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Science For Medicine Jess > Lipids > Flashcards

Lipids Flashcards

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1
Q

What is b-oxidation? Where does it occur? What are the products? What happens?

A

The degradation of Fatty Acids to produce energy. The mitochondrial matrix. Produces acetyl coA, NADH and FADH2 (ATP). 3 steps: ACTIVATION - FA to fatty acyl CoA in cytosol (uses ATP). TRANSPORTATION - Carnitine shuttle takes long chains into mitochondrial matrix. DEGRADATION (4 steps) - produces FADH2. NADH and ACETYL CoA.

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2
Q

What is the carnitine shuttle?

A

(CAT-1/2) Takes long chain FA from cytosol to mitochondrial matrix (activation step in b-oxidation). Removes CoA from fatty acyl CoA to make fatty acyl cartnitine to shuttle across. Then carnitine is removed again once mitochondrial matrix is reached. replaced by coA. Carnitine shuttled back again. Short chains do not require. Carnitine from diet/ made from lysine. From meat - lots of body builders use.

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3
Q

What is malonyl CoA?

A

A regulatory molecule that can stop b-oxidation.

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4
Q

What happens when no b-oxidation?

A

CAT-1 (in liver) deficiency, hypoglycaemia (low glucose) can lead to coma. Pressure on using glucose through glucogenesis. CAT-2 (in muscle) deficiency, avoid strenuous exercise.

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5
Q

Long chain fatty acids in b-oxidation? Problems?

A

Undergo preliminary b-oxidation in peroxisomes. Broken down to shorter FA chains. Carnitine shuttle. Defects result in long FA chain accumulation in blood and tissue.

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6
Q

Why cant you convert fatty acids to glucose?

A

Thermodynamically impossible - acetyl coA cannot go to pyruvate (irreversible).

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7
Q

Ketosis - what is happening?

A

When ketone body production >utilisation. Starvation/ uncontrolled diabetes - lots of FAs being broken down. Increased gluconeogenesis (oxaloacetate converting to pyruvate) so excess acetyl CoA (normally would react with oxaloacetate to enter citric acid cycle). Excess Acetyl coA forms ketone bodies. Stereotypical fruity odour on breath (acetone). Ph of body decreases.

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8
Q

What are ketone bodies? How are they used? Where are they produced?

A

Ketone bodies are formed in the liver, but cannot be used by the liver (need FAs and glycerol). Cardiac and skeletal muscle use ketone bodies as energy source. Can be good in moderation.

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9
Q

What does(n’t) the brain use for energy?

A

Cannot use FAs. But can use ketone bodies when starving.

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10
Q

FA synthesis location?

A

Cytosol! Mainly in liver , lactating gland (milk), adipose tissue.

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11
Q

FA degradation location?

A

Mitochondrial matrix

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12
Q

ATP net yield per b-oxidation cycle?

A

FADH2 - 2ATP
NADH - 3ATP
Acetyl-CoA - 12 ATP
total = 131

HOWEVER, 2 ATP neded for palmitoyl coA= 129 ATP

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13
Q

Fatty acid synthesis - What are the enzymes, what does it ‘need’, what is the reactant/ product?

A

Acetyl CoA from excess proteins, carbohydrates and fats, (in mitochondria), becomes citrate, which is shuttled into the cytosol using the CITRATE SHUTTLE. Enzymes: Acetyl CoA, fatty acid synthase. Needs: Acetyl CoA and NADPH. Product: Palmitic acid.

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14
Q

What is the citrate shuttle? When and where does it occur? What does it produce?

A

Occurs when citrate concentration of mitochondria is high. Acetyl CoA transforms to citrate, which is then shuttled to the cytosol, which either turns back to acetyl CoA, or to oxaloacetate. Oxaloacetate acted on to produce pyruvate, which is then shuttled back to mitochondria to again convert to oxaloacetate. NADPH produced.

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15
Q

What process produces palmitic/palmitate acid?

A

Fatty acid synthesis. Acetyl CoA to malonyl CoA to This is the basic fatty acid. It then changes from there.

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16
Q

Where does the NADPH needed for the synthesis of palmitic acid come from?

A

Some from the pentose-phosphate pathway and some from the citrate shuttle.

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17
Q

What are the fates of fatty acids once synthesised?

A

Transported to tissues in VLDL, stored as energy in adipose tissue.

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18
Q

What is malonyl coA?

A

Intermediate between acetyl coA and palmitic acid (fatty acid synthesis). Binds carbons onto it (synthesis).

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19
Q

What can inhibit b-oxidation?

A

High levels of malonyl coA.

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20
Q

What are steroids?

A

Major class of LIPIDS, chemicals that serve as chemical messengers. Have a ring structure.

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21
Q

What is cholesterol? Where is it made? What can it form?

A

Class of LIPIDS. Starting material for STEROID synthesis. Made in liver. Can form bile salts, plasma lipoproteins, vitamin D, steroid hormones.

