Oxidative

lipolysis

TAG breakdown to glycerol + free fatty acids.

Main fast-acting hormone for lipolysis

Glucagon.

What other acute hormone promotes lipolysis?

Epinephrine.

Which hormone chronically increases lipolysis?

Cortisol.

lipogenesis

De novo fatty acid synthesis and TAG formation.

Main hormone that stimulates lipogenesis

Insulin.

What are TAGs?

Storage/transport form of fat.

How do free fatty acids travel in blood?

Bound to albumin.

Tissues that commonly oxidize fatty acids

Liver, muscle, adipose.

Where does β-oxidation occur?

Mitochondria.

Immediate products of β-oxidation

Acetyl-CoA, NADH, FADHI.

Where does acetyl-CoA go after β-oxidation?

TCA cycle.

What uses NADH/FADHI from β-oxidation?

Electron transport system (ETS).

What hormonal shift marks fasting/starvation?

↑ Glucagon/epinephrine/cortisol, ↓ insulin.

What rises in blood when adipose undergoes lipolysis?

Free fatty acids.

What happens to glycerol from lipolysis?

Used for gluconeogenesis.

ketogenesis

Hepatic production of ketone bodies from acetyl-CoA.

Physiologic settings that trigger ketogenesis

Fasting, starvation, low-carb intake, untreated type 1 diabetes.

Proximate trigger for ketogenesis

Acetyl-CoA exceeds TCA capacity.

Name the three ketone bodies

Acetoacetate, β-hydroxybutyrate, acetone.

Can the brain use ketones?

Yes (especially during prolonged fasting).

Can the liver use ketones?

No (it produces them but doesn't utilize them).

ketonemia

Elevated blood ketones.

ketonuria

Presence of ketones in urine.

Normal blood ketone level (approx.)

< 0.2 mmol/L.

Level consistent with ketoacidosis (approx.)

> 7 mmol/L.

Major causes of significant ketosis

Uncontrolled diabetes, starvation, fasting, low-carb diet.

Dual role of glucagon in fasting

Stimulates gluconeogenesis and lipolysis.

Key chronic effects of excess cortisol

Insulin resistance, hyperglycemia, muscle wasting, fat redistribution.

Where does de novo FA synthesis occur primarily?

Liver.

Nutritional state favoring FA synthesis

Energy/carbohydrate surplus (post-meal).

What happens to newly synthesized FA in liver?

Esterified to TAG and exported in VLDL.

Are lipogenesis and β-oxidation reverse pathways?

No—different enzymes, compartments, and regulation.

Cellular location of lipogenesis

Cytosol.

How do acetyl units reach cytosol for FA synthesis?

Via citrate export (malate-citrate shuttle).

What does cytosolic citrate become?

Acetyl-CoA + oxaloacetate.

What does insulin stimulate post-meal that supports FA synthesis?

Glycolysis and PDH → ↑ acetyl-CoA and ↑ citrate.

What happens to insulin during fasting?

It falls.

Effect of low insulin on pathways

↓ Lipogenesis, ↑ lipolysis and ↑ ketogenesis.

How are synthesized fatty acids stored?

Esterified to glycerol as TAG.

How are hepatic TAGs delivered to adipose?

Packed into VLDL.

Early effect of alcohol on liver fat handling

Inhibits FA oxidation → re-esterification to TAG → ↑ VLDL and hypertriglyceridemia.

Late effect in alcoholic fatty liver

Impaired VLDL production → TAG accumulates (steatosis).

One-line contrast of control: lipolysis vs lipogenesis

Glucagon/epi/cortisol ↑ lipolysis; insulin ↑ lipogenesis.

Quick pathway summary in fasting

Lipolysis → FFA → β-oxidation → acetyl-CoA → ketogenesis (if excess).

Quick pathway summary in fed state

Glucose surplus → citrate export → FA synthesis → TAG → VLDL → adipose storage.