Biochemistry · Enzyme
Hormone-sensitive lipase (HSL) !
Hormone-sensitive lipase releases fatty acids from stored fat when the body needs energy (fasting, stress, exercise).
Updated 2026-11-01
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Key facts
- In the adipocyte: mainly hydrolyses diacylglycerol to monoacylglycerol; ATGL makes the first cut of triacylglycerol.
- Glucagon and adrenaline activate it (β receptor, cAMP, PKA), phosphorylating it together with perilipin.
- Insulin switches it off: it activates phosphodiesterase, lowers cAMP and it is dephosphorylated.
- Fatty acids travel bound to albumin to liver and muscle; glycerol goes to the liver for gluconeogenesis.
Regulation
- Phosphorylation by PKA (adrenaline, glucagon, noradrenaline): activates.
- Insulin (phosphodiesterase 3B) and AMPK: inhibit.
Inhibitors and toxins
- Insulin (physiological)
- Experimental HSL inhibitors
Clinical notes
- Without insulin (type 1 diabetes) lipolysis runs free: many fatty acids reach the liver and ketones form.
- Loss-of-function LIPE variants cause partial lipodystrophy with insulin resistance.
Pathways
Related conditions
Related
- Palmitate (palmitic acid)
- Carnitine shuttle
- Carnitine palmitoyltransferase I (CPT-I)
- Acetyl-CoA carboxylase (ACC)
Test yourself
Think of the answer, then tap the question to see it.
Which hormones activate hormone-sensitive lipase?
Adrenaline, noradrenaline and glucagon, via cAMP and PKA.
How does insulin slow lipolysis?
It activates phosphodiesterase 3B, cAMP falls and HSL is left dephosphorylated and inactive.
What happens to the glycerol released by lipolysis?
It goes to the liver, where glycerol kinase phosphorylates it and it enters gluconeogenesis.
Educational information, not medical advice. For any symptom, see a health professional.
Sources: LIPE: Hormone-sensitive lipase (human) (UniProt, 2026); Triglyceride catabolism (Reactome, 2026); 8ZVQ: Cryo-EM Structure of Human Hormone-sensitive Lipase (HSL) (RCSB Protein Data Bank, 2026).
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Representative model, for educational purposes only.