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principles of normal function > week 3 lipids (revised) > Flashcards

week 3 lipids (revised) Flashcards

1
Q

what are 5 the major lipid classes

A
  • fatty acids
  • triacylglycerols
  • phospholipid
  • glycolipid
  • steroids
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2
Q

what kind of fatty acids are “good fats”

A
  • high in polyunsaturated fatty acids
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3
Q

what kind of fatty acids are “bad fats”

A
  • high in saturated fatty acids e.g. beef

- have a role in myelination and hormone production, important in maintaining health

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4
Q

what kind of fatty acids are “really bad fats”

A
  • trans unsaturated fatty acids

- result from hydrogenation of veg. oils e.g. margarine (man-made)

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5
Q

what are essential fatty acids

A
  • linoleic and alpha linoleic acids

- ones that you cannot make, must get them from diet

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6
Q

what can you make from linoleic acid (essential fatty acid)

A
  • arachidonic acid is a precursor of Eicosanoids and can be made from linoleic acid
  • omega 3 fatty acids derived from linoleic acids (lowers cholesterol and prevents atherosclerosis, lowers triacylglycerols, prevents obesity, reduces inflammation)
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7
Q

with happens if you have an essential acid deficiency

A
  • rare, most often in infants with diets deficient in EFA
  • signs are scaly dermatitis, alopecia, in children intellectual disability
  • ADHD = lower levels of omega 3
  • chronic intestinal disorders
  • depression = deficiency of lipid signalling molecules
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8
Q

what are triacylglycerols

A
  • major class of lipid
  • esters of fatty acids and glycerol (esters are neutral uncharged lipids)
  • water insoluble
  • dietary fuel and insulation
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9
Q

what are phospholipids

A
  • major class of lipids
  • glycerol bound to two fatty acids and a phosphate group
  • amphipathic (hydrophobic and hydrophilic)
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10
Q

what is the main site of digestion of lipids

A

small intestine

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11
Q

what is lipid digestion promoted by

A
  • lipid digestion by pancreatic enzymes (lipases) is promoted by emulsification by bile salts and peristalsis (mixing)
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12
Q

what are bile salts

A
  • act as biological detergents to form emulsions and mixed micelles
  • stop lipids grouping together in aqueous environment
  • derivatives of cholesterol
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13
Q

how are triacylglycerols digested

A
  • most TAG are degraded in small intestine by pancreatic lipase to monoacylglycrol and 2 fatty acids
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14
Q

how are cholesterol esters and phospholipids digested

A
  • cholesterol esters digested to cholesterol and free fatty acid
  • phospholipids hydrolysed to fatty acid and lysophospholipid
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15
Q

what is the uptake of digested lipids

A
  • products of lipid digestion form mixed micelles with bile salts
  • mixed micelles approach the border of the enterocytes (intestinal cells) and release lipid products which enter cells by diffusion
  • short and medium chain fatty acids do not require micelles for absorption
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16
Q

what is steatorrhea

A
  • excess fat in faeces
  • due to lipid malabsorption (defects in bile secretion, pancreatic function, or intestinal cell uptake, removal of gallbladder)
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17
Q

what happens to absorbed fatty acids

A
  • intestinal cells resynthesise TAG, phospholipids and cholesterol esters for export
  • insoluble so packaged into chylomicrons for export
  • chylomicrons released by exocytosis into lymph then blood
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18
Q

what happens when blood chylomicrons reach tissue

A
  • TAG in chylomicrons is hydrolysed to fatty acid and glycerol by lipoprotein lipase
  • resulting free fatty acid used for energy or re-esterified to TAG for storage
  • chylomicrons depleted of TAG are called chylomicron remnants and go to liver
  • glycerol used by liver to produce glycerol-3-phosphate (glycolysis and gluconeogenesis)
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19
Q

what is the digestion of fats

A
  • fats ingested
  • bile salts emulsify fats in small intestine forming mixed micelles
  • intestinal lipases degrade TAG
  • fatty acids and breakdown products taken up by intestinal mucosa and converted into TAG
  • TAG + cholesterol + apolipoproteins packaged into chylomicrons
  • chylomicrons move through lymphatics first then blood
  • lipoprotein lipase in capillary converts TAG to fatty acids and glycerol
  • fatty acids enter cell
  • fatty acids oxidised as fuel or re-esterified to TAG for storage
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20
Q

