FATTY ACID SYNTHESIS

What two enzymes are needed for FA synthesis?

acetyl Coa carboxylase - cat synthesis of malonyl Coa

FAS - cytoplasmic multi func enzyme, FA chain attaches to acyl carrier protein (ACP) of FAS, uses NADPH

What packaging system will use to export triglycerides out of the liver

VLDL

What catalzyes the reaction between pyruvate to be converted to OAA

PC

What catalzyes the reaction between pyruvate to be converted to acetyl Coa

PDC

Releases OAA which wil then be recycled in the cycle

What is the rate limiting step for FA synthesis

acetyl Coa carboxylase

cat rxn of acetyl CoA to malonyl CoA

Act via high acetyl CoA

When citrate is in excess in the cytosol what will happen?

It will be concerted to acetyl COA and OAA via citrate lyase

• requires ATP

• Induced via insulin

Where does OAA from cleavage of citrate go to?

Red to malate via malate dehydrogenase in teh presence of NADH and then converted to pyruvate through decarb rxn catalized via malic enzyme

**malic enzyme is not a dehydgranse thsu will go from NADPH to NADP

Where does NADPH go after being made via the malic enzyme?

Reductive synthesis of FAs, sterols, steroids

cyc p450

detox of oxygen species

What pathways made NADPH

PPP and malic enzyme (called the trans hydrogenation pathway)

***releases Co2 during this step

What hormone activates pyruvate dehydrogenase

Insulin —→ alos acts PDC phosphatase —→malic enzyme —→g-6-DH —>citrate lyase

Also activated via dephophorlization

Why is the activity of G6P needed for FA synthesis?

Glucose-6-phosphate feeds into the pentose phosphate pathway (PPP), also known as the hexose monophosphate shunt, where it plays a key role in generating NADPH.

A patient comes in with elevated citrate levels in the blood due to inh of isocitrate dehydrogenase. What is causing this?

NADH is the inhibitor of isocitrate dehydro

How is linoleic acid to arachindonic acid made?

Desat at carbon 6 —> elongated by 2 carbons —>desat at carbon 5 —>arachidonyl -CoA

Desat —>makes double bond

Where does desaturation occur and what does this process require?

Occurs in teh ER and requires O2, NADH, and cyc b5

cyc derived via succinyl CoA

Describe the process of FA enlongation

2 carbons at a time donated via malonyl CoA

NADPH provides reducing power

Palm —>stearyl CoA (18C) —>very long chain ***important for brain

Describe palmitate elongation and activation.

needs biotin ie carboxy rxn to acetyl CoA carboxylase

What is needed for the conversion of acetyl CoA to malonyl CoA

Bitoin, ATP

***acetyl CoA arboxylase is the RLS of FA synthesis

How is acetyl carboxylase regualted?

Act via citrate ande insulin

INh via palmitoyl CoA nad phosphilization via AMP activated protein kinase

What happens when glucagon is high, then what about insulin.

glucagon inh

inlsuin act

🔁 How is ACC regulated by glucagon and insulin? 🟠 When Glucagon is High (Fasting State):

• Glucagon → Activates protein kinase A (PKA) via cAMP signaling.

• PKA phosphorylates ACC, rendering it inactive.

• Result:
  🔻 Fatty acid synthesis is inhibited
  🔺 Fatty acid oxidation is favored (since malonyl-CoA levels drop, removing the inhibition on CPT1)

👉 This happens during fasting, exercise, or low glucose — the body wants to mobilize fat, not store it.

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🟢 When Insulin is High (Fed State):

• Insulin → Activates protein phosphatase, which dephosphorylates ACC, making it active.

• Result:
  🔺 Fatty acid synthesis is stimulated
  🔻 Fatty acid oxidation is inhibited (due to ↑ malonyl-CoA)

👉 This happens during feeding, when glucose is abundant and the body wants to store energy as fat.

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🧠 Summary Table:

Hormone	ACC Phosphorylation	ACC Activity	FA Synthesis	FA Oxidation
Glucagon	✅ Phosphorylated (inactive)	🔻 Decreased	🔻 Inhibited	🔺 Increased
Insulin	❌ Dephosphorylated (active)	🔺 Increased	🔺 Stimulated	🔻 Inhibited