Lipids Flashcards by Aarav Patel

Lipid Structure Facts

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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Structure of fatty acids

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

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What are the types of lipids

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

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How are lipids stored

Triacylglycerol

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What is the structure of Triacylglycerol

Glycerol backbone attached to three fatty acids

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How are ketone bodies formed

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

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What is derived from Fatty Acids

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

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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What are the fat soluble vitamins

A, D, E and K.
derived from lipids

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Does Triacylglycerols Glycogen Muscle protein vary with heathy to obese people

Glycogen and Muscle protein remain constant

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

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What is Triacylglycerols derived from

Glycerol and Fatty acids in an esterification reaction

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What is Lipolysis

Triacylglycerols turning back in to Glycerol and fatty acids

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Function of Triacylglycerols,
Is it hydrophobic or hydrophilic

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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what is the benefit of Tricylglyerols being hydrophobic

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

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When and where does Metabolism of triacylglycerols occur

Stage 1
GI Tract (lumen) (Small interstine)
Extracellular

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

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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What is the colour when you disect the lymphatics

Looks milky due to the CHYLOMICRONS

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Fatty Acid Catabolism - Summary

FA is activated (by linking to coenzyme A outside the mitochondrion)
Transported across the inner mitochondrial membrane using a carnitine shuttle
FA cycles through sequences of oxidative reactions, with C2 removed each cycle

(C18 —> C16 + C2)

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How is fatty acid Activated

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

How are fatty acyl~CoA transported

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

How does the Carnitine Shuttle work

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

What does Carnitine acyltransferases do

Puts Acyl group onto Carnitine and helps move it across membrane

How is Carnitine shuttle transport regulated

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)

Why is called Beta - Oxidation

As its the Beta Carbon that gets oxidised

What is the final step of B-oxidation

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

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

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

Where does B-Oxidation occur

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

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

* 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

What happens to glycerol

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

What happens to Glycerol phosphate

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

Where and How ketone bodies generated

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

When is the production of ketone bodies higher

Production is much higher during fasting (and starvation)

What are Kentone bodies used for

* Used by peripheral tissues (muscle) * Alternative fuel to glucose (helps conserve glucose)

Why is ketone bodies an important energy source

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

What is the pKA of kentones What is Physiological ketosis

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

What is the Normal Plasma ketone conc

Normal plasma ketone body concentration < 1 mM

What is the Starvation, Ketones conc

Starvation 2-10 mM (physiological ketosis)

What happens in untreated Type 1 diabetes

Untreated Type 1 diabetes > 10 mM (pathological ketosis)

What are the steps in ketone production

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

What happens when Hydroxymethyl glutaryl-CoA. (HMG-CoA) interacts with HMG-CoA Reductase (staitin drug) When the insulin/glucagon ratio is high

Mevalonate ---> Cholesterol occurs when When the insulin/glucagon ratio is high, i.e. fed state: Lyase is inhibited+reductase activated --> cholesterol synthesis

Control of Ketone body production in the liver

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

What happens to Acetoacetate

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

What happens when the insulin/glucagon ratio is Low

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

What happens in Starvation / Diabetes

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.

What Is the role of Acetyl CoA in metabolism

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