3.
Acetoacetate : if not oxidized to form usable
energy, used as source of two other ketone
bodies
Acetone : cannot be used by brain for energy.
Generated through decarboxylation of
acetoacetate (enzyme : acetoacetate
decarboxylase) released by breathing it off, or
via urine excretion.
D-β-hydroxybutyrate : generated through the
action of the enzyme D-β-hydroxybutyrate
dehydrogenase on acetoacetate
4. Produced as “by-products” from
breakdown of fatty acids in liver.
Acetoacetic acid & D-β-hydroxybutyric
acid used as energy source in heart and
brain
( during fasting/ low blood-glucose
conditions)
Acetone = waste product= EXCRETED!!!
5. Modification of acetyl coA from fat
catabolism into ketone bodies, to be
delivered into other peripheral
tissues, then turn into CO2 and H2O
by oxidation process. (Lehninger
pg.213)
Other tissues : brain tissues, etc.
7.
Produced from acetyl CoA mainly in the
mitochondrial matrix of hepatocytes
Scarcity of carbohydrate -> fatty acid breakdown->
obtain energy
High level acetyl coA -> pyruvate dehydrogenase
complex is inhibited-> pyruvate carboxylase
activated.
High level of ATP & NADH inhibit the enzyme
isocitrate dehydrogenase in TCA cycle->increasing of
malate.
High level of NADH & ATP -> B-oxidation
Excess of acetyl coA-> rerouted to ketogenesis
8.
Low level of blood glucose : exhaustion,
fasting, sleeping, etc. -> body still needs
energy -> breakdown the fatty acid into
ketone bodies
Excessive of blood glucose -> unable to be
stored as glycogen -> fatty acid
synthesis can occur in response to unavailability of blood glucose. This is caused by low glucose level in the blood, after exhaustion, of cellular carbohydrate stores, such as glycogen or, synthesis of ketones can occur due to excessively high levels of blood glucose, that are unable to be stored as glycogen in liver and muscle.
Acetoacetate & D-β-hydroxybutyratetidakdioksidasidalamhati dibawakejaringanperifer