The regulation of aldosterone secretion by leptin: Implications in obesity-related cardiovascular disease

Jessica L. Faulkner, Thiago Bruder-Nascimento, Eric Jacques Belin de Chantemele

Research output: Contribution to journalReview article

10 Citations (Scopus)

Abstract

Purpose of review Although it has been known for some time that increases in body mass enhance aldosterone secretion, particularly in women, the origin of this elevation in aldosterone production is not well defined. Adipocyte-derived factors have emerged as potential candidates to increase aldosterone production in obesity. Recent findings Emerging evidence suggests the presence of a mechanistic link in which the adipocyte-derived hormone leptin stimulates aldosterone production in obesity, thereby creating a positive feedback loop for obesity-associated cardiovascular disease. In addition, recent reports give credence to the concept that this leptin-aldosterone stimulation pathway in obesity is an underlying mechanism for sex-discrepancies in obesity-associated cardiovascular disease. Summary Leptin appears as a new direct regulator of adrenal aldosterone production and leptin-mediated aldosterone production is a novel candidate mechanism underlying obesity-associated hypertension, particularly in females.

Original languageEnglish (US)
Pages (from-to)63-69
Number of pages7
JournalCurrent opinion in nephrology and hypertension
Volume27
Issue number2
DOIs
StatePublished - Mar 1 2018

Fingerprint

Leptin
Aldosterone
Cardiovascular Diseases
Obesity
Adipocytes
Hormones
Hypertension

Keywords

  • aldosterone
  • hypertension
  • leptin
  • obesity
  • sex differences

ASJC Scopus subject areas

  • Internal Medicine
  • Nephrology

Cite this

The regulation of aldosterone secretion by leptin : Implications in obesity-related cardiovascular disease. / Faulkner, Jessica L.; Bruder-Nascimento, Thiago; Belin de Chantemele, Eric Jacques.

In: Current opinion in nephrology and hypertension, Vol. 27, No. 2, 01.03.2018, p. 63-69.

Research output: Contribution to journalReview article

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