how are fatty acids released from stored TAG in adipose tissue

A
  • by hormone sensitive lipase (HSL)
  • HSL activated by phosphorylation in response to epinephrine
  • high plasma glucose and insulin promote desphosphorylation (inactivation) of lipase
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21
Q

how are fatty acids transported in the blood

A
  • free fatty acids transported in complex with serum albumin (plasma protein)
  • most fatty acids are esterified and carried in lipoproteins
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22
Q

what do lipoproteins transport

A
  • TAGs

- cholesterol esters

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23
Q

what are the classes of lipoprotein in order of least dense to most dense

A
  • chylomicrons (transport TAG from intestine to tissues)
  • VLDL (transports TAG from liver to tissues
  • LDL (transports cholesterol to extra hepatic tissues) :(
  • HDL (transports cholesterol from tissue to liver for elimination) :)
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24
Q

what is beta oxidation of fatty acids

A
  • occurs in mitochondrial matrix of tissues
  • degrades fatty acids two carbons at a time
  • produces acetyl coA, NADH and FADH which are sources of energy
25
Q

what are the three stages of beta oxidation of fatty acids

A
  • activation (of fatty acids in cytosol)
  • transport (into the mitochondria)
  • degradation (4 stages, degrade two carbons at a time as acetyl coA)
26
Q

where are fatty acids activated

A
  • cytosol
27
Q

how are fatty acids transported from cytosol to matrix for beta oxidation

A
  • carnitine shuttle
  • fatty acids becomes fatty acyl coA (via phosphorylation by ATP)
  • fatty acyl coA diffuses across outer mitochondrial membrane
  • coA diffuses across inner mitochondrial membrane and carnitine transports acyl across in the from acyl carnitine
  • enzyme on outer mitochondrial membrane is carnitine palmitoyl transferase 1
  • enzyme on inner mitochondrial membrane is carnitine palmitoyl transferase 2
28
Q

what is carnitine palmitoyl transferase inhibited by

A
  • malonyl coA (prevents degradation and synthesis happening simultaneously)
29
Q

wha happens if you have a carnitine palmitoyl transferase deficiency

A
  • no beta oxidation, hypoglycaemia
  • improved with IV glucose
  • therapy = give medium chain fatty acids, these do not require the enzyme for transport
30
Q

what are the four steps of beta oxidation of fatty acids

A
  1. dehydration (AKA oxidation) of FAD > FADH2
  2. hydration (requires H2O)
  3. dehydration of NAD > NADH
  4. thiolysis to produce acetyl coA
31
Q

what is the end result of one round of beta oxidation

A
  • FADH2
  • NADH
  • acetyl coA
  • fatty acids 2 carbon shorter than when it started (2 carbons = acetyl coA)
32
Q

what is beta oxidation in peroxisome

A
  • very long chain fatty acids >22 carbons undergo preliminary beta oxidation in peroxisomes
  • does not produce FADH2 so less energy efficient
  • shortened fatty acid linked to carnitine diffuses from peroxisome into mitochondria for further oxidation
33
Q

why can animals not convert fatty acid into glucose

A
  • due to irreversible step of pyruvate > acetyl coA, via pyruvate dehydrogenase
34
Q

what inhibits pyruvate dehydrogenase

A
  • acetyl coA
35
Q

what does pyruvate carboxylase do

A
  • pyruvate > oxaloacetate

- inhibited by acetyl coA

36
Q

since fatty acid cannot be converted into glucose, how do we get energy when desperately need it and no glucose

A
  • ketone bodies

- fuel molecules

37
Q

when do you get ketone bodies

A
  • during starvation/fasting, glucose is decreased and excess acetyl coA from fat metabolism can be converted into ketone bodies
  • cardiac and skeletal muscle use ketone bodies as energy source
  • brain can use ketone bodies during starvation (brain cannot use fatty acid as fuel source)
38
Q

where are ketone bodies formed

A
  • liver (mitochondrial matrix), liver cannot use them though
  • transported with blood to other cells where it is used as fuel, soluble so don’t need to be carried
  • ketones: acetone, D-B hydroxybutyrate, acetoacetate)
39
Q

how do you end up with excess ketone bodies and what happens

A
  • uncontrolled diabetes (or starvation) leads to very high levels of ketone body concentration in blood
  • ketonuria (KB in urine)
  • ketonaemia (KB in blood)
  • academia
  • fruity odour to breath due to acetone
  • diabetic ketosis results when insulin is absent
40
Q

where do we get fatty acids from

A
  • diet (essential fatty acids)

