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Gastrointestinal biology > Post Absorption Processing of Lipids. > Flashcards

Post Absorption Processing of Lipids. Flashcards

1
Q

List the steps in lipid metabolism.

A
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2
Q

What are features of Triglycerides?

A
  • Fatty-acids (95%) and glycerol (5%).
  • The principal storage form of energy in the body.
  • Too large & hydrophobic to move about freely in the circulation.
  • Transported in lipoprotein particles.
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3
Q

How is fat absorbed following digestion?

A
  • As 2-monoacylglycerol and free FAs.
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4
Q

What activates FAs?

A
  • Activated by Acyl-CoA Synthetase to acyl-CoA in the ER of intestinal mucosal cells.
  • Triglycerides are then re-synthesised from Acyl-CoA and 2-monoacylglycerol within the enterocyte.
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5
Q

What happens to the TGs after synthesis?

A
  • TGs are then incorporated into Chylomicron particles (98/99% lipids & 1-2% proteins).
  • Proteins synthesised at the Rough ER with the lipids added in the smooth ER & Golgi Complex.
  • The secretory pathway releases them into the
    extracellular space as small fat droplets.
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6
Q

How are lipid droplets transported?

A
  • They’re collected by local lymph ducts and are
    transported via the thoracic duct to the left
    brachycephalic vein.
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7
Q

What type of bond is in lipids?

A
  • An ester bond forms when a hydroxyl (-OH) group from the glycerol bonds with the carboxyl (-COOH) group of the fatty acid.
  • Monoacylglycerol: glycerol linked to a fatty acid via an ester bond.
  • Triacylglycerol: an ester derived from glycerol and three fatty acids.
  • Cholesteryl ester: ester bond formed between the carboxylate group of a fatty acid and the hydroxyl group of cholesterol.
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8
Q

What enzyme is needed for TGs use in tissues?

A
  • Lipoprotein Lipase (LPL) is needed.
  • Found in: adipose tissue, skeletal muscle,
    myocardium, mammary gland, spleen, lung, kidney & aorta.
  • Not found in: liver or brain.
  • LPL is attached to heparan sulphate glycoproteins on surface of the capillary endothelium.
  • Different LPL isoenzymes are found in different tissues
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9
Q

What isoform of LPL is up-regulated by insulin?

A
  • Adipose tissue LPL isoform.
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10
Q

What is the effect of different LPL isoenzymes on different tissues?

A
  • Going from fed state to fasting, TGs are rerouted from adipose tissue to muscle.
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11
Q

How are TGs used in tissue?

A
  • Chylomicrons bind to LPL and the TGs are hydrolysed.
  • FAs and monoglycerides diffusing into the tissues directly.
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12
Q

Discuss glycerol-3-phosphate formation.

A
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13
Q

Discuss TG formation from glycerol-3-phosphate.

A
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14
Q

What are the sites of the biosynthetic pathways of TGs?

A
  • Liver.
  • Adipose tissue.
  • Lactating Mammary glands.
  • Different from intestinal pathway (assembled in chylomicrons within enterocyte)!
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15
Q

Discuss the hormonal regulation of TG metabolism in adipose tissue.

A
  • Fat synthesis is stimulated by Insulin:
    1. Insulin increases the rate of glycolysis.
    2. Insulin increases LPL activity (releases FAs from chylomicron.
    3. Insulin induces the Glycerolphosphate-acyl transferase which catalyses the first step in TG
    biosynthesis.
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16
Q

How does insulin increase the rate of glycolysis?

A
  • Increases the number of glucose transporters in
    the adipocyte membrane.
  • Increases PFK1 activity via fructose 2,6 bisphosphate.
  • More glycerol-3-phosphate is produced.
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17
Q

Discuss lipolysis/ TG breakdown.

A
  • Requires the stepwise removal of 3 FAs.
  • The first cleavage, the rate-limiting step*, is catalysed by: adipose tissue lipase (Hormone-sensitive).
  • This enzyme catalyses the hydrolysis of TAG to diacylglycerol.
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18
Q

What hormone inhibits adipose tissue lipase and what activates it?

A
  • Insulin
  • Removal of insulin activates it.
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19
Q

When is lipase active?

A
  • When phosphorylated via the action of: cAMP-dependent Protein Kinase A (PKA)
20
Q

What hormone activates PKA pathway?

A
  • Glucagon.
    *The same enzyme acts in the regulation of
    glycogen metabolism.
21
Q

What are lipolytic agents? Give examples.

A
  • Cause cleavage of fats into fatty acids and glycerol.
  • E.g. Catecholamines: Noradrenaline & Adrenaline.
22
Q

How does noradrenaline trigger lipolysis?

A
  • Noradrenaline is released from sympathetic nerve termini in adipose tissue to trigger lipolysis.
  • It acts via a-adrenergic receptors, cAMP & Protein
    Kinase A to promote TG breakdown.
23
Q

What are other lipolytic hormones?

A
  • Glucocorticoids.
  • Growth Hormone.
  • Thyroid Hormones.
24
Q

How do lipolytic hormones act?

A
  • By inducing the synthesis of lipolytic proteins including the hormone-sensitive lipase.
  • These ^ the lipolytic response of adipose tissue to catecholamine release.
25
Q

Compare TG synthesis vs breakdown.

