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Human fat cell lipolysis: biochemistry, regulation and clinical role.
Abstract
Release of fatty acids (FAs) from adipose tissue through lipolysis in fat cells is a key event in many processes. FAs are not only energy substrates but also signalling molecules and substrates for lipoprotein production by the liver. Fat cells consist of>95% triglycerides that are hydrolysed during lipolysis to glycerol and FAs. The major rate-limiting factor for lipolysis is hormone-sensitive lipase, but additional lipases such as adipose tissue triglyceride lipase may also play a role. The regulation of human fat cell lipolysis is, in many ways, species unique. Only catecholamines, insulin and natriuretic peptides have pronounced acute effects. Catecholamines influence lipolysis through four different adrenoceptor subtypes, in contrast to rodents where only one subtype (beta(3)) is of major importance. There are regional variations in adipocyte lipolysis leading to more release of FAs from the visceral than subcutaneous adipose tissue during hormone stimulation (insulin, catecholamines). Since, only visceral fat is linked to the liver (by the portal vein), alterations in visceral adipocyte tissue lipolysis have direct effects on the liver through portal FA release. The regional variations in lipolysis are further enhanced in obesity and polycystic ovarian syndrome, and are of importance for dyslipidaemia, hyperinsulinaemia and glucose intolerance in these conditions. There is a marked elevation of circulating FA levels among the obese, which may be due to enhanced production of tumour necrosis factor alpha in adipose tissue. This cytokine stimulates lipolysis through so-called MAP kinases. Pharmacological agents in clinical practice such as nicotinic acid and glitazones exert lipid-lowering and glucose-lowering effects, respectively, by decreasing FA output from the adipose tissue. This review covers the biochemistry, regulation and clinical aspects of human fat cell lipolysis.
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“The counter-regulatory pathway involving catecholamine-related HSL stimulation is also attenuated in obesity, rendering adipocytes insensitive to catecholamines”
From Effect of Exercise Training on Fat Loss—Energetic Perspectives and the Role of Improved Adipose Tissue Function and Body Fat Distribution (2021) · cites this paper as Arner, 2005
In the citing paper
“Catecholamines act through β-adrenergic receptors in adipocytes, inducing an increase in cAMP levels, which activates PKA and ultimately enhances lipolysis (Arner, 2005).”
From Effect of Exercise Training on Fat Loss—Energetic Perspectives and the Role of Improved Adipose Tissue Function and Body Fat Distribution (2021) · cites this paper as Arner, 2005
In the citing paper
“In adipocytes, fat is stored as triacylglycerol in lipid droplets that make up > 95% of the intracellular content (Arner, 2005).”
From Effect of Exercise Training on Fat Loss—Energetic Perspectives and the Role of Improved Adipose Tissue Function and Body Fat Distribution (2021) · cites this paper as Arner, 2005
In the citing paper
“Insulin signaling in adipocytes through the insulin receptor increases glucose and fatty acid (FA) uptake into the adipocytes (Arner, 2005).”
From Effect of Exercise Training on Fat Loss—Energetic Perspectives and the Role of Improved Adipose Tissue Function and Body Fat Distribution (2021) · cites this paper as Arner, 2005
In the citing paper
“When insulin levels are relatively low, AT releases FFAs into the bloodstream, making them available for muscle and other tissues when needed (Arner, 2005).”
From Effect of Exercise Training on Fat Loss—Energetic Perspectives and the Role of Improved Adipose Tissue Function and Body Fat Distribution (2021) · cites this paper as Arner, 2005
In the citing paper
“Given that the effect of insulin on lipolysis is less pronounced in visceral fat than subcutaneous fat, 60 the slightly higher intraabdominal fat content may have contributed to the higher S-FFA concentrations in type 2 diabetic patients as compared with nondiabetic subjects.”
From Increased liver fat, impaired insulin clearance, and hepatic and adipose tissue insulin resistance in type 2 diabetes. (2008) · cites this paper as [60]
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Metadata
- Authors
- Arner, P.
- Affiliations
- Karolinska University Hospital (SE)
- Corresponding author
- Arner, Peter
- ORCID
- Arner, Peter
- Venue
- Best Practice & Research Clinical Endocrinology & Metabolism
- Publisher
- Elsevier BV
- Published
- 2005-12
- Volume
- 19
- Issue
- 4
- Pages
- 471-482
- ISSN
- 1521-690X (ISSN-L)
- OpenAlex
- W1981933686
- Cited by
- 401
- References
- 46
- Citations by year
- 2026: 15 · 2025: 8 · 2024: 12 · 2023: 9 · 2022: 19 · 2021: 20 · 2020: 19 · 2019: 17 · 2018: 10 · 2017: 18 · 2016: 14 · 2015: 14 · 2014: 27 · 2013: 30 · 2012: 25
- FWCI
- 2.63
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Best Practice & Research Clinical Endocrinology & Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Lipid metabolism and biosynthesis
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
- Keywords
- adipocyte lipolysis, fatty acid release, hormone-sensitive lipase, catecholamines, adrenergic receptors, insulin, natriuretic peptides, visceral adipose tissue, subcutaneous adipose tissue, portal vein, hepatic lipoprotein production, obesity, polycystic ovary syndrome, TNF-α, mitogen-activated protein kinase, nicotinic acid, thiazolidinediones, dyslipidemia, hyperinsulinemia, impaired glucose tolerance
- MeSH terms
- Catecholamines, Female, Humans, Insulin, Lipolysis, Obesity, Polycystic Ovary Syndrome, Triglycerides, Adipocytes, Natriuretic Peptides, Lipid Metabolism
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