11. Post Absorption Processing of Lipids Flashcards

1
Q

What are lipids transported in in circulation?

A

Lipoprotein particles: chylomicrons

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2
Q

What is fat principally absorbed as?

A

2-monoacylglycerol

FAs

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3
Q

What are FAs converted to?

A

Acyl-CoA

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4
Q

Where are FAs converted to Acyl-CoA?

A

ER of intestinal mucosal cells

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5
Q

What converts FAs to acyl-CoA?

A

Acyl-CoA Synthetase

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6
Q

What happens once proteins and lipids are secreted from the smooth ER and golgi?

A

Released into extracellular space as fat droplets
Collected by local lymph
Transported via the thoracic duct to the left brachycephalic vein

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7
Q

What is the structure of monoacylglycerol?

A

Glycerol linked to a FA via an ester bond

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8
Q

What is the structure of triacylglycerol?

A

Ester derived from glycerol and 3 FAs

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9
Q

What is the structure of cholesterol ester?

A

Ester bond formed between the carboxylate group of a fatty acid and the hydroxyl group of cholesterol

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10
Q

What does utilisation of TAGs require?

A

Lipoprotein Lipase

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11
Q

Where is lipoprotein lipase not found?

A

Liver

Brain

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12
Q

What is LPL attached to?

A

Heparan sulphate glycoproteins on the surface of the capillary endothelium on adipose

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13
Q

What increases the activity of LPL?

A

Insulin

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14
Q

What happens to TAGs when going from a fed state to a fasting one?

A

TAGs are re-routed from adipose to muscle

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15
Q

Where do most of the FAs used in TAG synthesis in adipose tissue come from?

A

Chylomicrons

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16
Q

Where do most of the FAs used in TAG synthesis after a high carb meal come from?

A

Acetyl CoA

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17
Q

What form do FAs participate in TAG synthesis as?

A

CoA-thioesters

18
Q

What form does glycerol participate in TAG synthesis as?

A

Glycerol-3-phosphate

19
Q

How does insulin regulate fat synthesis?

A

Increases rate of glycolysis
Increases LPL activity
Induces glycerolphosphate-acyl transferase which catalyses the first step in TAG synthesis

20
Q

What enzyme carries out the first cleavage of a FA from TAGs?

A

Hormone-sensitive adipose tissue lipase

21
Q

What activates adipose tissue lipase?

A

Phosphorylation by cAMP-dependent Protein Kinase A

22
Q

What are the most important human lipolytic agents?

A

Noradrenaline and adrenaline

23
Q

How does noradrenaline work to promote TAG breakdown?

A

Acts via beta-adrenergic receptors, cAMP, Protein Kinase A

24
Q

What are other lipolytic hormones?

A

Glucocorticoids
GH
Thyroid hormone

25
What conditions increase TAG hydrolisation?
Cold exposure Stress Physical exercise
26
What do free FAs bind to in circulation?
Albumin
27
Where does beta oxidation occur?
In the mitochondrion
28
What types of cells can't oxidise FAs?
Neurons | Erythrocytes
29
How do short FAs enter the mitochondrion?
Passive diffusion
30
How do longer FAs enter the mitochondrion?
Converted to CoA-thioesters by Fatty Acyl CoA Synthetase Carnitine transports acyl group across the membrane Known as the carnitine shuttle
31
What is the carnitine shuttle composed of?
Carnitine Palmitoyltransferase 1 and 2 | Carnitine-acylcarnitine translocase
32
What inhibits CPT-1?
Malonyl-CoA
33
What is the net result of beta oxidation?
Each cycle removes 2 carbons from the FA as acetyl-CoA | Production of NADH, H+ and FADH2
34
How does beta oxidation produce energy?
FADH2 and NADH feed into oxidative phosphorylation | Acetyl-CoA enteres TCA cycle
35
How is beta oxidation regulated?
Supply of free FAs Activity of hormone-sensitive adipose tissue lipase Inhibted by malonyl-CoA
36
Name 3 ketone bodies
Acetoacetate B-hydroxybutyrate Acetone
37
How are acetoacetate and B-hydroxybutyrate formed?
From Acetyl-CoA in the liver mitochondria by ketogenesis
38
How is acetone formed?
Spontaneous decarboxylation of acetoacetate
39
Where are ketone bodies especially important for energy?
Heart Adrenal glands Renal cortex
40
When are circulating ketone body levels high?
Fasting Diabetes mellitus Whenever fat breakdown exceeds carbohydrate breakdown
41
What is brown adipose tissue characterised by?
Good blood supply High mitochondria and cytochromes Low activity of ATP synthetase
42
What are the main clinical signs of Medium Chain Acyl-CoA Dehydrogenase Deficiency?
``` Intolerance to prolonged fasting Hypoglycaemia Impaired ketogenesis Hypoglycaemic coma Medium-chain dicarboxylic aciduria ```