Direct Effect of Glucocorticoids on Lipolysis in Adipocytes
Open accessAbstract
Hypercortisolemia and glucocorticoid treatment cause elevated level of circulating free fatty acids (FFAs). The basis of this phenomenon has long been linked to the effect of glucocorticoids permitting and enhancing the adipose lipolysis response to various hormones. In this study, we demonstrate that glucocorticoids directly stimulate lipolysis in rat primary adipocytes in a dose- and time-responsive manner; this lipolytic action was attenuated by treatment with the glucocorticoid antagonist RU486. Dexamethasone down-regulates mRNA and protein levels of cyclic-nucleotide phosphodiesterase 3B, thereby elevating cellular cAMP production and activating protein kinase A (PKA). On inhibition of PKA but not other kinases, the lipolysis response ceases. Furthermore, dexamethasone induces phosphorylation and down-regulation of perilipin, a lipid droplet-associating protein that modulates lipolysis; this effect is restored by RU486 or PKA inhibitor H89. Dexamethasone up-regulates mRNA and protein levels of hormone-sensitive lipase (HSL) and adipose triglyceride lipase; these effects, parallel to increased lipolysis, are attenuated by RU486 or actinomycin D. Phosphorylation at Ser-563 and Ser-660 residues of HSL and activity of cellular lipases are elevated on dexamethasone stimulation but abrogated by the coaddition of H89. However, dexamethasone does not induce HSL translocation to the lipid droplet surface in differentiated adipocytes. We show that elevated FFA concentration in plasma is associated with increased lipase activity and lipolysis in vivo in adipose tissues of dexamethasone-treated rats. Therefore, the lipolytic action of glucocorticoids liberates FFA efflux from adipocytes to the bloodstream, which could be a cellular basis of systemic FFA elevation in response to glucocorticoid challenge.
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Glucocorticoids enhance basal lipolysis in rodents.
“However, glucocorticoids enhance basal lipolysis in rodents,4, 23 which we did not observe in humans, highlighting species‐specific differences in the glucocorticoid regulation of lipolysis.”
From Acute physiological effects of glucocorticoids on fuel metabolism in humans are permissive but not direct (2017) · cites this paper as [4]
In vitro studies in adipocytes have shown lipolytic rates to be increased, unchanged or decreased by glucocorticoids.
“For example, in vitro studies in adipocytes have shown lipolytic rates to be increased,4 unchanged5 or decreased6 by glucocorticoids.”
From Acute physiological effects of glucocorticoids on fuel metabolism in humans are permissive but not direct (2017) · cites this paper as [4]
Additional genes outside the classic lipolytic pathway have been implicated in the lipolytic effects of glucocorticoids, such as phosphodiesterase 3b, pigment epithelium derived factor, and angiopoietin-like 4.
“Additional genes outside the classic lipolytic pathway have been implicated in the lipolytic effects of glucocorticoids, such as phosphodiesterase 3b,4 pigment epithelium derived factor24 and angiopoietin‐like 4;25”
From Acute physiological effects of glucocorticoids on fuel metabolism in humans are permissive but not direct (2017) · cites this paper as [4]
Previous studies have tested how glucocorticoids regulate the lipolytic pathway in rodents by increasing ATGL and HSL.
“Although previous studies have tested how glucocorticoids regulate the lipolytic pathway in rodents (by increasing ATGL and HSL),4, 23 this had not been tested in vivo in humans.”
From Acute physiological effects of glucocorticoids on fuel metabolism in humans are permissive but not direct (2017) · cites this paper as [4]
This had not been tested in vivo in humans.
“Although previous studies have tested how glucocorticoids regulate the lipolytic pathway in rodents (by increasing ATGL and HSL),4, 23 this had not been tested in vivo in humans.”
From Acute physiological effects of glucocorticoids on fuel metabolism in humans are permissive but not direct (2017) · cites this paper as [4]
The Animal studies section describes dexamethasone experiments in rats, and the Discussion reports increased ATGL and HSL in primary adipocytes. Neither passage says whether this pathway had previously been tested in vivo in humans; searches for human in vivo studies and an explicit research gap found no such statement in our copy. (LLM, conf=0.72)
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- Authors
- Xu, C., He, J., Jiang, H., Zu, L., Zhai, W., Pu, S., & Xu, G.
- Affiliations
- Peking University (CN)
- Zhengzhou University (CN)
- Corresponding author
- Xu, Guoheng
- Venue
- Molecular Endocrinology
- Publisher
- The Endocrine Society
- Published
- 2009-08
- Volume
- 23
- Issue
- 8
- Pages
- 1161-1170
- ISSN
- 0888-8809 (ISSN-L)
- 1944-9917
- PMC
- PMC5419195
- OpenAlex
- W2115274616
- Cited by
- 291
- References
- 46
- Citations by year
- 2026: 12 · 2025: 13 · 2024: 22 · 2023: 22 · 2022: 14 · 2021: 20 · 2020: 21 · 2019: 20 · 2018: 16 · 2017: 26 · 2016: 22 · 2015: 16 · 2014: 16 · 2013: 17 · 2012: 17
- FWCI
- 6.00
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Molecular Endocrinology (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- University of Pittsburgh
- National Natural Science Foundation of China (30770803, 30890042, 30670779)
- Peking University
- National Key Research and Development Program of China (2006CB 503910, 2009CB941603)
- Peking University Health Science Center
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Lipid metabolism and biosynthesis
- Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Peroxisome Proliferator-Activated Receptors
- Keywords
- glucocorticoids, dexamethasone, adipocyte lipolysis, free fatty acids, cyclic AMP, protein kinase A, PDE3B, perilipin, hormone-sensitive lipase, adipose triglyceride lipase, hypercortisolism, RU486, H89, lipid droplets
- MeSH terms
- Adipose Tissue, Animals, Dexamethasone, Dose-Response Relationship, Drug, Enzyme Inhibitors, Glucocorticoids, Isoquinolines, Lipolysis, Male, Models, Biological, Serine, Sulfonamides, Rats, Sprague-Dawley, Adipocytes, Rats, Cyclic Nucleotide Phosphodiesterases, Type 3
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