?

A

System e.g human
Tissue/Organ e.g brain, liver gut
Cellular e.g liver and muscle response to glucose levels changing
Subcellular e.g mitochondria
(Lecture 4, Slide 6)

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7
Q

What releases insulin and when?

A

pancreatic ß-cells release insulin when blood glucose levels increase
(Lecture 4, Slide 9)

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8
Q

What releases glucagon and when?

A

pancreatic α-cells release glucagon (glucose gone) when blood glucose levels fall
(Lecture 4, Slide 9)

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9
Q

What 3 things does the release of insulin into the blood trigger?

A

Increases glucose uptake into fat and muscle
Increases glycogen synthesis in the liver
Inhibits gluconeogenesis in the liver
(Lecture 4, Slide 10)

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10
Q

What does the release of insulin signal?

A

The “fed” state and he removal of glucose from the blood
(Lecture 4, Slide 10)

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11
Q

What 3 things does the release of glucagon into the blood trigger?

A

Stimulates gluconeogenesis
Inhibits glycogen synthesis in the liver
Triggers lipid breakdown
(Lecture 4, Slide 10)

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12
Q

What does the release of glucagon signal?

A

The release of glucose into the blood
(Lecture 4, Slide 10)

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13
Q

What occurs in the absorptive state?

A

Ingested nutrients enter bloodstream from GI tract, supporting energy requirements of the body and excess nutrients are stored
(Lecture 4, Slide 11)

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14
Q

Why are excess nutrients stored in the body?

A

For use in the post-absorptive state
(Lecture 4, Slide 11)

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15
Q

What occurs in the post-absorptive state?

A

No nutrients entering bloodstream from GI tract - body needs to switch to net catabolism of stores (e.g glycogen, fat, protein)
(Lecture 4, Slide 11)

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16
Q

What is the aim of the post-absorptive state?

A

To maintain blood glucose levels in the absence of absorption from the GI tract
(Lecture 4, Slide 11)

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17
Q

What is the main energy source used by cells in the post-absorptive state?

A

Fatty acids
(Lecture 4, Slide 12)

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18
Q

What is the difference between glycogen breakdown in the liver and glycogen breakdown in the skeletal muscle?

A

Glycogen breakdown in the liver releases glucose into the blood whereas glycogen breakdown in the skeletal muscle doesn’t release glucose into the blood
(Lecture 4, Slide 12)

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19
Q

What are hormones?

A

Chemical messengers which are released from a specific cell type in response to a specific signal
(Lecture 4, Slide 13)

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20
Q

How are hormones carried to their targets cells and organs?

A

By the circulatory system
(Lecture 4, Slide 13)

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21
Q

How do hormones have long-range effects?

A

As they are carried in the blood
(Lecture 4, Slide 13)

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22
Q

How do target cells and organs respond to a hormone?

A

As they express specific receptors which allow them to respond in the presence of the hormone
(Lecture 4, Slide 13)

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23
Q

Does insulin regulate metabolic events in the post-absorptive or absorptive state ?

A

Absorptive
(Lecture 4, Slide 14)

24
Q

What does binding of insulin to the insulin receptor lead to?

A

The receptor auto-phosphorylating
(Lecture 4, Slide 18)

25
Q

What happens in insulin binding after the receptor self-phosphorylates?

A

Phosphorylated residues on the insulin receptor act as binding sites for insulin receptor substrate (IRS) proteins
(Lecture 4, Slide 18)

26
Q

What happens in insulin binding after insulin receptor substrate (IRS) proteins bind to phosphorylated residues on the insulin receptor?

A

The insulin receptor phosphorylates 4 tyrosine residues in insulin receptor substrate (IRS) proteins
(Lecture 4, Slide 18)

27
Q

What happens in insulin binding after the insulin receptor phosphorylates 4 tyrosine residues in insulin receptor substrate (IRS) proteins?

A

The lipid kinase phosphoinositide 3-kinase binds to phosphorylated residues on IRS proteins and then converts phosphatidylinositol 4,5-bisphosphate (PIP2) into phosphatidylinositol 3,4,5-trisphosphate (PIP3)
(Lecture 4, Slide 18)

28
Q

What happens in insulin binding after phosphoinositide 3-kinase converts PIP 2 to PIP 3?

A

PDK1 binds to PIP3 and becomes activated, which then phosphorylates and activates kinases such as PKB (Akt)
(Lecture 4, Slide 18)

29
Q

What is GLUT4?

A

Glucose transporter
(Lecture 4, Slide 21)

30
Q

Where is GLUT4 contained inside the cell?

