Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MD1 > Biochemistry > Flashcards

Biochemistry Flashcards

1
Q

List the metabolic challenges to tumour cells

A
  1. Energy sources
  2. Protecting against oxidative stress
  3. Precursors for biosynthesis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Describe the Warburg effect and its role in cancer cell metabolism

A
  • 18F-FDG is a glucose derivative that is radiolabelled and used as a tracer and taken up by glucose utilising cells
    • Because of Warburg effect, tumour cells exhibit high capacity to take up 18F-FDG
    • FDG cannot be further metabolised and accumulates in cells resulting in intense radiolabelling in cancer cells (inability of phosphofructo-kinase-1)
      High capacity to take up FDG relates to the metabolic adaptation of cancer cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Why do cancer cells exhibit enhanced glucose uptake?

A

Cancer cells over-express GLUT-1, a foetal form of glucose transformer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Why do cancer cells exhibit enhanced glycolytic flux?

A

Glycolytic enzymes hexokinase, PFK1 and lactase dehydrogenase (LDH) are over-expressed in cancer cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Why do cancer cells exhibit diminished metabolic flux in TCA cycle?

A

Pyruvate dehydrogenase (PDH) activity is suppressed in cancer cells -> reduced rate of pyruvate metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What usually occurs in hypoxia?

A

ROS/superoxide production occurs -? ROS damage of nuclear and mitochondrial DNA -? damaged DNA causes activation of tumour suppressor p53 -> p53 induces cell death, DNA repair, senescence and cell cycle arrest

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How to cancer cells overcome/prevent hypoxia?

A

Glutathione (reduced) pairs with ROS and become oxidised -> reacts with NADPH to become reduced again (mopping up ROS)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How is NADPH produced in the context of cancer cells?

A

Through the pentose phosphate pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Explain the production of NADPH in the context of the PPP

A

hypoxia induces expression of glycogen synthase and glycogen phosphorylase -> hypoxic tumour cells store glycogen -> stored glycogen used to create glucose-6-phosphate -> creates NADPH for reducing glutathione

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What does the Warburg effect have to do with the PPP and hypoxia?

A

Warburg effect is the over-expression of GLUT-1 allowing for the excess storage of glucose which then allows for this glucose to be used by PPP to create NADPH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What enzymes are involved with glycolysis?

A

Phosphoglucomutase and Hexokinase II

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What enzymes are involved with glycogen metabolism?

A

Glycogen synthase 1, glycogen phosphorylase, glycogen branching enzyme 1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What enzyme is involved in the increased glucose uptake?

A

GLUT1 transporter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Hypoxia induces the activation of…

A

Hypoxia inducible factor (HIF-1)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Explain the role of glutamine metabolism in cancer cells

A

Increased expression of other enzymes to convert glutamine to form other amino acids like serine and glycine and also intermediates of TCA cycle like alpha-ketoglutarate to produce other precursors of biosynthesis of proteins and nucleic acids -> help with cancer cell proliferation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How to cancer cells undergo metabolic adaptations to maintain their high cell proliferation rate?

A

Non-oxidative phase of PPP -> generate precursors for DNA and protein synthesis

17
Q

Explain the role of pyruvate kinase M2 in metabolic adaptation of cancer cells

A
  • PKM2 has a lower activity than normal PK
  • Cancer cells over-express pyruvate kinase M2 (PKM2) feeding the glycolysis cycle (going through to lactate rather than the TCA cycle)
17
Q

Explain the role of pyruvate kinase M2 in metabolic adaptation of cancer cells

A
  • PKM2 has a lower activity than normal PK
  • Cancer cells over-express pyruvate kinase M2 (PKM2) feeding the glycolysis cycle (going through to lactate rather than the TCA cycle)
18
Q

What are some ways metabolic liabilities can be exploited for cancer cell therapy?

A
  1. dietary restrictions to limit glucose availability
  2. inhibitors of glycogen phosphorylase
  3. inhibitors of hexokinase
  4. inhibitors/activators of PKM2
19
Q

What is GLUT

A

glucose transporter

19
Q

What is GLUT

A

glucose transporter

20
Q

What are the kinases in glycolysis and what do they do?

A

hexokinase and glucokinase - turn glucose into phosphorylate glucose by using ATP trapping in the cell

21
Q

Describe the rate limiting step in glycolysis

A

fructose 6 phosphate -> PFK1 -> fructose 1, 6-bisphosphate

22
Q

What is the process that changes the rate of glycolysis when in a fed state

A

fed state -> insulin -> increased PFK2 -> fructose 2, 6-bisphosphate -> increased PFK1 = faster glycolysis

23
Q

What is the process that changes the rate of glycolysis when in a fasting state

A

fasting state -> glucagon -> less PFK2 -> less fructose 2, 6 bisphosphate -> less PFK1 = slower glycolysis

24
Q

In an anaerobic state what happens in glycolysis after fructose 1, 6-bisphosphate is made?

A

creation of ATP and converting until pyruvate kinase created pyruvate -> lactate dehydrogenase and NADH -> lactate + NAD+ (build up of lactate causes muscle soreness and NAD keeps glycolysis going)

25
Q

In an aerobic state what happens in glycolysis after fructose 1, 6-bisphosphate is made?

A

creation of ATP and converting until pyruvate kinase created pyruvate -> moves to mitochondria -> krebs cycle = ATP

26
Q

What is gluconeogenesis?

A

When in a prolonged fasting state gluconeogenesis allows the cells to make their own glucose for energy production, it is glycolysis in reverse with a couple of extra speedbumbs that requite the use of lactate, amino acids and glycerol

27
Q

Describe the progression of type 2 diabetes

A

Type 2 diabetes is a progressive disorder - starts with insulin resistance. Can no longer bring about the effect of reducing blood sugar. Body pancreas initially secretes enough insulin to overcome glucose, no longer happens with type 2 diabetes. Insulin-resistant muscle with reduced glucose transport.

28
Q

How does being overweight contribute to risk of diabetes?

A

Overweight = larger adipocytes
Pro-inflammatory state = enlarged adipocytes produce chemotaxis protein (MCP-1)
Chronic inflammation = macrophages infiltrate adipose tissue in response to MCP-1

Inhibit GLUT4, cannot access energy from glucose

29
Q

Why is cholesterol important?

A

Steroid hormones are formed from cholesterol

30
Q

Describe the steps used to synthesise thyroid hormones in the thyroid gland

A

Thyroglobulin -> thyroglobulin with iodinated Tyr residues -> Thyroxine (T4), Triiodothyronine (T3)

31
Q

Describe the steps of alcohol metabolism

A

Ethanol –(Alcohol dehydrogenase)–> Acetaldehyde –(Aldehyde dehydrogenase) –> Acetate

MD1 (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions