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MEH > Energy production - Lipids > Flashcards

Energy production - Lipids Flashcards

1
Q

lipids

A
  • structurally diverse
  • generally insoluble in water (hydrophobic)
  • soluble in organic solvents
  • contain C, H, O (phospholipids contain P, N)
  • more reduced than carbohydrates so release more energy when oxidised
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2
Q

3 classes of lipids

A

fatty acid derivatives
- fatty acids - fuel molecules
- triacylglycerols - fuel storage and insulation
- phospholipids - membrnaes + lipoproteins
- eicosanoids - local mediators

hydroxy-methyl-glutaric acid derivatives
- ketone bodies (C6) - water soluble fuel molecules
- cholesterol (C27) - membranes + steroid hormones
- cholesterol esters - cholesterol storage
- bile acids and salts (C24) - lipid digestion

vitamins
- A
- D
- E
- K

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3
Q

triacylglycerols

A
  • major dietary and storage lipid
  • three fatty acids esterified to glycerol
  • hydrophobic
  • stored in anhydrous form
  • stored in highly specialised storage tissue - adipose
  • used in prolonged aerobic exercise, starvation, pregnancy
  • storage/mobilisation under hormonal control
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4
Q

hormonal control of storage of triacylglycerols

A

promoted by
- insulin

reduced by
- glucagon
- adrenaline
- cortisol
- growth hormone
- thyroxine

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5
Q

stage 1 metabolism of triacylglycerols

A
  • hydrolysed by pancreatic lipase in the small intestine to release glycerol and fatty acids
  • requires bile salts and protein factor called colipase
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6
Q

fatty acids

A
  • hydrophobic
  • highly reduced molecules
  • saturated or unsaturated
  • ideal for energy storage
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7
Q

fatty acid catabolism

A
  1. FA activated by linking to coenzyme A outside mitochondrion
  2. transported across innner mitochondrial membrane using carnitine shuttle
  3. FA cycles through sequences of oxidative reactions with C2 removed each time
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8
Q

why does β oxidation not occur in cells of central nervous system

A

fatty acids do not readily cross the blood-brain barrier

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9
Q

lipolysis

A
  • adipose tissue triacylglycerols hydrolysed by hormone-sensitive lipase
  • fatty acids and glycerol diffuse from tissue
  • when body subjected to stress situations
  • activated by adrenaline, glucagon, growth hormone, cortisol and thyroxine
  • inhibited by insulin
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10
Q

how are fatty acids transported

A

carried to tissues via blood stream bound non-covalently to albumin (called NEFA or FFA)

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11
Q

what happens to glycerol

A
  • transported in blood to liver
  • converted to glycerol phosphate by glycerol kinase and ATP
  • used to synthesise triacylglycerols or enters glycolysis
  • enters glycolysis by being converted to dihydroxyacetone phosphate (DHAP) by glycerol 3-phosphate dehydrogenase and NAD+
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12
Q

fatty acid activation

A
  • outside mitochondria, in cytoplasm
  • fatty acids link to coenzyme A by action of fatty acyl CoA synthase and ATP
  • forms high energy hydrolysis bond via the S-atom
  • CoA contains vitamin B5 and free -SH group
  • activated fatty acids do not readily cross inner mitochondrial membrane
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13
Q

fatty acid transport into mitochondria

A
  • carnitine shuttles exchange acyl carnitine for free carnitine using CAT 1/2 (carnitine acyltransferases) to transport fatty acyls across mitochondrial membrane which rejoin with CoA in matrix
  • important in regulating rate of FA oxidation
  • regulated by AMP and insulin
  • CAT1 inhibited by malonyl CoA, prevents newly synthesised fatty acids being immediately transported into mitochondria
  • defective transport system = poor exercise tolerance, lipid droplets in muscle cells
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14
Q

β oxidation of fatty acids

A
  • generates acetyl CoA and reducing power (NADH and FADH2)
  • fatty acid is oxidised and **C2 unit (acetate) is removed **
  • shortened fatty acid is cycled, repeatedly removing C2 until 2 carbons remain
  • requires mitochondrial NAD+, FAD+ and oxygen (re-oxidise NADH and FADH2)
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15
Q

acetyl CoA

A
  • produced by catabolism of fatty acids, sugars, alcohol and amino acids
  • oxidised via stage 3 catabolism (Kreb’s cycle)
  • important intermediate in lipid biosynthesis
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16
Q

what are the 3 ketone bodies produced in the body

A
  • acetoacetate (in liver from acetyl Co-A)
  • β-hydroxybutyrate (in liver from acetyl Co-A)
  • acetone (spontaneous decarboxylation of acetoacetate)
17
Q

plasma concentrations of ketone bodies

A
  • normal <1mmol/L
  • starvation 2-10mmol/L (physiological ketosis)
  • untreated type 1 diabetes >10mmol/L (pathological ketosis)
18
Q

ketonuria

A

excretion of ketone bodies in urine

19
Q

properties of ketone bodies

A
  • water-soluble - allows high plasma concentrations and ketonuria
  • high concentrations of acetoacetate and β-hydroxybtyrate cause ketoacidosis
  • acetone is volatile and excreted through lungs (smell of acetone on breath of untreated type 1 diabetics)
20
Q

where are ketone bodies synthesised

A

liver mitochondria by actions of lyase and reductase enzymes that are reciprocally controlled by insulin/glucagon ratio

21
Q

ketone body synthesis pathway

A
  • acetyl Co-A
  • HMG-CoA (synthase)
  • acetoacetate (lyase)
  • β-hydroxybutyrate or acetone
22
Q

how do statins reduce cholesterol

A

they act as HMG-CoA reductase inhibitors so cholesterol can’t be formed from acetyl Co-A

23
Q

ketone body synthesis when insulin/glucagon ratio is high (fed)

A
  • lyase inhibited
  • reductase activated
  • cholesterol synthesis occurs
24
Q

ketone body synthesis when insulin/glucagon ratio is low (starvation)

A
  • lyase activated
  • reductase inhibited
  • ketone body synthesis occurs (ketogenesis)
25
Q

2 things the synthesis of ketone bodies requires

A
  • availability of fatty acids from excess lipolysis in adipose tissue to provide substrate by oxidation in the liver (excess acetyl Co-A)
  • low plasma insulin/glucagon ratio to activate lyase and inhibit reductase
26
Q

control of ketone body production in liver

A
  • high levels of triacylglycerols so conversion to acetyl Co-A uses up NAD+
  • low NAD+ inhibits TCA cycle (isocitrate dehydrogenase and α-ketoglutarate dehydrogenase)
  • acetyl Co-A diverted from TCA cycle to ketogenesis
27
Q

why are ketone bodies produced

A
  • important fuel molecules that can be used by all tissues containing mitochondria including the CNS
  • alternative fuel to glucose so way of conserving glucose in starvation/diabetes
28
Q

metabolism of ketone bodies

A
  • synthesised in the liver
  • transported in blood
  • acetone excreted through lungs
  • acetoacetate and β-hydroxybutyrate converted back to acetyl Co-A in muscle
  • acetyl Co-A enters TCA cycle
29
Q

amphipathic fatty acids

A

contain hydrophobic and hydrophilic groups

MEH (26 decks)

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