BIOC3022 Exam 4| Ques ons and answers | Updated
RATED A+ 2026
how is triglyceride mobilized from adipocytes?
lipolysis.
Uses lipases to release fa y acids from triglycerides. Lipolysis in adipose ssue is s mulated by
hormones that respond to fas ng (glucagon) or stress (epinephrine)
Hormone s mula on of GPCR ac vates adenylyl cyclase, increasing cAMP and ac va ng PKA
which then phosphorylates lipases to ac vate. These reac ons release fa y acid from glycerol
backbone
hormonal control of triacylglycerol lipase, then diacylglycerol lipase, then monoacylglycerol
lipase to liberate all 3 fa y acids from glycerol backbone.
what are the steps to B-oxida on?
B carbon undergoes oxida on to release acetyl CoA.
1. Dehydrogena on: of long chain fa y acid- creates C=C double bond. Enzyme: Acyl CoA
dehydrogenase. Electrons (H+) transferred to FAD and released as FADH2.
2. Hydra on: of double bond adds a hydroxyl group to B-carbon. Enzyme: Enol CoA hydratase
3. Dehydrogena on: using NAD as an electron acceptor. Enzyme: 3-hydroxyacyl dehydrogenase
4. Thiolysis: between C2 and C3. A new molecule of CoA breaks the bond by nucleophilic a ack
on C3. Releases C1 and C2 as acetyl CoA. Enzyme: B-ketothiolase
repeat to release 2nd acetyl CoA group
how are acyl-CoA molecules transferred into the mitochondria?
by having a carni ne group added to it. From CPT1. And then CACT (translocase for carni ne)
transfers it across the inner mito membrane.
How is cycling between fa y acid synthesis and degrada on avoided? why do we want to avoid
it?
, Quan es of malonyl CoA and citrate regulate whether synthesis or oxida on is occurring
Malonyl CoA is a regulatory molecule for Fa y acid synthesis and also inhibits CPT1
allosterically.
Reduced malonyl CoA enables FFA oxida on and energy produc on
Citrate also regulates PFK and glycolysis rates- excess signals to glycolysis to slow down and
pushes C through PPP producing NADPH to make FFA
how is glycerol used?
is converted to DHAP and sent to gluconeogenesis
what is the energy yield from FFA oxida on?
7 FADH2
7NADH
8 acetyl CoA
129 ATP
What are the pathways of ketogenesis and ketolysis? Know enzyma c pathways and how
specific ssues u lize these molecules.
Ketolysis: breakdown of ketone molecules
Ketogenesis: the movement of carbon units from the liver to other ssues during a starva on. B
oxida on is restricted to the muscle and liver. The heart and brain can use an alternate carbon
source: ketogenesis.
During starva on, the ketolysis makes acetyl CoA for the brain
KETONE BODIES: acetone, acetoacetate, 2-hydroxybutyric acid
ketone bodies are formed in the liver and require HMG CoA as a star ng material
HMG CoA produc on: Thiolase enzyme combines 2 acetyl-CoA into 4-C acetoacetyl CoA. HMG
CoA synthase adds a 3rd acetyl CoA to make HMG CoA
Making ketones: HMG-CoA reacted with HMG-CoA lyase to remove an acetyl CoA group to
make acetoacetate which then can be either non-ezyma cally decarboxylated into acetone or
B-hydroxoybutyrate dehydrogenase (removed double bond to add H) into D-B-hydroxybutyrate
RATED A+ 2026
how is triglyceride mobilized from adipocytes?
lipolysis.
Uses lipases to release fa y acids from triglycerides. Lipolysis in adipose ssue is s mulated by
hormones that respond to fas ng (glucagon) or stress (epinephrine)
Hormone s mula on of GPCR ac vates adenylyl cyclase, increasing cAMP and ac va ng PKA
which then phosphorylates lipases to ac vate. These reac ons release fa y acid from glycerol
backbone
hormonal control of triacylglycerol lipase, then diacylglycerol lipase, then monoacylglycerol
lipase to liberate all 3 fa y acids from glycerol backbone.
what are the steps to B-oxida on?
B carbon undergoes oxida on to release acetyl CoA.
1. Dehydrogena on: of long chain fa y acid- creates C=C double bond. Enzyme: Acyl CoA
dehydrogenase. Electrons (H+) transferred to FAD and released as FADH2.
2. Hydra on: of double bond adds a hydroxyl group to B-carbon. Enzyme: Enol CoA hydratase
3. Dehydrogena on: using NAD as an electron acceptor. Enzyme: 3-hydroxyacyl dehydrogenase
4. Thiolysis: between C2 and C3. A new molecule of CoA breaks the bond by nucleophilic a ack
on C3. Releases C1 and C2 as acetyl CoA. Enzyme: B-ketothiolase
repeat to release 2nd acetyl CoA group
how are acyl-CoA molecules transferred into the mitochondria?
by having a carni ne group added to it. From CPT1. And then CACT (translocase for carni ne)
transfers it across the inner mito membrane.
How is cycling between fa y acid synthesis and degrada on avoided? why do we want to avoid
it?
, Quan es of malonyl CoA and citrate regulate whether synthesis or oxida on is occurring
Malonyl CoA is a regulatory molecule for Fa y acid synthesis and also inhibits CPT1
allosterically.
Reduced malonyl CoA enables FFA oxida on and energy produc on
Citrate also regulates PFK and glycolysis rates- excess signals to glycolysis to slow down and
pushes C through PPP producing NADPH to make FFA
how is glycerol used?
is converted to DHAP and sent to gluconeogenesis
what is the energy yield from FFA oxida on?
7 FADH2
7NADH
8 acetyl CoA
129 ATP
What are the pathways of ketogenesis and ketolysis? Know enzyma c pathways and how
specific ssues u lize these molecules.
Ketolysis: breakdown of ketone molecules
Ketogenesis: the movement of carbon units from the liver to other ssues during a starva on. B
oxida on is restricted to the muscle and liver. The heart and brain can use an alternate carbon
source: ketogenesis.
During starva on, the ketolysis makes acetyl CoA for the brain
KETONE BODIES: acetone, acetoacetate, 2-hydroxybutyric acid
ketone bodies are formed in the liver and require HMG CoA as a star ng material
HMG CoA produc on: Thiolase enzyme combines 2 acetyl-CoA into 4-C acetoacetyl CoA. HMG
CoA synthase adds a 3rd acetyl CoA to make HMG CoA
Making ketones: HMG-CoA reacted with HMG-CoA lyase to remove an acetyl CoA group to
make acetoacetate which then can be either non-ezyma cally decarboxylated into acetone or
B-hydroxoybutyrate dehydrogenase (removed double bond to add H) into D-B-hydroxybutyrate
