Lipolysis equation

Lipolysis is the breakdown of triglycerides (stored fats) into glycerol and free fatty acids. The overall equation is:

Triglyceride + 3 H₂O → Glycerol + 3 Fatty Acids

Or more precisely:

C₅₅H₁₀₄O₆ + 3 H₂O → C₃H₈O₃ + 3 C₁₇H₃₅COOH (a generic tripalmitin example)

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Here is a complete breakdown of the lipolysis equation and its biochemistry, drawn from Harper's Illustrated Biochemistry and Mulholland & Greenfield's Surgery:

Lipolysis - The Overall Equation

Triglyceride (Triacylglycerol) + 3 H₂O → Glycerol + 3 Free Fatty Acids (FFA)

This is a sequential hydrolysis - it does NOT happen in a single step. Three separate lipase reactions cleave one fatty acid at a time:

Step-by-Step Reactions

Step	Enzyme	Reaction	Products
1	Hormone-sensitive lipase (HSL) - rate-limiting	Triacylglycerol (TG) → Diacylglycerol (DG) + FFA	DG + FFA
2	Diacylglycerol lipase	Diacylglycerol (DG) → Monoacylglycerol (MG) + FFA	MG + FFA
3	2-Monoacylglycerol lipase (2-MAGL)	Monoacylglycerol (MG) → Glycerol + FFA	Glycerol + FFA

Net result: 1 TG → 1 Glycerol + 3 FFA

What Happens to the Products?

Glycerol - enters glycolysis as dihydroxyacetone phosphate (DHAP); also used as a substrate for gluconeogenesis in the liver
Free Fatty Acids (FFA) - transported in blood bound to albumin; taken up by heart, skeletal muscle, and liver; undergo beta-oxidation in the mitochondria to generate acetyl-CoA → ATP

Hormonal Control of Lipolysis

The diagram below (from Harper's Illustrated Biochemistry) shows the full regulatory cascade:

Control of adipose tissue lipolysis - hormone-sensitive lipase activation cascade

Lipolysis is stimulated by:

Catecholamines (epinephrine, norepinephrine) - via β-adrenergic receptors → adenylate cyclase → ↑ cAMP → cAMP-dependent protein kinase → phosphorylates and activates HSL
Glucagon, ACTH, TSH, GH - similar cAMP-mediated pathway
Glucocorticoids - via cAMP-independent pathway (new lipase protein synthesis)

Lipolysis is inhibited by:

Insulin - inhibits adenylate cyclase, activates phosphodiesterase (degrades cAMP), activates lipase phosphatase (inactivates HSL)
Nicotinic acid, Prostaglandin E₁ - inhibit adenylate cyclase via Gᵢ protein
Adenosine - inhibits adenylate cyclase
High concentrations of FFA (negative feedback)

Key Points

HSL is the rate-limiting enzyme of lipolysis (not the first enzyme in fat synthesis)
Adipose tissue is extremely sensitive to insulin - even small rises in insulin powerfully suppress lipolysis
Excess lipolysis (as in starvation or uncontrolled diabetes) floods the liver with acetyl-CoA, leading to ketone body production
Methylxanthines (caffeine, theophylline) enhance lipolysis by blocking phosphodiesterase (preventing cAMP degradation)

Sources: - Harper's Illustrated Biochemistry, 32nd Ed., p. 268 | Mulholland & Greenfield's Surgery, 7e, p. 83

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Lipolysis example

Here is a concrete worked example of lipolysis using a real triglyceride molecule.

Worked Example: Lipolysis of Tripalmitin

Tripalmitin (glyceryl tripalmitate) is a common saturated triglyceride made of glycerol + 3 palmitic acid (C16:0) chains.

Molecular Formula

Tripalmitin: C₅₁H₉₈O₆
Palmitic acid: C₁₅H₃₁COOH (CH₃-(CH₂)₁₄-COOH)

The Reaction

C₅₁H₉₈O₆ + 3 H₂O → C₃H₈O₃ + 3 C₁₆H₃₂O₂

Tripalmitin + Water → Glycerol + 3 Palmitic acid

Step-by-Step Hydrolysis

Step 1 (HSL - rate-limiting):
Tripalmitin → Dipalmitin + Palmitic acid (1 FFA released)

Step 2 (Diacylglycerol lipase):
Dipalmitin → Monopalmitin + Palmitic acid (2nd FFA released)

Step 3 (2-Monoacylglycerol lipase):
Monopalmitin → Glycerol + Palmitic acid (3rd FFA released)

What Happens Next - Energy Accounting

Each palmitic acid (C16) undergoes beta-oxidation:

Product	Quantity	ATP yield
Acetyl-CoA	8 per palmitate	8 × 10 = 80 ATP
NADH	7 per palmitate	7 × 2.5 = 17.5 ATP
FADH₂	7 per palmitate	7 × 1.5 = 10.5 ATP
Activation cost	-1 per palmitate	-2 ATP
Net per palmitate		~106 ATP

3 palmitates × 106 = ~318 ATP from fatty acids alone, plus a small yield from glycerol entering glycolysis.

Clinical Example: Diabetic Ketoacidosis (DKA)

A type 1 diabetic with no insulin experiences uncontrolled lipolysis:

No insulin → HSL is not inhibited → massive TG breakdown in adipose
Flood of FFA enters the liver
Liver overwhelmed → excess acetyl-CoA cannot enter TCA cycle
Acetyl-CoA diverted → ketone bodies (acetoacetate, β-hydroxybutyrate, acetone)
Result: metabolic acidosis, fruity breath, Kussmaul breathing

This is exactly why insulin is the treatment - it re-inhibits HSL and stops the lipolytic cascade.

Another Example: Fasting/Exercise

During a 12-hour fast or aerobic exercise:

Blood glucose drops → insulin falls, glucagon rises
Glucagon → ↑ cAMP → activates HSL in adipocytes
FFAs released → skeletal muscle and heart switch to fat as primary fuel
Glycerol released → liver uses it for gluconeogenesis to maintain blood glucose

This is the normal, controlled version of lipolysis - the body's way of mobilizing stored energy.

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