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Semester 1 - MCBG > 7. Energy Production: Lipids > Flashcards

7. Energy Production: Lipids Flashcards

1
Q

describe features of lipids

A 
• Structurally diverse
• Generally insoluble in water (hydrophobic)
• Most only contain C, H, O
– (phospholipids contain P, N)
• More reduced than carbohydrates
– release more energy when oxidised
– complete oxidation requires more O
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2
Q

what are the 3 classes of lipids?

A
  1. Fatty acid derivatives
  2. Hydroxy-methyl-glutaric acid derivatives (C6
    compound)
  3. Vitamins
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3
Q

what are the 4 types of fatty acid derivatives?

A

Fatty acids – fuel molecules.
Triacylglycerols (triglycerides) – fuel storage and insulation
Phospholipids – components of membranes and plasma
lipoproteins
Eicosanoids – local mediators

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4
Q

what are the 4 types of Hydroxy-methyl-glutaric acid derivatives?

A

Ketone bodies (C4
) – water soluble fuel molecules
Cholesterol (C27) – membranes and steroid hormone synthesis
Cholesterol esters – cholesterol storage
Bile acids and salts (C24) – lipid digestion

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5
Q

what are the 4 types of lipid vitamins?

A

A, D, E and K.

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6
Q

describe the structure of Triacylglycerols (TAG)

A

glycerol backbone and fatty acid sidechain

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7
Q

how are Triacylglycerols (TAG) formed

A

formed by esterification - attachment of fatty acids to glycerol and loss of water

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8
Q

where are Triacylglycerols stored?

A

adipose tissue

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9
Q

which form is Triacylglycerols stored in and why?

A
  • Triacylglycerols are hydrophobic

* Therefore stored in an anhydrous form

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10
Q

when are stored Triacylglycerols utilised?

A

Utilised in prolonged exercise, ‘starvation’, during pregnancy

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11
Q

what controls Triacylglycerols storage and mobilisation?

A

Storage / mobilisation under hormonal control

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12
Q

describe an overview of triglyceride metabolism

A
  1. triglycerides broken down into glycerol and fatty acids
  2. the glycerol is transported to the blood and then to the liver
  3. the fatty acid is repackaged into chylomicrons to enter blood and is taken to adipose tissue to be stored.
  4. when needed, the fatty acid is released into the blood as fatty acid but its is hydrophobic so cannot dissolve in blood so are carried on albumin
  5. the fatty acid is then transported to tissues that need it like muscles
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13
Q

where does stage 1 of triacylglycerol metabolism occur?

A

extracellular - GI tract

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14
Q

describe stage 1 of triacylglycerol metabolism

A
  1. Lipids (TAG) in diet are hydrolysed in small intestine by
    pancreatic lipases to fatty acids and glycerol
  2. Recombined in small intestine epithelia and packaged transported as TAG by lipoproteins (Chylomicrons)
  3. Released into circulation via lymphatics
  4. Carried to adipose tissue or directly to tissues where fatty acid metabolism occurs
  5. Stored as triglyceride (TAG)
  6. Released as fatty acids when needed
  7. Carried to tissues as albumin-fatty acid complex
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15
Q

which hormones are involved in fat mobilisation?

A

Hormone-sensitive lipase:
glucagon/adrenaline - increases fat mobilsation
insulin - decreases fat mobilisation

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16
Q

which cells do not oxidise fatty acids to release energy?

A
  • cells without mitochondria, e.g. RBC
  • brain; FA do not easily pass blood-brain
    barrier
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17
Q

describe the Triglyceride/fatty acid cycle in adipose tissue

A
  1. glucose transported from extracellular fluid to adipose tissue when in excess
  2. glycolysis occurs in adipose tissue using the glucose
  3. glycerol-1-P that feeds out from glycolysis is combined with fatty acyl-CoA to form triglyceride - esterification
  4. lysis: triglyceride is broken down into fatty acid and glycerol
  5. the glycerol is released and used in glycolysis in other tissues
  6. the fatty acids are not released, but converted to fatty acyl-CoA which is used in the cycle again to form triglyceride
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18
Q

what happens to the Triglyceride/fatty acid cycle in adipose tissue when extracellular glucose concentrations are low?

A

Low extracellular [glucose] results in fatty acid release as alternative fuel

  • low glucose means less glycerol-1-p is created so less triglyceride formed
  • thus, fatty acid that is produced by break down of triglyceride is released into the blood stream and not converted to fatty acyl-CoA
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19
Q

describe features of fatty acids

A

• saturated or
• unsaturated ( ie one or more double bonds C=C)
• amphipathic (contain hydrophilic & hydrophobic groups)
• certain polyunsaturated FA are essential (i.e. required in diet)
(because mammals cannot introduce a double bond beyond
C9), e.g. linolenic acid

20
Q

summarise fatty acid catabolism

A
  1. FA is activated (by linking to coenzyme A outside the mitochondrion
  2. Transported across the inner mitochondrial membrane using a carnitine shuttle
  3. FA cycles through sequence of oxidative reactions, with C2 removed each cycle
21
Q

where does fatty acid catabolism occur?

A

mitochondria

22
Q

describe fatty acid activation

A

Occurs outside the mitochondria, in cytoplasm
• Fatty acids activated by linking to coenzyme A (via high energy bond) by the action of fatty acyl CoA synthase
• Activated fatty acids (fatty acyl~CoA) do not readily cross the inner mitochondrial membrane
requires ATP

23
Q

how is the fatty acyl-CoA transported across the mitochondrial membrane?

