Research
Hormonal
Insulin is the primary hormonal inhibitor of lipolysis, acting by activating phosphodiesterase-3B to lower cAMP levels and preventing hormone-sensitive lipase (HSL) activation.
Insulin is the body's main signal to stop breaking down fat. High insulin levels (e.g., from high carbohydrate intake) will inhibit lipolysis. To maximize fat mobilization, managing insulin through dietary composition and timing is important, but it is just one part of the complex regulation involving catecholamines and other factors.
StrongSupportsVERY_HIGH confidence
Among all endocrine factors, insulin is quantitatively and qualitatively the most relevant one... Insulin powerfully inhibits catecholamine-induced lipolysis and basal phosphorylation (via a PKB/Akt-dependent action) of phosphodiesterase-3B (PDE-3B). The phosphodiesterase catalyses the breakdown of cAMP to its inactive form, thereby decreasing cAMP levels, which in turn reduces PKA activation and, therefore, also translates into preventing HSL stimulation.
Why this rating
This is a foundational concept in metabolic physiology, extensively reviewed and cited in the paper.
Source
Regulation of adipocyte lipolysis
Gema Frühbeck et al. · Nutrition Research Reviews · 2014
DOI 10.1017/s095442241400002x
narrative_reviewCited 427×
Read the paper DOI resolved against Crossref · corpus check 2026-06-10
More from this paper
- Catecholamines (adrenaline and noradrenaline) stimulate lipolysis by binding to beta-adrenergic receptors, increasing cAMP, and activating Protein Kinase A (PKA) to phosphorylate Hormone-Sensitive Lipase (HSL) and Perilipin.Strong
- Caffeine and methylxanthines stimulate adipocyte lipolysis by antagonizing A1-adenosine receptors and inhibiting phosphodiesterase, thereby increasing intracellular cAMP levels.Good
- Adiponectin inhibits spontaneous and catecholamine-induced lipolysis in non-obese humans via AMPK-dependent mechanisms, and its levels are decreased in obesity.Good
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