beta oxidation of fatty acids

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1

trans fatty acid

hydrogens on opposite side of chain; formed in industrial hydrogenation of fish and plant oils; it improves thermal and oxidation stability

2

fatty acids are stored as what?

triacylglycerols

3

triacylglycerol lipase

enzyme that cuts fatty acids

4

where does beta oxidation occur?

mitochondrial matrix

5

beta oxidation

oxidation/burning of fatty acids in the mitochondrial matrix

6

what activate the lipases?

cAMP

7

how is fatty acids circulate in blood?

they are bound to serum albumin

8

albumin

major serum protein; make up 60% of total plasma protein; binds free fatty acids, steroid hormones and bilirubin

9

how can longer chain of FA enter the matrix?

they are converted to acylcarnitine derivatives by carnitine:acylcarnitine translocase

10

carnitine:acylcarnitine translocase

transport long chain fatty acids across inner membrane of mitochondria

11

fatty acids in the body are always bound to what 3 things?

CoA or glycogen or carnitine:acylcarnitine translocase

12

how many membranes do fatty acids cross to get inside the mitochondria?

3 membranes: plasma membrane, outer mitochondrial membrane, inner mitochondrial membrane

13

how does carnitine:acylcarnitine translocase (CAT) work?

it sends carnitine out and acylcarnitine in; this is done to recycle the concentration of carnitine on the outside of the mitochrondrial membrane so it can bind to fatty acids and be transported into the inner mitochondrial membrane

14

what is the cofactor for fatty acids breakdown?

NAD+/NADH

15

what is the cofactor for fatty acids synthesis?

NADP+/NADPH

16

how many carbons does the beta-oxidation pathway degrade from fatty acids at a time?

2

17

3 main stages of beta-oxidation pathway

activation of fatty acids in the cytosol; transport into mitochondria; degradation to 2 carbon fragments in the mitochondrial matrix in the 4 steps repeated as a spiral

18

4 key repeated reactions in b-oxidation

oxidation; hydration; oxidation; thiolysis

19

each round of reaction generates one molecule each of what?

QH2, NADH, acetyl CoA, fatty acyl CoA that is 2 carbons shorter each round

20

how many acetyl CoA, QH2, NADH is produced when a 16-carbon fat is burned?

8 acetyl CoA, 7 QH2, 7 NADH

21

how many ATPs is produced when a 16-carbon fat is burned?

106 ATP

22

what are 2 exceptions when fatty acids can be made into glucose?

odd number of carbons on a fatty acid (because any 3-carbon molecule can be converted to pyruvate) and glycerol

23

very long chain fatty acids are oxidized first where?

peroxisomes

24

last cleavage of odd-chain length fatty acids give you what?

acetyl CoA and propionyl CoA (a 3-carbon molecule)

25

peroxisomes break down fatty acids in order to do what?

detoxify and make hydrogen peroxide (H2O2) to destroy bacteria

26

what happens if some one has carnitine deficiency?

hypoglycemia, reduced carnitine in tissues and impaired long chain fatty acids metabolism

27

MCAD (medium chain acylCoA dehydrogenase) defect

show intermittent hypoglycemia, onset in 2nd year of life, dicarboxylic aciduria extensive during attacks but undetectable when healthy

28

what is the primary fuel during fasting?

fatty acids

29

where is ketone bodies produced?

liver

30

where is ketone bodies converted back to acetyl CoA?

muscle and tissues

31

ketone bodies are sources of energy for what during fasting?

brain, heart, skeletal muscles

32

ketone bodies synthesis occurs only where?

mitochondria matrix

33

what are ketone bodies?

fatty acid derivatives that are easy to transport in blood without albumin or other fatty acid binding proteins

34

what is the preferred energy source for kidney cortex cells and cardiac muscle?

acetoacetate and beta-hydroxybutyrate

35

what is the ratio of acetoacetate:b-hydroxybutyrate?

1:1; these are readily interchangable

36

how does hyperclycemia causes dehydration?

reduces excretion of ketone bodies in urine, this causes increase in plasma [H+] and leads to ketoacidosis

37

how does diabetes mellitus leads to excess ketone bodies adn ultimately ketoacidosis?

cells are starving in the midst of plenty and turn to breakdown of fats and proteins and gluconeogenesis to increase the blood glucose level; this leads to excess acetyl CoA which then lead to formation of excess ketone bodies

38

normal accumulation of ketone bodies in urine?

<125 mg/24 h

39

normal accumulation of ketone bodies in blood

<3 mg/100 mL

40

adipocytes prefer what energy source?

ketone bodies

41

gluconeogenesis

process of making glucose from non-carbohydrate intermediates, except for fatty acids (although 3-c fatty acids can be used for gluconeogenesis)

42

where does NADPH come from?

pentose phosphate pathway

43

why is NADPH important?

it is used to synthesize molecules, whereas NADH is used as a cofactor to break down molecules