A

GLUT4 storage vesicles (GSV)
(Lecture 4, Slide 21)

31
Q

What does the protein AS160 do?

A

Retains GLUT4 storage vesicles (GSV)
inside the cell preventing them from moving to the plasma membrane
(Lecture 4, Slide 21)

32
Q

How does PKB, activated by insulin, stimulate glucose uptake into adipocytes and muscle?

A

Activated PKB phosphorylates AS160 and inactivates it, allowing GLUT4 storage vesicles (GSV) to fuse with the plasma membrane leading to increased levels of the glucose transporter at the cell surface
(Lecture 4, Slide 21)

33
Q

What way are coupled metabolic reactions set up in?

A

In that there is a net overall change in free energy which favours one direction
(Lecture 4, Slide 23)

34
Q

What is glycogen synthase?

A

The enzyme which catalyses the reaction to synthesise glycogen
(Lecture 4, Slide 26)

35
Q

What is the activity of glycogen synthase regulated by and how?

A

Phosphorylation - GSK can phosphorylate glycogen synthase to inactivate it
(Lecture 4, Slide 26)

36
Q

How does insulin activating PKB lead to an increase in glycogen synthesis?

A

PKB phosphorylates and inactivates GSK leading to an increase in the active (unphosphorylated) form of glycogen synthase, leading to an increase in glycogen synthesis
(Lecture 4, Slide 30)

37
Q

Where in the cell is Fox01 synthesised?

A

In the cytosol
(Lecture 4, Slide 33)

38
Q

Where in the cell is Fox01’s target?

A

The nucleus
(Lecture 4, Slide 33)

39
Q

What is Fox01?

A

A transcription factor which regulates expression of genes which mediate gluconeogenesis
(Lecture 4, Slide 33)

40
Q

How does PKB stop glucose production?

A

PKB phosphorylates Fox01, preventing it from entering the nucleus which leads to a loss of expression of gluconeogenic genes and hence a loss of glucose production
(Lecture 4, Slide 34)

41
Q

Are the enzymes which catalyse the reversible reactions to convert glucose-1-P to glycogen and vice versa regulated reciprocally?

A

No, when one is active, the other is not and vice versa
(Lecture 4, Slide 37)

42
Q

What type of receptor is the glucagon receptor?

A

A g-protein coupled receptor (GPCR)
(Lecture 4, Slide 40)

43
Q

What does binding of glucagon to its receptor lead to?

A

An elevation in cAMP levels and activation of protein kinase A (PKA)
(Lecture 4, Slide 40)

44
Q

How does protein kinase A(PKA) block glycogen synthesis?

A

It directly phosphorylates and therefore inactivates glycogen synthase, blocking glycogen synthesis
(Lecture 4, Slide 41)

45
Q

How does protein kinase A (PKA) increase glycogen breakdown?

A

Activates glycogen phosphorylase, leading to increased glycogen breakdown
(Lecture 4, Slide 41)

46
Q

What is glycogen phosphorylase?

A

The enzyme which catalyses the conversion of glycogen to glucose-1-phosphate
(Lecture 4, Slide 41)

47
Q

How does protein kinase A increase glucose production?

A

Activates a key enzyme activity involved in gluconeogenesis
(Lecture 4, Slide 41)

48
Q

What does activation of leptin lead to?

A

Changes in the sensation of hunger
(Lecture 4, Slide 43)

49
Q

When is leptin released?

A

When fat storage hits a certain level
(Lecture 4, Slide 43)

50
Q

What releases leptin?

A

Adipocytes
(Lecture 4, Slide 43)

51
Q

What does the release of ghrelin do?

A

increase hunger sensation
(Lecture 4, Slide 43)

52
Q

When is ghrelin released?

A

When the stomach is empty
(Lecture 4, Slide 43)

53
Q

What releases gherlin?

A

Cells in the Gi tract
(Lecture 4, Slide 43)

54
Q

How does type 1 diabetes arise?

A

Due to a loss of insulin release from pancreatic ß-cells as a result of autoimmune destruction of the ß-cells
(Lecture 4, Slide 44)

55
Q

What is type 2 diabetes associated with?

A

Insulin resistance of target cells and decreased insulin secretion, also has a strong association with obesity
(Lecture 4, Slide 44)

56
Q

At what ages are type 1 and 2 diabetes usually diagnosed?

A

Type 1 is usually diagnosed in childhood/adolescence whereas Type 2 diabetes generally occurs in adulthood
(Lecture 4, Slide 44)

BM 210: Introduction to Biochemistry (12 decks)

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