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Nutrition and Metabolism > Lipid Synthesis and Transport > Flashcards

Lipid Synthesis and Transport Flashcards

1
Q

How is TAG used in the body (general)?

A

TAG in small intestine transferred into blood.
Liver TAG transfered into blood.
Moves into muscle to be oxidised to generate ATP.
Moves into adipose tissue to be stored.

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2
Q

Where does fatty acid synthesis occur?

A

In the cytosol of liver cells

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3
Q

What hormone stimulates fatty acid synthesis?

A

Insulin

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4
Q

What is the starting molecule in fatty acid synthesis?

A

Acetyl CoA

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5
Q

How is acetyl CoA transported from mitochondrial matrix into the cytosol?

A

In mitochondria: Acetyl CoA + oxaloacetate > citrate

Citrate passes through mitochondrial membrane.

In cytosol: citrate > acetyl CoA + oxaloacetate

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6
Q

Outline step 1 of fatty acid syntheis. Reaction, enzyme etc.

A

Acetyl CoA + HCO3- > Malonyl CoA
Enzyme: acetyl CoA carboxylase
Uses ATP > ADP + Pi

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7
Q

How is acetyl CoA carboxylase activated, what does it do?

A

Activated by insulin.

Coverts Acetyl CoA into Malonyl CoA.

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8
Q

How does malonyl CoA signify the fed state?

A

Malonyl CoA inhibits carnitine transferase

  • prevents transferral of fatty acids into the mitchondria to be oxidised.
  • stops fatty acid breakdown.
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9
Q

Outline steps 2 and 3 in fatty acid synthesis.

A

Step 2: Malonyl reacts with another acetyl CoA and loses a carbon. (Adds 2 and loses 1).
Step 3: Subsequent addition of a malonyl CoA and removal of one carbon. (Adds 3, loses 1)
CATALYSES BY FATTY ACID SYNTHETASE.

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10
Q

What co-factor is needed for fatty acid synthesis?

A

NADPH - acts as a reducing agent.

Provided by hexose monophosphate shunt.

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11
Q

How are triacylglycerides synthesised in liver cell?

A

Glycerol is activated by phosphorylation to glycerol phosphate.
Glycerol phosphate + 3fatty acids > Triacyl glyceride + phosphate

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12
Q

What is a lipoprotein?

A

Protein-lipid complex used to transport TAG in blood.

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13
Q

What are the 4 main types of lipoprotein and what do they carry?

A

Chylomicrons (carry mainly TAG - biggest + lowest density)
Very-low density lipoprotein (VLDL) - Endogenous TAG, Produced in the liver.
Low-density lipoprotein (LDL) - mainly carries cholesterol
High density lipoprotein (HDL) - takes cholesterol to liver

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14
Q

What is the general structure of lipoproteins?

A

Inner core = triacyl glycerol + choesterol esters

Outer surface = single layer of phsopholipid, cholesterol and apoproteins.

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15
Q

What are the 3 roles of apoproteins? Give examples.

A
  1. Some required as structural components:
    - Apo B-48 in chylomicrons
    - Apo B-100 in VLDL
  2. Some activate enzymes:
    - apo C-II on chylomicrons activates lipoprotein lipase (removes fatty acids from TAG)
  3. Some as destination targetting signals - bind to specific receptors on cel surface to allow uptake of lipoprotein into cell.
    - apo B-100 on LDL binds to LDL receptors
    - apo E on chylomicrons bind to liver remnant receptors.
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16
Q

How is exogenous fat (from intestinal lumen) transported?

A
  1. Chylomicron bound to apo-48 enters circulation.
  2. Picks up apo E and apo C-II.
  3. TAG in chylomicron broken down by lipoprotein lipase to fatty acids and glycerol. Fatty acids enter adipocyte where they are stored.
  4. Chylomicron remnant is still bound to apo E and apo B-48.
  5. Apo E binds to receptor on liver surface casing uptake of the chylomicron remnant into the liver.
17
Q

What apoprotein activates lipoprotein lipase?

A

Apo C-II

18
Q

What apoprotein stabilises chylomicrons?

A

Apo B-48

19
Q

What apoprotein allows uptake of chylomicron remnant into liver cells?

A

Apo E binds to apo E receptors on liver cell surface.

20
Q

What sort of lipoprotein transports exogenous fat?

A

Chylomicrons

21
Q

What sort of lipoprotein transports endogenous fat?

A

VLDL/LDL

22
Q

How is endogenous fat transported around the body?

A
  1. Starts in liver as VLDL bound to apo B-100 - trnasported out of liver into blood.
  2. apo E and apo C-II is transferred from HDL onto the VLDL.
  3. Apo C-II activates lipoprotein lipase - stores fat in adipocyte.
  4. VLDL becomes LDL as TAG is removed into adipocyte.
  5. apo C-II and apo E are returned to HDL.
  6. LDL associated with B-100. B-100 receptors on peripheral tissue and liver. 50/50 uptake.
23
Q

What is the function of HDL?

A

Transports cholesterol out of cells.

24
Q

What enzyme esterifies cholesterol to form cholesterol esters?

A

LCAT enzyme - converts phosphatidy choline to lipophosphatidy simualtaneously.

25
Q

How does HDL transport cholesterol out of cells?

A

HDL bound to apo A-1 takes up cholesterol esters.
Some cholesterol ester is transferred from HDL to VLDL by cholesterol ester transfer protein.
SR-B1 receptor for HDL binds to apo A-1 allowing uptake of HDL containing cholesterol ester into the liver.

26
Q

How does choelsterol control its own synthesis?

A

Cholesterol acts as a steroid hormone on the nucleus and inhibits the synthesis of enzymes that synthesise cholesterol.
It also controls the number of cholesterol receptors on the cell surface.
High cholesterol = fewer receptors

27
Q

How is choesterol synthesised from acetyl-CoA?

A

Acetyl CoA + Acetyl CoA > HMG-CoA > Mevalonate > cholesterol

28
Q

What enzyme converts HMG-CoA to mevalonate?

A

HMG-CoA reductase.

Cholesterol inhibits production of HMG-CoA reductase - negative feedback.

29
Q

What drugs inhibit cholesterol synthesis and how?

A

Statins - inhibit HMG-CoA reductase.

30
Q

What are hyperlipidaemias?

A

Hypercholesterolaemia - high cholesterol

Hypertriglyceridaemia - high TAG

31
Q

What are risk factors of hyperlipidaemia?

A
  • obesity
  • diabetes mellitus
  • dietary cholesterol
  • dietary fatty acid (saturated)
  • alcoholism (increases LDL)
32
Q

What is lipoprotein-a? What does it do?

A

LDL + apo A

  • In high concentration increases risk of coronary heart disease.
  • Levels are genetic - can be increased by trans-fat intake and decreased by oestrogen.
  • Slows breakdown of blood clots by competing with plasminogen.
33
Q

What is atherosclerosis?

A

Disease where plaque builds up in blood vessels causing obstruction.

34
Q

What is a plaque?

A

Complex structure involving inflammation and proliferation of smooth muscle in the arterial wall.
Contains connective tissue and a pool of cholesterol rich lipid.

35
Q

What is a foam cell?

A

A macrophage filled with cholesterol.

Nutrition and Metabolism (11 decks)

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