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MEH Sem 1 > Lecture 5 - Energy Storage & Lipid Transport > Flashcards

Lecture 5 - Energy Storage & Lipid Transport Flashcards

1
Q

Desc. the diff major energy stores

A
  1. Muscle glycogen: converted to glucose –> glycolysis
    (no G-6-phosphatase)
  2. Liver glycogen: glucose –> blood
    (granules in cytoplasm)
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2
Q

Desc. glycogen structure and its functions

A
  • Has α-1,6 form branch points, α-1,4 join chains
  • Has osmotic effect: draw in H2O
  • Many branches: phosphorylated for energy
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3
Q

Desc. glycogenesis

A 
1. Glucose ---> G-6-P 
[Hexokinase, needs ATP]
2. G-6-P --> G-1-P
[Phosphoglucomutase] *catalyse both ways
3. G-1-P + UTP + H20 --> UDP-glucose 
[G1P-uridyltransferase, needs ATP]
4. Glycogen + UDP-glucose --> Glycogen 
[Glycogen Synthase/Branching enzyme]
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4
Q

Desc. glycogenolysis

A
  • Glycogen –> G-1-P
    [Glycogen Phosphorylase/De-branching enzyme]
  • G-1-P –> G-6-P
    [Phosphoglucomutase]
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5
Q

What occurs to G-6-P after formed in glycogenolysis in muscle & liver?

A
  • To muscle: Glycolysis for energy
    (lacks enzyme glucose-6-phosphatase)
  • To liver: G-6-P –> Glucose –> blood (buffer for plasma glucose)
    [Glucose-6-phosphatase]
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6
Q

What are some examples and causes of glycogen storage diseases? What happens when there is an excess/diminished glycogen storage?

A
  • Arise from deficiency of enzymes of glycogen metabolism
  • Excess: lead to tissue damage, Diminished: Hypoglycaemia & poor exercise tolerance
  • Von Gierke’s disease: Glucose-6-phosphatase deficiency
  • McArdle disease: muscle glycogen phosphorylase deficiency
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7
Q

What are the 3 major precursors to gluconeogenesis?

A
  1. Lactate
  2. Glycerol: From lipolysis
  3. A.a (alanine)
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8
Q

Desc. gluconeogenesis

A
  1. Glucogenic a.a & lactate –> pyruvate
  2. Pyruvate –> oxaloacetate
  3. Oxaloacetate –> phosphoenolpyruvate
    [PEPCK]
  4. Fructose -1,6-bisphosphate –> fructose-6-P
    [fructose-1,6-bisphosphatase] [reverse is PFK, phosphofructokinase]
  5. G-6-P –> Glucose
    [G-6-Phosphatase] [Reverse is glucokinase]
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9
Q

What regulates gluconeogenesis?

A
  • Fructose-1,6-bisphosphatase, PEPCK (Phosphoenolpyruvate carboxykinase)
  • Stimulate: glucagon, cortisol
  • Inhibit: Insulin
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10
Q

Why is TAGs efficient energy store?

A
  • Energy content higher than carbohydrate

- Utilise in prolonged exercise, stress, starvation

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11
Q

Desc. lipogenesis. (location, reaction, enzymes)

A
  • Occurs mainly in liver, require ATP & NADPH
  • Pyruvate enter mitochondria –> acetyl CoA & OAA –> citrate
  • Citrate leaves and goes to cytoplasm –> acetyl CoA & OAA
  • OAA recycled to form pyruvate again
  • Acetyl CoA –> Malonyl CoA
    [Acetyl-CoA carboxylase, require ATP]
  • Malonyl CoA –> F.A synthase complex (donate 2C) –> F.A
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12
Q

What is the key regulatory enzyme of lipogenesis? What regulates it?

A
  • Acetyl-CoA decarboxylase
  • ⬆️insulin and citrate
  • ⬇️glucagon/adrenaline & AMP
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13
Q

What is the difference between fatty acid synthesis and β-oxidation?

A

Synthesis

  1. Add 2C (added as malonyl CoA)
  2. Occurs in cytoplasm
  3. Require NADPH and ATP (large)
  4. Regulated by acetyl CoA decarboxylase
  5. Glucagon, adrenaline inhibit & insulin stimulate

β-oxidation

  1. Remove 2c (removed as acetyl CoA)
  2. Occurs in mitochondria
  3. Produces NADH & FADH2
  4. Require ATP (small amount) to activate FA
  5. Regulated indirectly by amount of FA
  6. Insulin inhibits
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14
Q

How lipids are transported in blood?

A
  • 2% bound to albumin, limited capacity (~3mmol/L)
  • 98% carried by:
    i) Chylomicrons: Transport TAG from liver to adipose tissue
    ii) VLDL: Transport TAG from liver to adipose tissue
    iii) IDL: Transport cholesterol from liver to adipose tissue. Short half life, precursor for LDL
    iv) LDL: Transport cholesterol from liver to tissue
    v) HDL: Transport excess cholesterol from tissue to liver for disposal as bile salts/give cholesterol to cells requiring add.
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15
Q

Where is cholesterol synthesised and what are its functions? What is it transported as in the blood?

