Obesity, estrogens and adipose tissue dysfunction: implications for pulmonary arterial hypertension

Research output: Contribution to journalArticle

Abstract

Obesity is a prevalent global public health issue characterised by excess body
fat. Adipose tissue is now recognised as an important endocrine organ releasing an abundance of bioactive adipokines including, but not limited to, leptin, adiponectin and resistin. Obesity is a common co-morbidity amongst pulmonary arterial hypertension (PAH) patients, with 30-40% reported as obese, independent of other co-morbidities associated with PAH (e.g. obstructive sleep apnoea). An “obesity paradox” has been observed, where obesity has been associated with subclinical RV dysfunction but paradoxically may confer a protective effect on RV function once pulmonary hypertension develops.

Obesity and PAH share multiple pathophysiological mechanisms including
inflammation, oxidative stress, elevated leptin (pro-inflammatory) and reduced
adiponectin (anti-inflammatory). The female-prevalence of PAH 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 post-menopausal women and men with PAH. This review discusses the functions of adipose tissue in both health and obesity and the links between obesity and PAH. Shared pathophysiological mechanisms and the contribution of specific fat depots, metabolic and sex-dependent differences are discussed.
Original languageEnglish
JournalPulmonary Circulation
DOIs
Publication statusAccepted/In press - 2 Sep 2020

Keywords

  • aromatase
  • metabolic syndrome
  • sex differences

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