Ketogenesis Flashcards

(68 cards)

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
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