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MEH > Lipids > Flashcards

Lipids Flashcards

1
Q

Lipid Structure Facts

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 O2
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2
Q

Structure of fatty acids

A

Alaphatic chain od methyl groups with acid (carboxylic) group on one end

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3
Q

What are the types of lipids

A

Fatty acids, triacylglycerols and ketone bodies are the types of lipid used as fuel molecules.

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4
Q

How are lipids stored

A

Triacylglycerol

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5
Q

What is the structure of Triacylglycerol

A

Glycerol backbone attached to three fatty acids

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6
Q

How are ketone bodies formed

A

In the liver fatty acids are turned in to ketone bodies
Derived from fatty acids

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7
Q

What is derived from Fatty Acids

A

Fatty acids - Fuel molecules
Triacylglycerols (Triglycerides) - Fuel Storage and insulation
Phospholipids – components of membranes and plasma
lipoproteins
Eicosanoids – local mediators (signaling molecules)

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8
Q

What is derived from Hydroxy-methyl-glutaric acid derivatives (C6 compound)

A

Kentone Bodies (C4) - Water soluble fuel molecules
Cholesterol (C27) – membranes (fluidity) and steroid hormone synthesis
Cholesterol esters – cholesterol storage
Bile acids and salts (C24) – lipid digestion

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9
Q

What are the fat soluble vitamins

A

A, D, E and K.
derived from lipids

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10
Q

Does Triacylglycerols Glycogen Muscle protein vary with heathy to obese people

A

Glycogen and Muscle protein remain constant

Triacylglycerols go up with from heathy to obese by the weight increase

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11
Q

What is Triacylglycerols derived from

A

Glycerol and Fatty acids in an esterification reaction

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12
Q

What is Lipolysis

A

Triacylglycerols turning back in to Glycerol and fatty acids

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13
Q

Function of Triacylglycerols,
Is it hydrophobic or hydrophilic

A
  • Triacylglycerols are hydrophobic
  • Therefore stored in ananhydrous form
  • Stored in specialised tissue– adipose tissue
  • Utilised in prolonged exercise, ‘starvation’,
    and also during pregnancy
  • Storage/ mobilisation is under tight hormonal control
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14
Q

what is the benefit of Tricylglyerols being hydrophobic

A

As its in an Anhydrous form
When stored they can hold alot more fuel per gram of weight

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15
Q

When and where does Metabolism of triacylglycerols occur

A
  • Stage 1
  • GI Tract (lumen) (Small interstine)
  • Extracellular
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16
Q

What happens to fatty acids after metabolism of triacylglycerols (in to fatty acids and Glycerol)

A
  • Converted back to triglycerides in G.I. tract in the cells
  • Packaged into lipoprotein particle ( this stabilises them as they interact with many other pathways eg, amino acid pathway)
  • The packages are called CHYLOMICRONS
  • Released into circulation via lymphatics
  • Carried to adipose tissue
  • Stored as triglyceride (triacylglycerols)
  • Released as fatty acids when needed
  • Carried to tissues as albumin-fatty acid complex ( different transport process as lipids aren’t water soluble)
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17
Q

What is the colour when you disect the lymphatics

A

Looks milky due to the CHYLOMICRONS

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18
Q

Fatty Acid Catabolism - Summary

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 sequences of oxidative reactions, with C2 removed each cycle

(C18 —> C16 + C2)

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19
Q

How is fatty acid Activated

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 :

CH3(CH2)nCOOH (FATTY ACID) + ATP + CoA —> CH3(CH2)nCO~CoA (fatty acyl~CoA) + AMP + 2Pi

20
Q

How are fatty acyl~CoA transported

A

Activated fatty acids (fatty acyl~CoA) do not readily cross the inner mitochondrial membrane
thus
Carnitine shuttle transports fatty acyl~CoA across the mitochondrial membrane

21
Q

How does the Carnitine Shuttle work

A
  1. Acyl Coa is put on to the carnitine making it Acl Carnitine using Carnitine acyltransferases 1
  2. Carnitie shuttle swaps Acyl carnitine for carnitine across membrane
  3. Acyl transferred back on to the CoA again using
    Carnitine acyltransferases 2
22
Q

What does Carnitine acyltransferases do

A

Puts Acyl group onto Carnitine and helps move it across membrane

23
Q

How is Carnitine shuttle transport regulated

A
  • Regulated (AMP, insulin), so controls the rate of FA oxidation
  • CAT1 inhibited by malonyl~CoA (biosynthetic intermediate)
  • Defects can occur in this transport system (exercise intolerance, lipid droplets in muscle)
24
Q