A
  • Antagonism between insulin and lipolytic hormones.
  • Adipose tissue is very sensitive to Insulin, so TGs are synthesised after a meal and degraded in fasting.
  • The SNS ensures that TGs are hydrolysed in response to cold exposure, stress and physical exercise.
    *HSL-hormone sensitive lipase.
26
Q

How are TG breakdown products mobilised?

A
  1. Adipose tissue releases free (unesterified) FAs.
  2. Free FAs bind reversibly to Serum Albumin for
    transport to distant sites.
    *Rapid turnover- 3 mins.
27
Q

How do adipocytes synthesise glucose from glycerol?

A
  • Adipocytes lack glycerol kinase and cannot synthesise glucose from glycerol.
  • Therefore glycerol is released into circulation and is taken up by the liver for the synthesis of glucose.
28
Q

Where des B oxidation happen?

A
  • In the mitochondrion.
29
Q

How is FAs transported into mitochondrion?

A
  • Shorter FAs enter by passive diffusion.
  • Longer FAs (>12 carbons atoms) are converted to their CoA-thioesters by Fatty Acyl CoA Synthetase (Thiokinase).
  • These are transported by Carnitine.
30
Q

What is Carnitine?

A
  • A specialised carrier that transports the acyl (FA) group across the membrane.
  • Known as Carnitine Shuttle:
    1. Carnitine Palmitoyltransferase (CPT) I & II.
    2. Carnitine-acylcarnitine translocase.
31
Q

Can FA synthesis and -oxidation happen
at the same time?

A
  • No.
  • Malonyl-CoA, the first intermediate in FA biosynthesis in the cytosol, inhibits CPT-I.
32
Q

Describe the process of B oxidation.

A
  • A cyclic reaction
  • Each cycle removes two carbons from the FA as acetyl-CoA.
  • Each cycle produces 1 NADH+H+ and 1 FADH2.
  • It is the -carbon (i.e. carbon 3) which is oxidised each time, hence the name.
33
Q

List the enzymes involved in B oxidation.

A
  1. Acyl-CoA dehydrogenase.
    - Deficiencies: Long chain (LCAD), medium chain (MCAD) and short chain (SCAD).
  2. Enoyl-CoA dehydratase.
  3. 3-L-hydroxyacyl-CoA dehydrogenase.
  4. B-ketothiolase.
34
Q

How does B oxidation produce energy (ATP)?

A
  • FADH2 and NADH feed ‘reducing equivalents’ into ETC.
  • Acetyl-CoA can go through the TCA Cycle= Oxidative Phosphorylation or used in biosynthetic reactions.
35
Q

Is Acetyl coA a substrate for Gluconeogenesis?

A
  • No.
  • But it is a positive allosteric regulator of pyr carboxylase stimulating oxaloacetate production.
36
Q

What are the energy yield of one mole of palmitic acid?

A
  • 129 moles of ATP (~ 40% efficiency).
37
Q

How is B oxidation regulated?

A
  • By the supply of free FAs.
  • Metabolism of FAs by tissues is proportional to plasma free FA level & thus responds to the activity of HSL.
38
Q

How is FA oxidation inhibited during FA synthesis?

A
  • Carnitine-palmitoyl transferase is allosterically
    inhibited by Malonyl-CoA.
39
Q

List ketone bodies.

A
  • Acetoacetate.
  • B -hydroxybutyrate.
  • Acetone.
40
Q

Where are ketone bodies formed?

A
  • Acetoacetate & B-hydroxybutyrate are formed from AcetylCoA in liver mitochondria only = the process of Ketogenesis.
  • Acetone is formed in small amounts by spontaneous decarboxylation of acetoacetate.
41
Q

What is the function of ketone bodies?

A
  • They are released from the liver into the blood are a major energy source for other tissues (ultimately enter TCA cycle as AcetylCoA).
  • Particularly important in heart, adrenal gland & renal cortex.
42
Q

Which ketone bodies enter TCA cycle as Acetyl CoA?

A
  • Acetoacetate & B-hydroxybutyrate.
  • Acetone is released on the breath.
43
Q

When are Ketone bodies elevated in the blood?

A
  • Normally low.
  • Rise in fasting or in diabetes mellitus or whenever fat breakdown exceeds carbohydrate breakdown.
  • Uncontrolled DM = excessive ketogenesis = acetone on the breath – “fruity” smell)
    **Ketosis (Keto-acidosis can be fatal!)
44
Q

What is Brown adipose tissue?

A
  • Involved in metabolism when heat (not ATP) must be generated.
  • Function:
    1. Arousal from hibernation
    2. Non-shivering thermogenesis
    3. Heat production in newborns
45
Q

What are the characteristics of brown adipose tissue?

A
  • Good blood supply.
  • High content of mitochondria & cytochromes.
  • Low activity of ATP Synthase.
  • Metabolic emphasis on oxidation of glucose & FAs.
46
Q

What is MCAD deficiency?

A
  • Main clinical signs:
    1. Intolerance to prolonged fasting
    2. Hypoglycaemia
    3. Impaired ketogenesis
    4. Recurrent episodes of hypoglycaemic coma with
    an associated medium-chain dicarboxylic aciduria.
47
Q

How is MCADD managed?

A
  • Via diet:
    1. Avoid fasting.
    2. Glucose supplements.

Gastrointestinal biology (24 decks)

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