Cited by 276Estrogen and related hormone effectsAdipose Tissue and MetabolismLipid metabolism and biosynthesis

Estrogen Controls Lipolysis by Up-Regulating α2A-Adrenergic Receptors Directly in Human Adipose Tissue through the Estrogen Receptor α. Implications for the Female Fat Distribution

Pedersen, Steen B., Kristensen, Kurt, Hermann, Pernille A., Katzenellenbogen, John A., Richelsen, Bjørn·2004·The Journal of Clinical Endocrinology & Metabolism

Abstract

Estrogen seems to promote and maintain the typical female type of fat distribution that is characterized by accumulation of adipose tissue, especially in the sc fat depot, with only modest accumulation of adipose tissue intraabdominally. However, it is completely unknown how estrogen controls the fat accumulation. We studied the effects of estradiol in vivo and in vitro on human adipose tissue metabolism and found that estradiol directly increases the number of antilipolytic α2A-adrenergic receptors in sc adipocytes. The increased number of α2A-adrenergic receptors caused an attenuated lipolytic response of epinephrine in sc adipocytes; in contrast, no effect of estrogen on α2A-adrenergic receptor mRNA expression was observed in adipocytes from the intraabdominal fat depot. These findings show that estrogen lowers the lipolytic response in sc fat depot by increasing the number of antilipolytic α2A-adrenergic receptors, whereas estrogen seems not to affect lipolysis in adipocytes from the intraabdominal fat depot. Using estrogen receptor subtype-specific ligands, we found that this effect of estrogen was caused through the estrogen receptor subtype α. These findings demonstrate that estrogen attenuates the lipolytic response through up-regulation of the number of antilipolytic α2A-adrenergic receptors only in sc and not in visceral fat depots. Thus, our findings offer an explanation how estrogen maintains the typical female sc fat distribution because estrogen seems to inhibit lipolysis only in sc depots and thereby shifts the assimilation of fat from intraabdominal depots to sc depots.

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Crossref · 10.1210/jc.2003-031327

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  • The mechanisms behind the hormonal regulation of adipose tissue distribution are complex and still incompletely characterized, but may arise from effects on lipolysis and lipogenesis, adipocyte differentiation, and insulin sensitivity.

    “Although the mechanisms behind the hormonal regulation of AT distribution are complex and still incompletely characterized, they may arise from effects on lipolysis and lipogenesis, adipocyte differentiation, and insulin sensitivity [9,24,[28][29][30].”

    From Adipose tissue estrogen production and metabolism in premenopausal women (2021) · cites this paper as [28]

    The introduction says the pathways by which estrogen affects adipose-tissue metabolism are not understood and discusses lipolysis and fat uptake through lipoprotein lipase. The Discussion links estrogen’s effects on lipolysis to fat distribution. Our copy does not establish adipocyte differentiation or insulin sensitivity as mechanisms of hormonal fat distribution; those terms appear in the retrieved references, not as findings of this paper. (LLM, conf=0.86)

    Experimental — accuracy not yet measured
  • Estrogen upregulates α2-adrenergic receptors in abdominal subcutaneous adipocytes.

    “estrogen upregulates α2-adrenergic receptors in abdominal subcutaneous adipocytes (55).”
  • Estradiol directly increases the number of antilipolytic α2A-adrenergic receptors in subcutaneous adipocytes.

    “Estradiol directly increases the number of antilipolytic α2A-adrenergic receptors in subcutaneous adipocytes [69].”

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Authors
Pedersen, S. B., Kristensen, K., Hermann, P. A., Katzenellenbogen, J. A., & Richelsen, B.
Affiliations
  • Aarhus University Hospital (DK)
  • University of Illinois Urbana-Champaign (US)
  • Aarhus University (DK)
Corresponding author
Pedersen, Steen B.
Venue
The Journal of Clinical Endocrinology & Metabolism
Published
2004-04-01
Volume
89
Issue
4
Pages
1869-1878
ISSN
  • 0021-972X (ISSN-L)
  • 1945-7197
OpenAlex
W2068408721
Cited by
276
References
50
Citations by year
2026: 6 · 2025: 23 · 2024: 19 · 2023: 16 · 2022: 15 · 2021: 19 · 2020: 17 · 2019: 15 · 2018: 12 · 2017: 16 · 2016: 6 · 2015: 10 · 2014: 15 · 2013: 8 · 2012: 11
FWCI
5.30
Type
journal article
Language
en
Open access
closed
Locations
  • The Journal of Clinical Endocrinology & Metabolism (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Sundhed og Sygdom, Det Frie Forskningsråd
  • National Institutes of Health
  • National Institute of Diabetes and Digestive and Kidney Diseases (R37DK015556)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
  • Health Sciences › Medicine › Physiology › Adipose Tissue and Metabolism
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Lipid metabolism and biosynthesis
Keywords
estrogen, estradiol, lipolysis, alpha2A-adrenergic receptor, estrogen receptor alpha, subcutaneous adipose tissue, visceral adipose tissue, epinephrine, adipocyte metabolism, receptor up-regulation
MeSH terms
Abdomen, Adipose Tissue, Adrenergic alpha-Antagonists, Sterol Esterase, Estradiol, Estrogens, Female, Humans, Lipolysis, Lipoprotein Lipase, Receptors, Adrenergic, Receptors, Estrogen, RNA, Messenger, Sex Characteristics, Yohimbine, Up-Regulation, Adipocytes, Receptors, Adrenergic, alpha-2, Subcutaneous Tissue, Estrogen Receptor alpha, In Vitro Techniques

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