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22
Q

What do statins do?

A

Inhibit synthesis of cholesterol, lowering LDL levels, which lessens the risk of developing CVD.

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23
Q

What is LDL?

A

A lipoprotein. Carries ‘bad’ cholesterol to tissues. Too much leads to atherosclerosis (clogging of arteries).

24
Q

What are thromboxanes, prostaglandins and leukotrienes? What do they do?

A

Types of EICOSANOIDS, which are LIPIDS. Regulatory molecules. inflammatory responses, pain and fever (PROSTAGLANDINS), blood pressure, blood-clotting induction (THROMBOXANE-take aspirin), reproductive functions (PROSTAGLANDINS), sleep/wake cycle.

25
Q

What does a leukotriene antagonist help?

A

Asthma.

26
Q

What is a COX inhibitor?

A

Inhibits prostaglandins that cause inflammation and thromboxanes that causes clotting.

27
Q

What do thromboxanes do?

A

Cause blood-clotting.

28
Q

What do prostaglandins do?

A

Regulate pain and fever.

29
Q

What do leukotrienes do?

A

Cause inflammation. Problem in asthma.

30
Q

What are classes of lipids?

A

Fatty acids, triacylglycerol, phospholipids, glycolipids, steroids.

31
Q

What are lipids?

A

water-insoluble molecules, functions include hormones, enzyme cofactors, structural elements of membranes, stored forms of energy.

32
Q

What is TAG? Where does it come from? What does it do?

A

Esterified fatty acid - triacylglycerol. Made up of 3 fatty acid chains, and 1 glycerol. Main fuel source from diet, stored in adipose tissue, used for fuel and insulation.

33
Q

What are phospholipids?

A

structural components of membranes, amphipathic (hydrophobic tail, hydrophilic head)

34
Q

What are essential fatty acids?

A

Fatty acids which the body cannot synthesise - we must get them from plants. Eg Linoleic acid.

35
Q

What are ‘good’ fats?

A

Fats high in polyunsaturated fatty acids (double bonds) including veg oils, sunflower oil etc.

36
Q

What are ‘bad’ fats?

A

Fats high in saturated fatty acids (single bonds) eg beef.

37
Q

Importance of saturated fats?

A

Huge role in mylenation of nerve fibres and hormone production.

38
Q

What are ‘really bad’ fats?

A

Trans fatty acids- from hydrogenation of veg oils eg margarine.

39
Q

What are omega fatty acids?

A

Types of essential FAs, derived from linoleic acid. 3 and 6.

40
Q

What are the benefits of omega 3 FA?

A

lowers plasma cholesterol, resolves inflammation. Omega 6 does not have these benefits. Can affect depression and behavioural issues.

41
Q

What are the dietary lipids?

A

TAG, phospholipids, cholesterol, free FAs.

42
Q

What is the main site of lipid digestion?

A

Small intestine.

43
Q

Outline the steps of lipid digestion?

A

Lipase enzymes break up the lipid, followed by emulsification and peristalsis (mixing) by bile salts. TAG degraded by lipase to from glycerol and 2 FAs. Bile salts and products form mixed micelles. Micelles transports FA into cell, TAG resynthesized, packaged with soluble protein to form CHYLOMICRON, which are released by exocytosis into lymph then to blood. turned back to FA and glycerol. Free FAs used for energy or re-esterified into TAG for storage. Glycerol used by liver to produce G-3-P for glycolysis and gluconeogenesis.

44
Q

What makes bile salts? What do they do?

A

Cholesterol. Form micelles to transport long FAa into cells.

45
Q

What are chylomicrons?

A

insoluble TAG coupled with soluble protein to transport into lymph.

46
Q

What does lipoprotein lipase do?

A

TAG in chylomicrons hydrolysed to FA and glycerol.

47
Q

Free FA fate after reached tissue?

A

re-esterified to TAG for storage OR released as energy.

48
Q

Glycerol fate after reached tissue

A

Goes to liver to produce G-3-P to enter glycolysis and gluconeogenesis.

49
Q

When are FAs used as an energy source?

A

When energy supply is low. Brain cannot use FAs directly.

50
Q

How are free FAs transported in the blood?

A

Plasma protein serum albumin, carried in lipoproteins.

51
Q

What do lipoproteins transport in the blood?

A

TAGS and cholesterol esters (insoluble). egs include chylomicrons, VLDL, LDL, HDL

52
Q

What is atherosclerosis?

A

Too much LDL.

53
Q

What is HDL?

A

A lipoprotein. Removes cholesterol from tissue, takes it to the liver.

54
Q

Why can FAs not be converted to glucose?

A

As pyruvate to acetyl coA, in glycolysis, is irreversible. So acetyl coA cannot then produce pyruvate.

55
Q

What does liver mitochondria do to excess acetyl coA?

A

creates water-soluble ketone bodies.

Science For Medicine Jess (28 decks)

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