Lipids 2 Flashcards Preview

Science for Medicine > Lipids 2 > Flashcards

Flashcards in Lipids 2 Deck (36):
1

Can fatty acids be converted to glucose?

No because pyruvate to acetyl conenzyme A is irreversible

2

What does the beta-oxidation pathway do?

Degrades fatty acids two carbons at a time, producing acetyl coenzyme A, NADH and FADH2

3

Where does beta-oxidation occur?

Mitochondiral matrix

4

5

Why can red blood cells not perform beta-oxidation?

They have no mitochondria

6

What are the 3 stages of beta-oxidation?

  1. Activation of fatty acid in cytosol
  2. Transport into the mitochondria
  3. Degradation to two carbon as acetyl coenzyme A

7

What do fatty acids form when they are activated?

Fatty acyl coenzyme A

8

Where does the activation of fatty acids occur?

The cytosol

9

What does the reaction of the activation of a fatty acid looking like?

10

Can fatty acyl coenzyme A pass the membrane without help?

No, it needs to use the carmitine shuttle

11

What is the process of the carnitine shutle?

  1. Carnitine reacts with acyl coenzyme A to produce acyl carnitine which crosses the mitochondrial membrane
  2. Inside the mitochondria acyl carnitine reactions with coenymze A to produce acyl conenzyme A
  3. Carnitine crosses the membrane and returns to the cytosol to be used again

12

What does the carnitine shuttle look like?

13

What enzymes are used in the carnitine shuttle?

Carnitine palmityl transferase I and II

14

What can inhibit carnitine polmityl transerase?

Malonyl coenzyme A when their is enough broken down fatty acids

15

What does malonyl coenzyme A ensure?

That synthesis and degradation do not happen at the same time

16

Where does carnitine come from?

The diet

Made from lysine or methionine

17

What does carnitine palmitoyl transferase dificiency lead to?

No beta-oxidation (hypoglycemia)

Coma

 

18

What is the treatment of carnitine palmitoyl transferase difficiency?

Eating medium and short chain fatty acids that do not require the carnintine shuttle

19

What are the stages of the degradation of beta-oxidation occurs in four stages?

  1. Dehydrogenation to produce FADH2
  2. Hydration
  3. Dehydrogenation to produce NADH
  4. Thiolysis (cleaved) to produce acetyl coenzyme A

20

What does each beta-oxidation cycle produce?

1 acetyl coenzyme A

Spieces of carbon 2 carbons shorter than the original

21

What would 7 beta-oxidation pathways produce?

8 acetyl coenzyme A

7 NADH

7 FADH2

22

What is the total net energy yield of beta-oxidation?

129 ATP molecules

23

What do very long chain fatty acids (>22 carbons) need to undergo before beta-oxidation?

Preliminary beta-oxidation in peroxisomes

24

How are very long chain fatty acids (>22 carbons) degraded?

  1. Preliminary beta-oxidation in peroxisomes, does not produce FADH2 so not as efficient as shorter chains
  2. Shortened fatty acid links to carntine and diffuses into the mitochondria for beta-oxidation

25

Why are very long chain fatty acids not as efficient as shorter ones?

Preliminary beta-oxidation in peroxisomes does not produce FADH2

26

What happens during starving/fasting?

  1. Liver flooded with acetyl coenzyme A
  2. Acetyl coenzyme A inhibits pyruvate dehydrogenase (pyruvate to acetyl coenzyme A) and activates pyruvate carboxylase (pyruvate to oxaloacetate)
  3. Oxaloacetate is used to produce glucose for gluconeogenesis

27

What happens to excess acetyl coenzyme A during fasting?

Converted into ketone bodies

28

What tissues can use ketones for fuel?

Cardiac and skeletal muscle

29

When can brain cells use ketones for fuel?

During starvation

30

Where are ketone bodies made?

In the liver (mitochondrial matrix) and then transported in the blood to other tissues

31

What cannot use ketones for energy?

The liver

32

What cannot use fatty acids for energy?

The brain

33

Why do ketones not need albumin or lipoprotein to transport in the blood?

They are soluble

34

What leads to high ketone concentration?

Uncontrolled diabetes or starvation

35

What happens when the rate of ketone production becomes greater than the rate they are used?

Body becomes acid (ketosis) which causes a fruity oddur in breath due to acetone

36

What ensure that fatty acid synthesis and degradation do not happen at the same time?

Inhibition and the two happening in different places