Why is called Beta - Oxidation

A

As its the Beta Carbon that gets oxidised

25
Q

What is the final step of B-oxidation

A

CO.CH2.CO-CoA gets cleaved and and addition of CoA to form CO-CoA + CH3.CO-CoA

26
Q

What is ultimately produced by B-oxidation and what are they used for

A

β-oxidation ultimately generates acetyl CoA and reducing power.
These intermediates are used to generate ATP in stages 3 and 4 of catabolism

27
Q

Where does B-Oxidation occur

A

Most tissues and white blood cells
DOESNT OCCUR IN BRAIN as fatty acids can’t get though brain barrier
Doesn’t occur in RBC as there is no mitochondria

28
Q

Fatty acid and glycerol metabolism
(B-oxidation)
(8) - Key Points

A
  • Mitochondrial
  • Cycle of reactions
  • Removal of 2C units per cycle
  • β-carbon oxidation
  • H+ and e- transferred to NAD+ and FAD
  • Stops in absence of O2
  • Regulated by AMP (insulin – liver)
  • No direct ATP synthesis
29
Q

What happens to glycerol

A

Glycerol can be transported in the blood to the liver, where it is metabolised
By Glycerol kinase using ATP
forming
Glycerol phosphate

30
Q

What happens to Glycerol phosphate

A

There are two pathways

It can enter glycolysis, using
glycerol 3-phosphate dehydrogenase
It will create Dihydroxyacetone - P

or

It can be stored as Fat (triacylglycerol)
This requires fatty acids

31
Q

Where and How ketone bodies generated

A

The liver mitochondria constantly generates ketone bodies from acetyl CoA

Adipose tissue release fatty acids
liver sensors pick this up
Thus generates Ketone bodies

Produced when Acetyl CoA is in excess

32
Q

When is the production of ketone bodies higher

A

Production is much higher during fasting (and starvation)

33
Q

What are Kentone bodies used for

A
  • Used by peripheral tissues (muscle)
  • Alternative fuel to glucose
    (helps conserve glucose)
34
Q

Why is ketone bodies an important energy source

A

They are water soluble
(whilst fatty acids are NOT thus finite amount of fatty acids can be transported)
Thus provided more fuel molecules

35
Q

What is the pKA of kentones

What is Physiological ketosis

A

acidic – pKa ~4 (deporotonated) making blood ph more acidic
Blood becomes more acidic due to higher ketone conc

36
Q

What is the Normal Plasma ketone conc

A

Normal plasma ketone body concentration < 1 mM

37
Q

What is the Starvation, Ketones conc

A

Starvation 2-10 mM (physiological ketosis)

38
Q

What happens in untreated Type 1 diabetes

A

Untreated Type 1 diabetes > 10 mM (pathological ketosis)

39
Q

What are the steps in ketone production

A

1.Acetly CoA (CH3CO-CoA) is sythesised in to
2.Hydroxymethyl glutaryl-CoA. (HMG-CoA) which is lysed by the enzyme lyase in to
3. acetoacetate and β-hdroxybutyrate these are used as biological fuels

40
Q

What happens when Hydroxymethyl glutaryl-CoA.
(HMG-CoA) interacts with HMG-CoA
Reductase (staitin drug)

When the insulin/glucagon ratio is high

A

Mevalonate —> Cholesterol occurs when

When the insulin/glucagon ratio is high, i.e. fed state:
Lyase is inhibited+reductase activated –> cholesterol synthesis

41
Q

Control of Ketone body production in the liver

A

1.Triacyglycerols levels get high
2. Fatty acids levels thus rise
3. Low NAD+ substrate
4. High NADH
5. This inhibits the TCA cycle
6. Thus acetyl-CoA gets diverted to produce Ketone Bodies

42
Q

What happens to Acetoacetate

A

Acetoacetate -
Acetone-
Acetoacetate - (using Sunccinyl CoA) turns to
Acetoacetyl CoA - Then another CoA added to form
Acetyl CoA (x2)- which is used in the TCA cycle
Which is used to generate ATP

43
Q

What happens when the insulin/glucagon ratio is Low

A

When the insulin/glucagon ratio is Low, i.e. starvation state: Lyase is activated + reductase inhibited  ketone body

44
Q

What happens in Starvation / Diabetes

A

Ketone bodies gets used preferably rather than glucose
glucose only used by cells that need it eg brain

Diabetes this is uncontrolled
all systems switched on
blood glucose is very high
Ketone levels gets very high
no insulin generated
no brake mechanism
Kentone lavels build up
leads to Ketoacidosis / Ketosis
Blood Ph becomes acidic
Can damage brain
Leads to coma and can even Die

Given Insulin to bring all process back under control
lowers glucose and ketone levels.

45
Q

What Is the role of Acetyl CoA in metabolism

A

Its main function is to deliver the acetyl group to the citric acid cycle (Krebs cycle) to be oxidized for energy production.

MEH (13 decks)

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