A
  • Synthesised in liver
  • Component of membrane (modulate fluidity)
  • Synthesise steroid hormones (cortisol, aldosterone, oestrogen)
  • Transported as cholesterol ester
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16
Q

Desc. the structure of lipoproteins

A
  • Surface coat: phospholipid, cholesterol and apoproteins

- Hydrophobic core: TAG, cholesterol ester, ADEK

17
Q

Why does blood collected from a patient have a whitish-creamy appearance?

A
  • Chylomicrons give creamy appearance.

- Present 4-6hr after meal

18
Q

What is the function of apolipoproteins?

A
  • Co-factor for enzyme
  • Ligands for cell-surface receptor
  • Packaging water insol. lipid
19
Q

What is the function of lipoprotein lipase?

A
  • Hydrolyse TAG in chylomicrons and VLDL to FA & glycerol
  • ApoC-II cofactor
  • Found on surface of endothelial cells
20
Q

Why is LDL considered ‘bad cholesterol’?

A
  • Longer half life = more susceptible to oxidative damage
  • Do not have apoC or E = X efficiently cleared by liver
  • Macrophages engulf LDL –> foam cells accumulate in intima–> fatty streak –> atherosclerotic plaque –> invades lumen –> rupture –> thrombosis –> stroke/myocardial infarction
21
Q

How does LDL enter cell?

A
  • Cell has LDL receptors –> apoB on LDL act as ligand to receptors –> endocytosis –> fuse w lysosomes –> cholesterol, FA release
22
Q

Desc. reverse cholesterol transport in HDL

A
  • HDL remove cholesterol from cells –> liver
  • Reduces likelihood of foam cells and atherosclerotic plaque
  • ABCA1 protein facilitates transfer –> cholesterol converted to cholesterol ester by LCAT
23
Q

What happens to mature HDL?

A
  • Taken up by liver
  • Cells requiring additional cholesterol (steroid hormone synthesis) use scavenger receptor to obtain cholesterol from HDL
  • Exchange cholesterol ester for TAG w VLDL via cholesterol exchange transfer protein (CETP)
24
Q

What is the function of Lecithin: Cholesterol Acyltransferase (LCAT)? Deficiency results in?

A
  • Removal of core lipids from lipoprotein particles –> unstable due to ⬆️ratio of surface:core lipids
  • LCAT converts cholesterol –> c.ester –> stable
  • Deficiency: unstable lipoprotein –> failure lipid transport process
25
Q

What are some underlying causes of hyperlipoproteinemia?

A
  • Defective lipoprotein lipase (remove TAG from chylomicrons and VLDL)
  • Defective LDL receptor
  • Defective apoE –> raised IDL & chylomicron remnants
26
Q

What are some clinical signs of hypercholesterolaemia? (⬆️cholesterol in blood)

A
  • Xanthelasma: yellow patches on eyelids
  • Tendon Xanthoma: nodules on tendons
  • Corneal arcus: white circle around eye (common in old ppl, but if in young its hyper…)
27
Q

Suggest treatment for hyperlipoproteinaemia

A
  • 1st approach:
    i) Diet = reduced cholesterol, saturated lipids & ⬆️fibre)
  • fibre binds to bile salts –> excrete in faeces –> bile salts X recycled, more cholesterol removed
    ii) Lifestyle = ⬆️exercise, X smoke reduce cardiovascular risk
  • If X response, drugs:
    i) Statin = reduce cholesterol by inhibiting enzyme HMG- CoA reductase, e.g Atorvastatin
    ii) Bile salts sequestrants = bind bile salts in GI tract, more bile acid –> ⬆️cholesterol removed, e.g. Colestipol
28
Q

What are the ranges for ideal cholesterol in body?

A
  • Total cholesterol: HDL-C: if above 6 = high risk, the lower the better
  • TAG: <2mmol in fasted sample
29
Q

How do tissues obtain lipid needed?

A
  • TAG = chylomicrons and VLDLs
    lipoprotein lipase present on surface of cell–> hydrolyses TAG to FA & glycerol
  • (in cell) FA –> TAG
    [glycerol phosphate, from glucose metabolism]
  • Cholesterol = LDLs (receptor mediated endocytosis)
  • LDL particles bind to LDL receptors on the surface of target cells. Receptor & LDL —> cell (endocytosis) –> fuse with lysosome –> lysosomal enzyme –> release cholesterol & receptor protein destroyed
  • Cholesterol –> C. ester for storage
  • When the cell has enough cholesterol = synthesis of new LDL receptors and the uptake of cholesterol is reduced
30
Q

Desc. lipid metabolism

A
  • Cytoplasm: fatty acid activation
    FA –> FA acyl coA
    (fatty acyl coa synthase)
  • Enter via carnitine shuttle (controls rate of FA oxidation, inhibited by malonyl coA)
  • β-oxidation: Remove 2C every time, NADH & FADH2 formed
  • X ATP formed, needs O2

MEH Sem 1 (18 decks)

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