Lipedema and the Potential Role of Estrogen in Excessive Adipose Tissue Accumulation

Lipedema is a painful fat disorder that affects ~11% of the female population. It is characterized by bilateral, disproportionate accumulation of subcutaneous adipose tissue predominantly in the lower body. The onset of lipedema pathophysiology is thought to occur during periods of hormonal fluctuat...

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Autores principales:	Kaleigh Katzer, Jessica L. Hill, Kara B. McIver, Michelle T. Foster
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	lipedema adipose tissue estrogen receptor lipoprotein lipase GLUT4 peroxisome proliferator-activated receptor gamma Biology (General) QH301-705.5 Chemistry QD1-999
Acceso en línea:	https://doaj.org/article/60e60c55367c4b41bb2cc74cf1484691
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spelling	oai:doaj.org-article:60e60c55367c4b41bb2cc74cf14846912021-11-11T17:10:49ZLipedema and the Potential Role of Estrogen in Excessive Adipose Tissue Accumulation10.3390/ijms2221117201422-00671661-6596https://doaj.org/article/60e60c55367c4b41bb2cc74cf14846912021-10-01T00:00:00Zhttps://www.mdpi.com/1422-0067/22/21/11720https://doaj.org/toc/1661-6596https://doaj.org/toc/1422-0067Lipedema is a painful fat disorder that affects ~11% of the female population. It is characterized by bilateral, disproportionate accumulation of subcutaneous adipose tissue predominantly in the lower body. The onset of lipedema pathophysiology is thought to occur during periods of hormonal fluctuation, such as puberty, pregnancy, or menopause. Although the identification and characterization of lipedema have improved, the underlying disease etiology remains to be elucidated. Estrogen, a key regulator of adipocyte lipid and glucose metabolism, and female-associated body fat distribution are postulated to play a contributory role in the pathophysiology of lipedema. Dysregulation of adipose tissue accumulation via estrogen signaling likely occurs by two mechanisms: (1). altered adipocyte estrogen receptor distribution (ERα/ERß ratio) and subsequent metabolic signaling and/or (2). increased release of adipocyte-produced steroidogenic enzymes leading to increased paracrine estrogen release. These alterations could result in increased activation of peroxisome proliferator-activated receptor γ (PPARγ), free fatty acid entry into adipocytes, glucose uptake, and angiogenesis while decreasing lipolysis, mitochondriogenesis, and mitochondrial function. Together, these metabolic alterations would lead to increased adipogenesis and adipocyte lipid deposition, resulting in increased adipose depot mass. This review summarizes research characterizing estrogen-mediated adipose tissue metabolism and its possible relation to excessive adipose tissue accumulation associated with lipedema.Kaleigh KatzerJessica L. HillKara B. McIverMichelle T. FosterMDPI AGarticlelipedemaadipose tissueestrogen receptorlipoprotein lipaseGLUT4peroxisome proliferator-activated receptor gammaBiology (General)QH301-705.5ChemistryQD1-999ENInternational Journal of Molecular Sciences, Vol 22, Iss 11720, p 11720 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	lipedema adipose tissue estrogen receptor lipoprotein lipase GLUT4 peroxisome proliferator-activated receptor gamma Biology (General) QH301-705.5 Chemistry QD1-999
spellingShingle	lipedema adipose tissue estrogen receptor lipoprotein lipase GLUT4 peroxisome proliferator-activated receptor gamma Biology (General) QH301-705.5 Chemistry QD1-999 Kaleigh Katzer Jessica L. Hill Kara B. McIver Michelle T. Foster Lipedema and the Potential Role of Estrogen in Excessive Adipose Tissue Accumulation
description	Lipedema is a painful fat disorder that affects ~11% of the female population. It is characterized by bilateral, disproportionate accumulation of subcutaneous adipose tissue predominantly in the lower body. The onset of lipedema pathophysiology is thought to occur during periods of hormonal fluctuation, such as puberty, pregnancy, or menopause. Although the identification and characterization of lipedema have improved, the underlying disease etiology remains to be elucidated. Estrogen, a key regulator of adipocyte lipid and glucose metabolism, and female-associated body fat distribution are postulated to play a contributory role in the pathophysiology of lipedema. Dysregulation of adipose tissue accumulation via estrogen signaling likely occurs by two mechanisms: (1). altered adipocyte estrogen receptor distribution (ERα/ERß ratio) and subsequent metabolic signaling and/or (2). increased release of adipocyte-produced steroidogenic enzymes leading to increased paracrine estrogen release. These alterations could result in increased activation of peroxisome proliferator-activated receptor γ (PPARγ), free fatty acid entry into adipocytes, glucose uptake, and angiogenesis while decreasing lipolysis, mitochondriogenesis, and mitochondrial function. Together, these metabolic alterations would lead to increased adipogenesis and adipocyte lipid deposition, resulting in increased adipose depot mass. This review summarizes research characterizing estrogen-mediated adipose tissue metabolism and its possible relation to excessive adipose tissue accumulation associated with lipedema.
format	article
author	Kaleigh Katzer Jessica L. Hill Kara B. McIver Michelle T. Foster
author_facet	Kaleigh Katzer Jessica L. Hill Kara B. McIver Michelle T. Foster
author_sort	Kaleigh Katzer
title	Lipedema and the Potential Role of Estrogen in Excessive Adipose Tissue Accumulation
title_short	Lipedema and the Potential Role of Estrogen in Excessive Adipose Tissue Accumulation
title_full	Lipedema and the Potential Role of Estrogen in Excessive Adipose Tissue Accumulation
title_fullStr	Lipedema and the Potential Role of Estrogen in Excessive Adipose Tissue Accumulation
title_full_unstemmed	Lipedema and the Potential Role of Estrogen in Excessive Adipose Tissue Accumulation
title_sort	lipedema and the potential role of estrogen in excessive adipose tissue accumulation
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/60e60c55367c4b41bb2cc74cf1484691
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Lipedema and the Potential Role of Estrogen in Excessive Adipose Tissue Accumulation

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