Post-absorption processing of fats. Flashcards

1
Q

Cholesterol is a precursor for:

A

Bile salts, steroid hormones, vitamin D and membranes

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2
Q

Where are chylomicrons formed? Where are they released?

A

Intestinal epithelial cells. Released into lymph.

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3
Q

How do fatty acids arrive at peripheral tissues?

A

In chylomicrons/VLDL (released by lipoprotein lipase). From adipose tissue (broken down by hormone-sensitive lipase, transported bound to albumin).

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4
Q

What is the first step of fatty acid oxidation?

A

Activation to fatty acyl CoA in cytosol.

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5
Q

Where does the oxidation of fatty acids take place?

A

Mitochondria

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6
Q

What is required for the transport of long-chain fatty acids?

A

Carnitine and carnitine carrier protein - transports them across mitochondrial inner membrane.

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7
Q

What is produced from the oxidation of fatty acids?

A

Acetyl CoA - Krebs cycle

NADH and FADH - oxidised by electron transport chain

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8
Q

How many molecules of ATP are produced from the oxidation of one fatty acid?

A

108

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9
Q

What controls fatty acid metabolism?

A

Regulated by access of fatty acids to the mitochondria - controlled by conc. of malonyl CoA (produced by 1st step of fatty acid synthesis). Inhibits breakdown when energy is plentiful.

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10
Q

What are ketone bodies formed from?

A

Excess acetyl CoA

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11
Q

Where does the synthesis of ketone bodies occur?

A

Mitochondria of liver cells when body is fasting or during diabetes.

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12
Q

What is the most important step in cholesterol biosynthesis?

A

1st - acetyl CoA to mevalonate

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13
Q

How is cholesterol synthesis controlled?

A

Adjusting the activity or amount of HMG CoA reductase - controlled by cholesterol levels and energy levels.

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14
Q

What is the effect of insulin of HMG-CoA reductase

A

Stimulation (via dephosphorylation)

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15
Q

What effect do saturated fats have on lipoprotein levels?

A

Increase LDL

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16
Q

What effect do trans fats have on lipoprotein levels.

A

Can raise LDL and lower HDL

17
Q

What is the aetiology of familial hypercholesterolaemia?

A

Lack of LDL receptors.

18
Q

How does cholesterol contribute to the negative feedback loop that contributes to a reduction in the txn of HMG-CoA reductase (hence reduction in cholesterol synthesis).

A

Inhibits txn-enhancing signal.

19
Q

Why is HDL considered ‘good cholesterol’?

A

Involved in reverse cholesterol transport - returning cholesterol from peripheral cells to the liver.

20
Q

What is the initiating factor in atherosclerosis?

A

Damage to endothelial cells allows LDL to access subintimal space.

21
Q

What happens to subintimal LDL to contribute to atherosclerosis?

A

Becomes oxidised and is internalised by macrophages. Accumulation of foam cells create bulge in vessel wall - atherosclerotic plaque. Fibrous collagen cap forms.

22
Q

Why might an atherosclerotic plaque rupture?

A

There is a continued inflammatory response - induces macrophages to produce proteinase enzymes which degrade the fibrous cap.

23
Q

What is the cause of alcoholic steatohepatitis?

A

Metabolism of large amounts of alcohol inhibits fatty acid oxidation and activated excess triglyceride synthesis (caused by high NADH).

24
Q

What is the cause of non-alcoholic steatohepatitis?

A

Insulin resistance leads to increased insulin secretion - stimulates fatty acid synthesis.