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Biochemistry 2 > Ketogenesis > Flashcards

Ketogenesis Flashcards

0
Q

What does B oxidation produce

A

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

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1
Q

Ketogenesis reduces what levels

A

Acetyl CoA and allows B Oxidation to continue

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2
Q

Ketogenesis is

A

Low no carbs

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3
Q

What are substances that make ketone bodies?

A

Acetyl CoA or things that can turn into Acetyl CoA

Ketogenic amino acids

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4
Q

What are the amino acids that are only Ketogenic?

A

Leucine and lysine

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5
Q

What are the amino acids that are Ketogenic and glucogenic?

A

Isoleucine phenylalanine tryptophan tyrosine threonine

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6
Q

What does fats turn into?

A

Acetyl CoA OHOT

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7
Q

What can fats not turn into?

A

Glucose

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8
Q

What can Acetyl CoA not turn into?

A

Glucose

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10
Q

Is pyruvate dehydrogenase a reversible reaction?

A

No Its only irreversible

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11
Q

what are ketone bodies the result of?

A

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

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12
Q

where are ketone bodies transported to?

A

the extrahepatic tissue

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13
Q

ketone bodies in the extrahepatic tissues are converted to what?

A

acetyl CoA

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14
Q

what are ketone bodies oxidized for?

A

oxidized for energy

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15
Q

what organ can make ketone bodies?

A

the liver

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16
Q

what can the liver not do to ketone bodies?

A

cannot oxidize ketone bodies

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17
Q

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

A

true

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18
Q

what are functional ketone bodies?

A

transported from the liver to target blood to target tissues

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19
Q

what are functional ketone boies converted to?

A

converted to acetyle CoA

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20
Q

functional ketone bodies run what cycles

A

krebs cycle and ETS

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21
Q

what are the functional (primary) ketone bodies?

A

acetoacetate and B-hydroxybutyrate

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22
Q

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

A

acetone

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23
Q

what does the brain prefer from energy?

A

glucose

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24
Q

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

A

yes it can

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25
Q

the liver has more …..

A

mitochodrial HMG CoA Synthase

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26
Q

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

A

HMG CoA Synthase

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27
Q

what version is present in significant quantities in the liver?

A

the isoenzyme

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28
Q

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

A

HMG CoA Synthase

29
Q

what are ketone bodies and cholesterol made from?

A

both start from acetyl CoA

both have HMG CoA as a precursor

30
Q

what conditions are ketones made under?

A

excessive fat bruning in the liver

31
Q

what condition is cholesterol made under?

A

excessive sugar and insulin results in cholesterol

32
Q

what happens in response to low carbohydrates?

A

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
Q

what does the liver receive large quantities of?

A

fat

34
Q

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

A

you will burn more fat

35
Q

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

A

fat burning

36
Q

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

A

liver glycolysis

37
Q

what does fat oxidation OHOT in the liver yield

A

lots of acetyl CoA

38
Q

what does acetyl CoA inhibit?

A

pyruvate dehydrogenase (prep step)

39
Q

what does acetyl CoA stimulate?

A

pyruvate carboxylase (gluconeogenesis)

40
Q

what is krebs cycle intermediates used to make

A

glucose (gluconeogenesis)

41
Q

krebs cycle intermediates used to make glucose

A

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
Q

what is the protein sparing effect?

A

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

43
Q

what is rare for a ketogenic diet?

A

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

44
Q

what are common side effect in a ketogenic diet?

A

constipation
acidosis
decreased weight gain but not loss

45
Q

what are less common side effects in a ketogenic diet?

A 
elevated cholesterol
kidney stones 
slow growth pattern (5th percentile)
GI upset 
decreased bone density (similar to medication effect)
46
Q

do ketone bodies cross the BBB

A

yes they do for brain energy metabolism

47
Q

low carbs mean

A

burn more fat and make more glucose

48
Q

what else can carbs be made from

A

protein

49
Q

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

A

no it is bad idea

50
Q

what does increased FA oxidation stimualte the production of

A

ketones

51
Q

what can ketones do instead of glucose

A

they can be oxidized

52
Q

does it take more protein or carbs

A

it takes more carbs and less protein

53
Q

what are acetoacetate and b-hydroxybuturate transported in and to

A

in the blood to the extraheptatic tissues

54
Q

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

A

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

55
Q

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

A

ketosis

56
Q

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

A

it lowers the blood ph

57
Q

lowering the blood ph leads to

A

acidosis (ketoacidosis)
coma
death

58
Q

what is a ketogenic diet (example atkins die)

A

high fat
low carb
moderate amount of protein

59
Q

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

A

from oxidized fat to be used for primary metabolic energy source

60
Q

type I diabetes

A

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

61
Q

type II diabetes

A

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

62
Q

what is the fourth most common neurological problem

A

epilepsy

63
Q

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

A

migraine stroke and alzheimers disease

64
Q

what is a refractory epilepsy

A

medication is not controling it

65
Q

how is ketoacidosis able to be avoided

A

by monitoring the blood levels

66
Q

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

A

relying of FA metabolism for energy

67
Q

ketogenic diet mechanisms

A

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

68
Q

GABA and glutamate

A

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

Biochemistry 2 (13 decks)

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