Journal September 25, 2026 7 min read

What markers track lipolysis?

A marker-focused review of lipolysis readouts across cell, animal and human research models, covering AMPK-centred signalling, hormone-sensitive lipase, FGF21, EPO and depot-specific differences.

peptides-pro Editorial

Lipolysis is the hydrolytic cleavage of triacylglycerol stored in lipid droplets into glycerol and free fatty acids, and the markers used to track it fall into three broad classes: enzymatic readouts (hormone-sensitive lipase, HSL, and adipose triglyceride lipase activity), circulating analytes (glycerol, free fatty acids, and the lipolytic hormones ghrelin and FGF21), and upstream signalling phospho-events (AMPK phosphorylation, ACC phosphorylation, PKA-dependent cAMP signalling). No single marker is sufficient; the literature typically reports a panel, and the choice of panel depends on whether the model is a cultured adipocyte, a rodent tissue, or a human serum sample.

The pathway most frequently invoked across the evidence assembled here is the AMP-activated protein kinase (AMPK) axis and its downstream transcriptional and autophagic arms, with a second cluster of work centred on G-protein-coupled receptor signalling through glucagon receptor (GCGR) and cAMP-PKA, and a third on sympathetic-driven FGF21 induction.

Research Studies

Sulforaphane and AMPK-centred lipid metabolism in cell and animal models

Sulforaphane (SFN) is an isothiocyanate produced from glucoraphanin in cruciferous vegetables. A narrative review evaluated AMPK-centred mechanisms and drew a distinction between pathway association and experimentally demonstrated AMPK dependence [1]. In cell and animal models, SFN treatment was associated with ACC phosphorylation, inhibition of mTORC1-SREBP signalling, CPT-1-related fatty acid oxidation, PGC-1α/PPAR-α transcriptional regulation, and ULK1-mediated lipophagy [1]. The review notes that most studies measured AMPK phosphorylation without pharmacological or genetic confirmation of dependence, so the marker evidence is associative rather than causal in much of the dataset [1].

Neu1, GCGR desialylation and hepatic cAMP-PKA signalling in old mice

Neuraminidase 1 (Neu1) removes sialic acid from glycoproteins and glycolipids and influences hepatic glycolipid metabolism. Liver-specific Neu1 knockout mice were constructed to probe liver gluconeogenesis and bile acid metabolism, and glucagon-stimulated HepG2 cells were used alongside the animal work [2]. The study links hepatic Neu1 deficiency to metabolic dysregulation via GCGR desialylation-dependent cAMP-PKA signalling and an inflammatory response in old mice [2]. Here the relevant lipolysis-adjacent markers are receptor-level post-translational modification and downstream PKA activity rather than a direct lipolytic rate.

Ethanol, ghrelin secretion and adipose lipolysis in in vitro models

Ghrelin is a stomach-derived orexigenic peptide that typically rises during fasting. Chronic alcohol consumption elevates circulating ghrelin, and ghrelin is reported to promote adipose lipolysis while inhibiting insulin secretion [3]. The cited work investigated how ethanol modulates ghrelin production and disrupts nutrient sensing in ghrelin-secreting cells, using in vitro mechanistic approaches [3]. In this context, circulating ghrelin is the marker of interest, with adipose lipolysis treated as a downstream consequence rather than a directly measured endpoint in the cell system.

hCG and IGF-I as lipolysis-linked analytes in dried blood spot analysis

A technical note described a UHPLC-MS/MS method for analysing hCG and IGF-I from dried blood spots [4]. Both hormones appear on the WADA list of banned molecules; male athletes may use pharmaceutical hCG to stimulate testosterone production before competition, and IGF-I to stimulate muscle protein synthesis, promote glycogen storage, and improve lipolysis [4]. The methodological relevance to lipolysis tracking is indirect: the paper concerns analytical detection in a dried matrix, not the physiology of fat mobilisation.

Erythropoietin and lipolysis in adipose tissue, skeletal muscle and liver

Erythropoietin (EPO) is a key regulator of erythrocyte production, and mice lacking EPO or its receptor die in utero from severe anaemia [5]. Beyond haematopoiesis, EPO influences non-haematopoietic tissues including glucose and fat metabolism in adipose tissue, skeletal muscle, and the liver [5]. EPO enhances lipolysis while inhibiting lipogenic gene expression in white adipose tissue, brown adipose tissue, skeletal muscle, and other sites [5]. The marker set here combines lipolytic enhancement with suppression of lipogenic gene expression, which is a useful reminder that lipolysis markers are often reported alongside lipogenesis markers.

