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Med 2024-2028 > Metabolism 3.2 > Flashcards

Metabolism 3.2 Flashcards

1
Q

State why lipids release more energy when oxidised compared to carbohydrates

A

More ‘reduced’

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2
Q

State why complete oxidation of lipids requires more O2

A

More ‘reduced’

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3
Q

State 3 classes of lipids

A
  1. Fatty acid derivatives
    -fatty acids. fuel molecules
    -triacylglycerols. from diet, fuel storage
    -phospholipids. membrane components
  2. HMG Derivatives
    -ketone bodies, alternative fuel molecules, water soluble
    -cholestrol, membrane + steroid hormone synthesis
    -cholestrol esters, cholestrol storage
    -bile acids + salts, lipid digestion
  3. Vitamins (A,D,E,K)
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4
Q

Where are triacylglycerols stored?

A

Adipose tissue
(anhydros form)

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5
Q

State function of TGs (triacylglycerols)

A

Used during

  1. Prolongued exercise
  2. Starbation
  3. Pregnancy (because pregnancy has increased metabolic load on women)
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6
Q

State which hormones control metabolism of TGs

A
  1. Glucagon -mobilisation
  2. Adrenaline - mobilsation
  3. Growth hormone- mobilisation
  4. Cortisol - mobilsation
  5. Thyroxine - mobilisation
  6. Insulin - promotes TGs storage
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7
Q
A
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8
Q

State why the brain uses glucose instead of fatty acids

A

FAs do not easily pass blood brain barrier

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9
Q

Why do RBCs and WBCs not use FAs?

A

No mitochondira

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10
Q

Stage 1 Catabolism of TGs

A

Triacylglycerols = triglycerides

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11
Q

Four stages of catabolism

A
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12
Q

When is fatty acid released as an alternative fuel?

A

Low glucose conc

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13
Q

State the location of stage 2 catabolism of fatty acids

A

Mitochonria (intracellular)

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14
Q

Describe what happens in stage 2 catabolism of fatty acids

A
  1. Fatty acids transported to adipose tissue, liver tissue, skeletal muscle
  2. Fatty acids are oxidised
  3. Requires h+ carriers which are reduced (NAD+ → NADH⁺ + H⁺)
  4. Reducing power released
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15
Q

Define amphipathic

A

Fatty acid containing hydrophilic + hydrophobic groups mainly

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16
Q

State essential polyunsaturated FAs

A

α-linolenic acid

linoleic acid

REQUIRED IN DIET AS WE CANNOT INTRODUCE DOUBLE BOND BEYOND C9

17
Q

Give an overview of the stage2 of fatty acid catabolism

A
  1. FAs activated: FAs linked to coenzyme A by action of fatty acyl CoA synthase (in cytosol) (Fatty Acid + CoA = Fatty Acyl CoA)
  2. Activated FAs transported across inner mitochondrial membrane using carnitine shuttle transporter - Look at diagram. FA transport inhibited bt malonyl CoA-intermediate in FA stnthesis, prevents transport of newly synthesised FAs to mitochondria
  3. FAs oxidised in sequence of oxidative reactions, 2Cs removed with each reaction, occurs in mitochondrial matrix
    Acetyl CoA goes to TCA cycle
    “reducing power” foes to oxidative phosphorylation
18
Q

Diagram showinf Carnitine Shuttle Transport

A
19
Q

Which is a higher energy fuel, Fat or Gluocse?

A

FAT

20
Q

Describe triacylglycerol catabolism stage 2 in terms of glycerol

A

Cytosol
Glycerol transported to liver (metabolised)

21
Q

Which Vitamin is CoA derived from ?

A

Vit B5 - (Pantothenic acid)

22
Q

Describe the consequences of B5 deficiency

A

CoA derived from B5
Less CoA
Impaired activation of FAs
Less intermediate metabolites during oxidation

23
Q

State anabolic functions acetyl coA

A
24
Q

State when ketobodies are used

A

Alternative fuel molecule

Used when glucose levels depleted (prolonged exercise, fasting)

  1. Starvation - glucose levels depleted
    Body increases ketone production as alternative fuel molecule (Physiological ketosis)
  2. Untreated type I diabetes
    Lack of insulin, uncontrollably high glucose levels
    Insulin deficiency presents cells from taking up glucose for energy (cells starved from glucose)
    To compensate, body increases fat breakdown, so, elevated ketone production
    If diabetes untreated, level of ketone bodies in blood stay high, leading to pathological ketosis, this can lead to ketoacidosis + ketonuria (renal threshold exceeded, kidneys can no longer remove it, ketone bodies excreted in urine)
    Volatile acetone excreted by lungs - characteristic smell of acetone (nail varnish remover) can be smelt on breath of type 1 diabetes patient
25
Q

Statge where ketogenesis occurs

A

Ketone bodies synthesis
Liver mitochondria

26
Q

Why would you recommend a ketogeneic diet to a patient with epilepsy?

A

Patient with epilepsy has damage to GLUT 3
This transports glucose to brain, so no glucose to brain, so no energy, seizures

With ketogenic diet, ketone bodies can be used in brain, used to produce energy

27
Q

State the side effects of a ketogenic diet

A

Short term: Nausea, vomiting, headache, constipation, insomnia, dizziness

Long term: hepatic steatosis (fatty liver disease), kidney stones, nutrient deficiencies, high cholestrol

Med 2024-2028 (56 decks)

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