- synthesis (from excess carbohydrates, fat and protein components (acetyl coA))

41
Q

where does FA synthesis occur

A
  • liver (cytosol)
  • lactating mammary gland
  • (adipose tissue)
42
Q

what are fatty acids synthesised from

A
  • acetyl coA

- uses NADPH and ATP

43
Q

why does acetyl coA have to be transferred across the membrane in fatty acid synthesis

A
  • acetyl coA formed in mitochondrial matrix so needs to be transferred to cytosol (site of FA synthesis)
44
Q

how is acetyl coA transported from the mitochondria to the cytosol for fatty acid synthesis

A
  • citrate shuffle

- occurs when concentration in mitochondria is high

45
Q

how does the citrate shuffle work

A
  • citrate transfers acetyl coA across the membrane through a protein
  • (mitochondria) pyruvate > oxaloacetate > citrate in mitochondria(carries acetyl coA across) > (cytosol) citrate (drops acetyl coA off in cytosol) > oxaloacetate >(NADH used here) malate > (NADPH produced in this reaction) pyruvate (pyruvate goes back across membrane to mitochondria)
46
Q

what does fatty acid synthesis need

A

enzymes
- acetyl coA carboxylase (activation/regulation)
- fatty acid synthase (multifunctional enzyme)
needs:
- acetyl coA
- NADPH (P!!!!)

  • product is palmitic acid
47
Q

what is acetyl coA carboxylase (ACC) needed for in fatty acid synthesis

A
  • needed for formation of malonyl coA (activation step)
  • ACC is key regulatory enzyme (activated by citrate - signals there is enough glucose so make FA), also activated by insulin
  • ACC deactivated by palmitoyl coA (enough FA made so halt synthesis), also deactivated by glucagon and epinephrine
48
Q

what are the 4 steps in fatty acid synthesis

A
  1. elongation (acyl-malonyl ACP condensing enzyme forms acetoacetyl-ACP, ACP=acyl carrier protein)
  2. reduction
  3. dehydration
  4. reduction
  • elongation cycle is repeated 6x more using malonyl coA each time to produce palmityl ACP
  • a thioesterase then cleaves the palmityl-coA from the ACP (acyl carrier protein)
49
Q

what is multifunctional fatty acid synthase

A
  • complex of 7 enzymes

- has role in fatty acid synthesis

50
Q

what is the fate of fatty acid

A

in order

  • acetyl coA
  • (liver) fatty acid
  • TAG
  • VLDL
  • adipose tissue
51
Q

does fatty acid degradation and synthesis run at the same time

A
  • no
52
Q

what are steroids

A
  • major class of lipids

- contain ring system

53
Q

what are the three classes of steroids

A
  • cholesterol (starting material for the synthesis of bile salts, steroid hormones and other components)
  • steroid hormones (chemical messengers e.g. corticosteroids)
  • bile salts (sodium salts of steroids used for emulsification)
54
Q

what is cholesterols

A
  • class of steroid
  • component of cell membranes
  • precursor to other substances (steroid hormones, vitamin D, bile acids)
55
Q

where is cholesterol made

A
  • mainly in liver

- only found in food substances e.g. milk, meat

56
Q

what are statins

A
  • inhibit HMG-CoA reductase that is essential in cholesterol synthesis
  • lowers LDL levels
  • lowers risk of cardiovascular disease
57
Q

what are Eicosanoids

A
  • lipid class derived from 20 carbon unsaturated fatty acids and synthesised throughout body
  • signalling molecule derived from omega 3 or 6 fatty acids
  • precursors to prostaglandins, thromboxanes and leukotrienes
  • short half life (metabolised rapidly), produced and act locally
58
Q

what do Eicosanoids regulate

A
  • inflammatory response
  • pain and fever (prostaglandins)
  • blood clotting induction/platelet homeostasis (thromboxane)
  • blood pressure regulation (prostacyclin)
  • many reproductive functions (e.g. labour induction, menstrual cramps, sperm mobility - prostaglandins)
  • smooth muscle construction and bronchoconstriction (leukotrienes)
  • mucous production in stomach (prostaglandins)

principles of normal function (15 decks)

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