Combined training and serum myostatin and hormone-sensitive lipase in overweight and obese men

A randomized controlled trial examined upper body-based versus lower body-based combined training and serum levels of myostatin (MSTN) and hormone-sensitive lipase (HSL) in overweight and obese men [7]. Myostatin is a myokine involved in skeletal muscle growth and adipose tissue metabolism, while HSL is a key enzyme in lipolysis and fat mobilisation [7]. Thirty-six overweight and obese men were assigned to an upper body combined training group, a lower body combined training group, or a non-exercising control group, with 10 weeks of combined resistance and aerobic training three times per week [7]. Serum MSTN and HSL were the measured outcomes.

Marker	Class	Model in which reported	Source
Hormone-sensitive lipase (HSL)	Lipolytic enzyme	Overweight and obese men, serum	[7]
Myostatin (MSTN)	Myokine	Overweight and obese men, serum	[7]
Ghrelin	Orexigenic peptide	In vitro ghrelin-secreting cells	[3]
ACC phosphorylation	AMPK substrate	Cell and animal models	[1]
GCGR desialylation / PKA	Receptor modification, kinase	Liver-specific Neu1 knockout mice; HepG2	[2]
EPO	Haematopoietic cytokine	Adipose tissue, skeletal muscle, liver	[5]

Alpha ketoglutarate and the surgical stress response in older CABG patients

The AEGIS trial addresses alpha ketoglutarate and geroprotection in surgery [6]. Coronary artery bypass grafting is performed in approximately 400,000 patients in the United States each year, and it invokes a large surgical stress response, with systemic epinephrine increasing 33-fold and norepinephrine increasing 3-fold [6]. Local tissue injury produces sterile inflammation and release of damage-associated molecular patterns, which activate neutrophils and a cascade of cytokines, complement, and coagulation changes; nociceptor activation produces a neurometabolic response involving the sympathetic nervous system and the hypothalamus-pituitary axis [6]. Catecholamines are canonical lipolytic drivers, so this trial is relevant to lipolysis markers chiefly through the sympathetic arm of the stress response rather than through a direct lipolytic assay.

Diet, hepatic transcriptomics and lipidomics in pre-diabetes

Non-alcoholic fatty liver disease affects 25% to 30% of the global population and nearly one third of the population in North America, and is defined as excessive lipid accumulation within hepatocytes without significant alcohol consumption or other chronic liver disease causes [8]. Patients typically present with hepatic steatosis on imaging and elevated liver enzymes alongside insulin resistance features including pre-diabetes, type 2 diabetes, arterial hypertension, dyslipidaemia, and visceral obesity; the minimum criterion for a histological diagnosis is greater than 5 percent steatosis [8]. This trial uses hepatic transcriptomics and lipidomics as the readout layer, which places it at the tissue-composition end of the marker spectrum rather than the circulating-enzyme end.

Depot-specific differences in human visceral and subcutaneous adipose tissue

Paired visceral adipose tissue (VAT) and subcutaneous adipose tissue (SAT) samples were collected from 22 patients with obesity undergoing elective Roux-en-Y surgery, in a study of depot-specific functional differences [11]. The work addresses factors limiting fat cell expandability, an area the authors describe as scarcely explored, and notes that comprehensive functional comparisons of human adipose depots are limited [11]. Depot identity is therefore itself a variable that conditions which lipolysis markers are meaningful in a given sample.

Central lactate, hypothalamic FGF21 and systemic fat mobilisation in rats

Fibroblast growth factor 21 (FGF21) regulates lipid metabolism, and lactate may act centrally to modulate energy homeostasis [12]. Using male Wistar rats, the study examined whether central FGF21 contributes to exercise-induced fat oxidation and whether central lactate regulates its induction and sympathetic-driven lipolysis [12]. This places FGF21 in the marker panel as a centrally induced signal with peripheral lipolytic consequences.

Canagliflozin and adipocyte-intrinsic remodelling in 3T3-L1 cells

Canagliflozin shows anti-obesity effects in clinical practice, but its direct adipocyte-intrinsic functions are less well characterised [9]. The reported work found that canagliflozin promoted 3T3-L1 preadipocyte differentiation, with an AMPK/autophagy-dependent pro-adipogenic effect coupled to enhanced lipid mobilisation and thermogenesis [9]. This is a cell-model finding and should be read as such.

Omentin-1 and in vitro porcine oocyte maturation

Omentin-1 enhanced in vitro oocyte maturation in porcine cells, increasing the percentage of oocytes in metaphase II, progesterone levels, mitochondrial function, and lipolysis via ERK1/2 and PRKAA1, without effect on preimplantation embryo development [10]. The lipolysis readout here is embedded in a reproductive-cell model rather than an adipocyte model.

If you are reading this for personal health reasons

The materials described on this page are sold for laboratory research only, and we do not provide dosing, administration, or medical guidance of any kind. Nothing here is a recommendation to use any compound, and no statement on this page should be read as one. If you are considering a compound for yourself, speak to a licensed clinician.