Research
Hormonal
Visceral fat accumulation activates the Renin-Angiotensin-Aldosterone System (RAAS) and Sympathetic Nervous System (SNS), leading to hypertension and sodium retention, independent of dietary salt intake.
High blood pressure in obesity is driven by hormones from belly fat, not just salt. Reducing visceral fat helps normalize these hormones and lower blood pressure.
GoodSupportsHIGH confidence
Visceral fat is associated with a 'within normal range' increase in plasma aldosterone concentrations, supported by the production of adipokines and angiotensinogen... This form of 'inappropriate secondary hyperaldosteronism'... further favors greater sodium reabsorption.
Why this rating
Narrative review explaining a well-established pathophysiological pathway.
Source
Adipocentric origin of the common cardiometabolic complications of obesity in the young up to the very old: pathophysiology and new therapeutic opportunities
Riccardo Sarzani et al. · Frontiers in Medicine · 2024
DOI 10.3389/fmed.2024.1365183
narrative_reviewCited 13×
Read the paper DOI resolved against Crossref · corpus check 2026-06-10
More from this paper
- GLP-1 receptor agonists (GLP1-RA) and SGLT2 inhibitors (SGLT2-i) are effective interventions for obesity-related cardiometabolic complications by reducing body weight and addressing pathophysiological derangements.Strong
- Visceral adipose tissue (VAT) is the primary driver of cardiometabolic complications (hypertension, T2DM, dyslipidemia) through endocrine dysfunction, RAAS activation, and inflammation, rather than total body weight alone.Good
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