Cell metabolism 2 - Lipids Flashcards

1
Q

What is the main product of fatty acid metabolism?

A

Acetyl CoA

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2
Q

What 3 primary sources are fats derived from?

A
  1. The diet
  2. De nonvo synthesis(liver:
  3. Storage depots in adipose tissue
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3
Q

Where are bile salts made and stored?

A

Made - Liver

Stored - Gall bladder

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4
Q

What do bile salts do during digestion?

A

They pass from the bile duct to the intestine.

They emulsify fats aiding their digestion and absorption of fats and also that of fat-soluble viamins, e.g. A, D, E, K

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5
Q

What is orlistat?

A

A medicine which reduced fat absorption by 30%, which is then secreted by the faecal route. It is a inhibitor of gastric and pancreatic lipases.
This can help treat patients with obesity.
Side effects are abdominal pain, urgency to defecate, increased flatus and steatorrhea.

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6
Q

What are lipoproteins?

A

Molecules in the blood that transport lipids

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7
Q

What is a lipoprotein?

A

A molecule that has a cholesterol monolayer and apoproteins, which surround a core of cholesterol esters and triacylglycerols

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8
Q

Where do chylomicrons get apoproteins from?

A

From HDLs in the bloodstream

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9
Q

Where are chylomicrons obtained from and how do they enter the body?

A

From digested food that are absorbed by entrocytes are on the border of the small intestine

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10
Q

How do chylomicrons travel through the body?

A

Through the lymphatic system

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11
Q

Where are lipoprotein lipases found?

A

On the capillary endothelial cells lining adipose, heart and skeletal muscle tissues

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12
Q

What is the life cycle of a chylomicron?

A
  1. Nascent chylomicron absorbed by intestinal villi
  2. Nascent chylomicron gains apoproteins from HDLs
  3. Chylomicrons with apoproteins can recognise and activate lipoproteins on the surface of endothelial cells lining adipose and muscle tissue. This results in the hydrolysis of triglycerides into free fatty acids(FFA) and glycerol. FFA can be taken up by tissues and glycerol is taken up by the liver for gluceoneogenesis.
  4. The empty/near empty chylomicrons then gain more apoproteins from HDLs and they are used up in the liver to produce VLDL
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13
Q

Draw the life cycle of VLDLs, IDLs, HDLs and LDLs

A

Look on one note

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14
Q

Why are HDLs referred to as ‘good cholesterol’ and LDLs as ‘bad cholesterol’?

A

HDLs:
Take cholesterol from peripheral tissues back to the liver for use or disposal. Help lower total serum cholesterol. Reverse cholesterol transport.
LDLs:
Prololonged elevation of LDLs leads to atherosclerosis. More than 40% of their weight are cholesterol esters.

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15
Q

What is Beta -oxidation of fatty acids?

A

When fatty acids are converted into an acyl CoA species

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16
Q

What is the carnitine shuttle?

A

The acyl CoA species formed in Beta-oxidation has to enter the matrix of the mitochondria so it couples with carnitine to form acyl carnitine. Carnitine and acyl carnitine and moved to a from the matrix by a transolcase in the mitochondrial membrane

17
Q

What is primary-carnitine deficiency?

A

It is a autosomal recessive disorder which causes a mutation to a carnitine transporter resulting in reduced ability for cells to uptake carnitine, needed for Beta-oxidation.
Symptoms can be encephalopathies, cardiomyopathies, muscle weakness and hypoglycaemia.

18
Q

When are ketone bodies formed?

A

When the Beta-oxidation > carbohydrate metabolism..

19
Q

What enzymes are involved in lipogenesis?

A

Acetyl CoA carboxylase and Fatty acid synthase

20
Q

How are fatty acids synthesised?

A

By decarboxylative condensation reactions involving acetyl-CoA and malonyl-CoA

21
Q

What are the distinctions between fatty acid synthesis and degradation?
Carriers?
Reducing power?
Location?

A
Carriers:
ACP(S) vs CoA(D)
Reducing power:
NADPH(S) vs FAD/NAD+(D)
Locations:
Cytoplasm(S) vs Mitochondrial matrix(D)