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Obesity, estrogens and adipose tissue dysfunction – implications for pulmonary arterial hypertension
Obesity is a prevalent global public health issue characterized by excess body fat. Adipose tissue is now recognized as an important endocrine organ releasing an abundance of bioactive adipokines including, but not limited to, leptin, adiponectin and resistin. Obesity is a common comorbidity amongst...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
SAGE Publications
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7506791/ https://www.ncbi.nlm.nih.gov/pubmed/32999709 http://dx.doi.org/10.1177/2045894020952023 |
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author | Mair, Kirsty M. Gaw, Rosemary MacLean, Margaret R. |
author_facet | Mair, Kirsty M. Gaw, Rosemary MacLean, Margaret R. |
author_sort | Mair, Kirsty M. |
collection | PubMed |
description | Obesity is a prevalent global public health issue characterized by excess body fat. Adipose tissue is now recognized as an important endocrine organ releasing an abundance of bioactive adipokines including, but not limited to, leptin, adiponectin and resistin. Obesity is a common comorbidity amongst pulmonary arterial hypertension patients, with 30% to 40% reported as obese, independent of other comorbidities associated with pulmonary arterial hypertension (e.g. obstructive sleep apnoea). An ‘obesity paradox’ has been observed, where obesity has been associated with subclinical right ventricular dysfunction but paradoxically may confer a protective effect on right ventricular function once pulmonary hypertension develops. Obesity and pulmonary arterial hypertension share multiple pathophysiological mechanisms including inflammation, oxidative stress, elevated leptin (proinflammatory) and reduced adiponectin (anti-inflammatory). The female prevalence of pulmonary arterial hypertension has instigated the hypothesis that estrogens may play a causative role in its development. Adipose tissue, a major site for storage and metabolism of sex steroids, is the primary source of estrogens and circulating estrogens levels which are elevated in postmenopausal women and men with pulmonary arterial hypertension. This review discusses the functions of adipose tissue in both health and obesity and the links between obesity and pulmonary arterial hypertension. Shared pathophysiological mechanisms and the contribution of specific fat depots, metabolic and sex-dependent differences are discussed. |
format | Online Article Text |
id | pubmed-7506791 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | SAGE Publications |
record_format | MEDLINE/PubMed |
spelling | pubmed-75067912020-09-29 Obesity, estrogens and adipose tissue dysfunction – implications for pulmonary arterial hypertension Mair, Kirsty M. Gaw, Rosemary MacLean, Margaret R. Pulm Circ Review Article Obesity is a prevalent global public health issue characterized by excess body fat. Adipose tissue is now recognized as an important endocrine organ releasing an abundance of bioactive adipokines including, but not limited to, leptin, adiponectin and resistin. Obesity is a common comorbidity amongst pulmonary arterial hypertension patients, with 30% to 40% reported as obese, independent of other comorbidities associated with pulmonary arterial hypertension (e.g. obstructive sleep apnoea). An ‘obesity paradox’ has been observed, where obesity has been associated with subclinical right ventricular dysfunction but paradoxically may confer a protective effect on right ventricular function once pulmonary hypertension develops. Obesity and pulmonary arterial hypertension share multiple pathophysiological mechanisms including inflammation, oxidative stress, elevated leptin (proinflammatory) and reduced adiponectin (anti-inflammatory). The female prevalence of pulmonary arterial hypertension has instigated the hypothesis that estrogens may play a causative role in its development. Adipose tissue, a major site for storage and metabolism of sex steroids, is the primary source of estrogens and circulating estrogens levels which are elevated in postmenopausal women and men with pulmonary arterial hypertension. This review discusses the functions of adipose tissue in both health and obesity and the links between obesity and pulmonary arterial hypertension. Shared pathophysiological mechanisms and the contribution of specific fat depots, metabolic and sex-dependent differences are discussed. SAGE Publications 2020-09-18 /pmc/articles/PMC7506791/ /pubmed/32999709 http://dx.doi.org/10.1177/2045894020952023 Text en © The Author(s) 2020 https://creativecommons.org/licenses/by/4.0/ Creative Commons CC-BY: This article is distributed under the terms of the Creative Commons Attribution 4.0 License (https://creativecommons.org/licenses/by/4.0/) which permits any use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage). |
spellingShingle | Review Article Mair, Kirsty M. Gaw, Rosemary MacLean, Margaret R. Obesity, estrogens and adipose tissue dysfunction – implications for pulmonary arterial hypertension |
title | Obesity, estrogens and adipose tissue dysfunction – implications for
pulmonary arterial hypertension |
title_full | Obesity, estrogens and adipose tissue dysfunction – implications for
pulmonary arterial hypertension |
title_fullStr | Obesity, estrogens and adipose tissue dysfunction – implications for
pulmonary arterial hypertension |
title_full_unstemmed | Obesity, estrogens and adipose tissue dysfunction – implications for
pulmonary arterial hypertension |
title_short | Obesity, estrogens and adipose tissue dysfunction – implications for
pulmonary arterial hypertension |
title_sort | obesity, estrogens and adipose tissue dysfunction – implications for
pulmonary arterial hypertension |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7506791/ https://www.ncbi.nlm.nih.gov/pubmed/32999709 http://dx.doi.org/10.1177/2045894020952023 |
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