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Flashcards in Ketogenesis Deck (68):
0

Ketogenesis reduces what levels

Acetyl CoA and allows B Oxidation to continue

1

What does B oxidation produce

Acetyl CoA in the citric acid cycle and ketone bodies in the liver

2

Ketogenesis is

Low no carbs

3

What are substances that make ketone bodies?

Acetyl CoA or things that can turn into Acetyl CoA
Ketogenic amino acids

4

What are the amino acids that are only Ketogenic?

Leucine and lysine

5

What are the amino acids that are Ketogenic and glucogenic?

Isoleucine phenylalanine tryptophan tyrosine threonine

6

What does fats turn into?

Acetyl CoA OHOT

7

What can fats not turn into?

Glucose

8

What can Acetyl CoA not turn into?

Glucose

10

Is pyruvate dehydrogenase a reversible reaction?

No Its only irreversible

11

what are ketone bodies the result of?

excess acetyl CoA from fat burning spilling over away from the krebs cycle

12

where are ketone bodies transported to?

the extrahepatic tissue

13

ketone bodies in the extrahepatic tissues are converted to what?

acetyl CoA

14

what are ketone bodies oxidized for?

oxidized for energy

15

what organ can make ketone bodies?

the liver

16

what can the liver not do to ketone bodies?

cannot oxidize ketone bodies

17

T/F the liver can produce ketone bodies but it cant consume ketone bodies

true

18

what are functional ketone bodies?

transported from the liver to target blood to target tissues

19

what are functional ketone boies converted to?

converted to acetyle CoA

20

functional ketone bodies run what cycles

krebs cycle and ETS

21

what are the functional (primary) ketone bodies?

acetoacetate and B-hydroxybutyrate

22

what is exhaled and is a by product of a ketone body?

acetone

23

what does the brain prefer from energy?

glucose

24

can the brain adapt to ketone bodies during starvation or lack of glucose

yes it can

25

the liver has more .....

mitochodrial HMG CoA Synthase

26

what is the rate limiting enzyme in the synthesis of ketone bodies?

HMG CoA Synthase

27

what version is present in significant quantities in the liver?

the isoenzyme

28

what enzyme is also in the cholesterol synthesis pathway but in the cytosol?

HMG CoA Synthase

29

what are ketone bodies and cholesterol made from?

both start from acetyl CoA
both have HMG CoA as a precursor

30

what conditions are ketones made under?

excessive fat bruning in the liver

31

what condition is cholesterol made under?

excessive sugar and insulin results in cholesterol

32

what happens in response to low carbohydrates?

increased fat burning> more acetyl CoA from OHOT going to the krebs cycle

increased gluconeogenesis> more AA are converted into glucose >more oxaloacetate stolen from the krebs cycle to make glucose(cant start with pyruvate or lactate low carbs)

OHOT makes excess acetyl CoA > not enough oxaloacetate to combine with it

excess acetyl CoA turns into ketone bodies

body uses the ketone bodies instead of glucose

GNG is diminished> less protein is consumed by GNG

33

what does the liver receive large quantities of?

fat

34

large quantities of fat in the liver what does low carbs mean?

you will burn more fat

35

large quantities of fat in the liver what does glucagon stimulate?

fat burning

36

large quantities of fat in the liver what does glucagon inhibit?

liver glycolysis

37

what does fat oxidation OHOT in the liver yield

lots of acetyl CoA

38

what does acetyl CoA inhibit?

pyruvate dehydrogenase (prep step)

39

what does acetyl CoA stimulate?

pyruvate carboxylase (gluconeogenesis)

40

what is krebs cycle intermediates used to make

glucose (gluconeogenesis)

41

krebs cycle intermediates used to make glucose

fasting or untreated diabetes
oxaloacetate stolen from krebs for GNG
slows krebs and acetyl CoA oxidation
stimulates the conversion of acetyl CoA to acetoacetate

42

what is the protein sparing effect?

by having ketones to burn, tissue doesnt have to rely on AA for glucose

43

what is rare for a ketogenic diet?

inflammation of pancreas
cardiac problems
selenium and carnitine deficiency
basal ganglia changes

44

what are common side effect in a ketogenic diet?

constipation
acidosis
decreased weight gain but not loss

45

what are less common side effects in a ketogenic diet?

elevated cholesterol
kidney stones
slow growth pattern (5th percentile)
GI upset
decreased bone density (similar to medication effect)

46

do ketone bodies cross the BBB

yes they do for brain energy metabolism

47

low carbs mean

burn more fat and make more glucose

48

what else can carbs be made from

protein

49

by burning protein to make carbs is it good for long term

no it is bad idea

50

what does increased FA oxidation stimualte the production of

ketones

51

what can ketones do instead of glucose

they can be oxidized

52

does it take more protein or carbs

it takes more carbs and less protein

53

what are acetoacetate and b-hydroxybuturate transported in and to

in the blood to the extraheptatic tissues

54

what can both acetoacetate and b-hydroxybuturate be converted to and what cycle can they both ente

can be converted acetyl CoA through a series of reactions and acetyl CoA can enter to krebs cycle

55

what is a increase ketone amount in the blood and urine called

ketosis

56

increased acetoacetate and b-hydroxybuturat in the blood does what to the ph

it lowers the blood ph

57

lowering the blood ph leads to

acidosis (ketoacidosis)
coma
death

58

what is a ketogenic diet (example atkins die)

high fat
low carb
moderate amount of protein

59

where does the production of ketone bodies come primarily from and what is it used for

from oxidized fat to be used for primary metabolic energy source

60

type I diabetes

is diagnosed early in life
insulin dependent
pancreas is not producing insulin

61

type II diabetes

diagnosed later in life
non insulin dependent
overproduction of insulin body is not using it properly

62

what is the fourth most common neurological problem

epilepsy

63

what are other common neurological problems that occur more then epilepsy?

migraine stroke and alzheimers disease

64

what is a refractory epilepsy

medication is not controling it

65

how is ketoacidosis able to be avoided

by monitoring the blood levels

66

what does a very low calorie (very low carb) diet rely on

relying of FA metabolism for energy

67

ketogenic diet mechanisms

neurotransmitters- GABA glutamate
decreased dopamine/ seratonin
regulation of adenosine
antooxidant effect

68

GABA and glutamate

inhibitory and excitatory
KB inhibit glutamate decarboxylase lowering glutamate (excitatory) and increasing conversion to GABA (inhibitory)
high GABA levels also inhibits sodium and calcium channels which are needed for neuronal excitation