Aldosterone directly affects apelin expression and secretion in adipocytes

Area of Science:

• Endocrinology
• Molecular Biology
• Metabolic Research

Background:

• Primary aldosteronism (PA) is linked to metabolic syndrome and adverse cardiometabolic outcomes.
• The molecular mechanisms connecting excess aldosterone to these conditions require elucidation.
• Apelin, a beneficial adipokine, plays a role in cardiovascular homeostasis and obesity-related disorders.

Purpose of the Study:

• To investigate the impact of elevated aldosterone on apelin expression and secretion in adipocytes.
• To identify the molecular pathways mediating aldosterone's effects on apelin.
• To explore apelin as a potential therapeutic target in PA-associated metabolic dysfunction.

Main Methods:

• In vivo studies involving aldosterone injection and assessment of serum/tissue apelin levels.
• In vitro experiments using 3T3-L1 adipocytes to study aldosterone's dose- and time-dependent effects on apelin.
• Analysis of glucocorticoid receptor (GR) involvement using antagonists and knockdown.
• Identification of hormone response elements (HREs) in the apelin promoter.
• Investigation of the p38 MAPK signaling pathway.

Main Results:

• Aldosterone injection acutely reduced serum and adipose tissue apelin levels in vivo.
• In 3T3-L1 adipocytes, aldosterone decreased apelin expression and secretion in a dose- and time-dependent manner.
• Glucocorticoid receptor (GR) activation mediated aldosterone's effect on apelin.
• The p38 MAPK signaling pathway was implicated in the observed effects.
• No synergistic effect was found between glucocorticoids and mineralocorticoids on apelin regulation via GR.

Conclusions:

• Aldosterone directly suppresses apelin expression and secretion in adipocytes through GR activation.
• This interaction provides a mechanistic link between primary aldosteronism and cardiometabolic syndrome.
• Apelin emerges as a potential therapeutic target for managing metabolic complications in PA.