Ketogenesis Flashcards
What does B oxidation produce
Acetyl CoA in the citric acid cycle and ketone bodies in the liver
Ketogenesis reduces what levels
Acetyl CoA and allows B Oxidation to continue
Ketogenesis is
Low no carbs
What are substances that make ketone bodies?
Acetyl CoA or things that can turn into Acetyl CoA
Ketogenic amino acids
What are the amino acids that are only Ketogenic?
Leucine and lysine
What are the amino acids that are Ketogenic and glucogenic?
Isoleucine phenylalanine tryptophan tyrosine threonine
What does fats turn into?
Acetyl CoA OHOT
What can fats not turn into?
Glucose
What can Acetyl CoA not turn into?
Glucose
Is pyruvate dehydrogenase a reversible reaction?
No Its only irreversible
what are ketone bodies the result of?
excess acetyl CoA from fat burning spilling over away from the krebs cycle
where are ketone bodies transported to?
the extrahepatic tissue
ketone bodies in the extrahepatic tissues are converted to what?
acetyl CoA
what are ketone bodies oxidized for?
oxidized for energy
what organ can make ketone bodies?
the liver
what can the liver not do to ketone bodies?
cannot oxidize ketone bodies
T/F the liver can produce ketone bodies but it cant consume ketone bodies
true
what are functional ketone bodies?
transported from the liver to target blood to target tissues
what are functional ketone boies converted to?
converted to acetyle CoA
functional ketone bodies run what cycles
krebs cycle and ETS
what are the functional (primary) ketone bodies?
acetoacetate and B-hydroxybutyrate
what is exhaled and is a by product of a ketone body?
acetone
what does the brain prefer from energy?
glucose
can the brain adapt to ketone bodies during starvation or lack of glucose
yes it can
the liver has more …..
mitochodrial HMG CoA Synthase
what is the rate limiting enzyme in the synthesis of ketone bodies?
HMG CoA Synthase
what version is present in significant quantities in the liver?
the isoenzyme
what enzyme is also in the cholesterol synthesis pathway but in the cytosol?
HMG CoA Synthase
what are ketone bodies and cholesterol made from?
both start from acetyl CoA
both have HMG CoA as a precursor
what conditions are ketones made under?
excessive fat bruning in the liver
what condition is cholesterol made under?
excessive sugar and insulin results in cholesterol
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
what does the liver receive large quantities of?
fat
large quantities of fat in the liver what does low carbs mean?
you will burn more fat
large quantities of fat in the liver what does glucagon stimulate?
fat burning
large quantities of fat in the liver what does glucagon inhibit?
liver glycolysis
what does fat oxidation OHOT in the liver yield
lots of acetyl CoA
what does acetyl CoA inhibit?
pyruvate dehydrogenase (prep step)
what does acetyl CoA stimulate?
pyruvate carboxylase (gluconeogenesis)
what is krebs cycle intermediates used to make
glucose (gluconeogenesis)
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
what is the protein sparing effect?
by having ketones to burn, tissue doesnt have to rely on AA for glucose
what is rare for a ketogenic diet?
inflammation of pancreas
cardiac problems
selenium and carnitine deficiency
basal ganglia changes
what are common side effect in a ketogenic diet?
constipation
acidosis
decreased weight gain but not loss
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)
do ketone bodies cross the BBB
yes they do for brain energy metabolism
low carbs mean
burn more fat and make more glucose
what else can carbs be made from
protein
by burning protein to make carbs is it good for long term
no it is bad idea
what does increased FA oxidation stimualte the production of
ketones
what can ketones do instead of glucose
they can be oxidized
does it take more protein or carbs
it takes more carbs and less protein
what are acetoacetate and b-hydroxybuturate transported in and to
in the blood to the extraheptatic tissues
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
what is a increase ketone amount in the blood and urine called
ketosis
increased acetoacetate and b-hydroxybuturat in the blood does what to the ph
it lowers the blood ph
lowering the blood ph leads to
acidosis (ketoacidosis)
coma
death
what is a ketogenic diet (example atkins die)
high fat
low carb
moderate amount of protein
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
type I diabetes
is diagnosed early in life
insulin dependent
pancreas is not producing insulin
type II diabetes
diagnosed later in life
non insulin dependent
overproduction of insulin body is not using it properly
what is the fourth most common neurological problem
epilepsy
what are other common neurological problems that occur more then epilepsy?
migraine stroke and alzheimers disease
what is a refractory epilepsy
medication is not controling it
how is ketoacidosis able to be avoided
by monitoring the blood levels
what does a very low calorie (very low carb) diet rely on
relying of FA metabolism for energy
ketogenic diet mechanisms
neurotransmitters- GABA glutamate
decreased dopamine/ seratonin
regulation of adenosine
antooxidant effect
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