A
  1. the Acyl from the fatty acyl-CoA is transferred to carnitine. this is catalysed by the carnitine transferase enzyme
  2. this releases the CoA to go back and activate more fatty acids.
  3. the acyl carnitine is transported through carnitine shuttle transporter into the mitochondrial matrix
  4. the acyl carnitine recombines to form acyl-CoA (requires another carnitine transferase enzyme)and releases carnitine which is transported back into the intermembrane space through the carnitine shuttle transporter
24
Q

why is the transport of fatty acyl~CoA

across the mitochondrial membrane regulated?

A

to control the rate of FA oxidation

25
Q

what inhibitsthe transport of fatty acyl~CoA

across the mitochondrial membrane?

A

• Inhibited by malonyl~CoA (biosynthetic intermediate)

26
Q

can problems occur in this transport of fatty acyl~CoA

across the mitochondrial membrane?

A

yes, Defects can occur in this transport system (exercise intolerance,lipid droplets in muscle)

27
Q

describe the B-oxidation stage of FA metabolism?

A
  • it occurs in the mitochondria
  • FA cycles through sequence of oxidative reactions, with C2 (acetyl CoA)removed each cycle
  • for each 2C released, 1 NADH, 1FADH2
  • a lot of energy is also produced
  • All intermediates are linked to coenzyme A (FA activation)
28
Q

is more energy derived from FA oxidation or glucose oxidation?

A

FA oxidation

29
Q

what is fatty acid metabolism also called?

A

B-oxidation

30
Q

whata re the key points of fatty acid metabolism?

A
  • Mitochondrial
  • Cycle of reactions
  • Removal of 2C units per cycle
  • Oxidation
  • H+ and e transferred to NAD+ and FAD
  • Stops in absence of O2
  • No ATP synthesis
31
Q

what happens to the glycerol that was released earlier?

A

Glycerol can be transported in the blood to the liver,

where it is metabolised

32
Q

describe glycerol metabolism

A
  1. glycerol converted to glycerol phosphate by hydrolysis of ATp in the presence of Glycerol kinase
  2. the glycerol phosphate can either be involved in Triacylglycerol synthesis(FA/TAG cycle) or be converted to Dihydroxyacetone phosphate(DHAP) by reduction of NAD. the DHAP can then be used in glycolysis
33
Q

where is the main convergence point for catabloic pathways?

A

Acetyl-CoA

34
Q

what are the functions of Acetyl CoA?

A

• A most important intermediate in both catabolic and
anabolic pathways
• it is involved in fatty acid synthesis
- make triglycerides
- make phospholipids
• it can form CO2
• it can form Hydroxymethyl glutaric acid (HMG) which is the precursor for Ketone bodies and Cholesterol
- cholesterol can then form steroid hormones

35
Q

what are the Three ketone bodies produced in the body?

A 
Acetoacetate: 
(liver)
– Acetone:
(spontaneous (non-enzymatic) decarboxylation of acetoacetate
– β-hydroxybutyrate:
(liver)
36
Q

what is the concentration of normal plasma ketone body concentration and during starvation and uintreated type 1 diabetes?

A
  • Normal plasma ketone body concentration < 1 mM
  • Starvation 2-10 mM (physiological ketosis)
  • Untreated Type 1 diabetes > 10 mM (pathological ketosis)
37
Q

where are ketone bodies synthesised?

A

Ketone bodies are synthesised by liver mitochondria:

38
Q

How are ketone bodies synthesised?

A

Acetyl-CoA is combined as a 3 to form hydroxymethyl glutaryl-CoA (in the presence of synthase enzyme )which can be converted to acetoacetate(in the presence of Lhasa enzyme) Which can then be converted to acetone or beta hydroxybutyrate.

Or acetyl-CoA in high energy state can go to form the substrate for cholesterol synthesis(in the presence of HMG-CoA reductase)

39
Q

What do statin drugs do?

A

Prevent acetyl-CoA being converted to cholesterol

40
Q

When does ketone body production occur?

A

When low in glucose, glycolysis is slowed down. Fatty acids are released which are metabolised to produce NADH. if there is high NADH, It will inhibit the enzymes in the TCA cycle. So acetyl CoA is no longer used so it can be Diverted out to produce ketone bodies

41
Q

Where are ketone bodies produced transported and used?

A

Produced in the liver, transported in the blood, used up In the muscle

42
Q

How are ketone bodies synthesis regulated by the insulin/glucagon ratio in the fed state.

A

When the Insulin/glucagonRatio is high HMG – CoA Is signalled to put hydroxmethyl glutaryl-CoA into store.

Lying is enzyme is inhibited and HMG –CoA reductase a is activated so less ketone made and more cholesterol made

43
Q

How are ketone bodies synthesis regulated by the insulin/glucagon ratio in the starvation state.

A

When the insulin/glucagon ration is low , Lyase is activated and reductase inhibited so leads to ketone body synthesis

44
Q

Why are ketone bodies produced?

A

When there is less glucose available during starvation/diabetes, ketones are transported to tissues and utilised to produce acetyl-CoA which is used to provide energy

45
Q

What happens in late starvation/diabetes?

A

In long-term starvation, fatty acid stores are depleted and protein in the muscles starts being degraded to amino acids which can enter the liver and be converted to pyruvate and enter Gluconeogenesis to sustain levels of glucose to sustain the brain.

46
Q

What is ketonuria?

A

Ketones in the urine as the exceed the rental threshold e.g. starving or diabetic patients

47
Q

What is ketoacidosis?

A

High levels of strong acidic acetoacetate and beta-hydroxybutyrate

Semester 1 - MCBG (18 decks)

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