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Updated: Mar 17, 2026

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Visceral adiposity syndrome.

Heno F Lopes1, Maria Lúcia Corrêa-Giannella2, Fernanda M Consolim-Colombo1

  • 1Universidade Nove de Julho-UNINOVE, Rua Vergueiro 235/249, 2 subsolo, Liberdade, São Paulo, CEP: 01504-001 Brazil ; Instituto do Coração do Hospital das Clinicas da Faculdade de Medicina da Universidade de São Paulo, São Paulo, Brazil.

Diabetology & Metabolic Syndrome
|July 21, 2016
PubMed
Summary

Metabolic syndrome, or visceral adiposity syndrome (VAS), involves abnormal fat distribution and metabolic changes. Autonomic nervous system dysfunction is a newly recognized factor contributing to VAS development and insulin resistance.

Keywords:
AdipocytokinesAdipose tissueInsulin resistanceParasympathetic activitySympathetic activityVisceral obesity syndrome

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Area of Science:

  • Endocrinology and Metabolism
  • Cardiovascular Physiology
  • Adipose Tissue Biology

Background:

  • Metabolic syndrome (MS), now termed visceral adiposity syndrome (VAS), links anthropometric and hemodynamic changes to metabolic dysfunction.
  • Historically, visceral obesity has been associated with hypertension, gout, and sleep apnea.
  • Chronic calorie excess drives visceral adipose tissue expansion, macrophage recruitment, and inflammatory cytokine release, impairing insulin signaling and causing insulin resistance (IR).

Purpose of the Study:

  • To review the multifaceted factors contributing to visceral adiposity syndrome (VAS).
  • To highlight the role of the autonomic nervous system (ANS) in regulating visceral adipose tissue (VAT) and its contribution to VAS.
  • To integrate the understanding of ANS dysfunction into the complex pathophysiology of VAS.

Main Methods:

  • Review of existing literature on metabolic syndrome, visceral adiposity, insulin resistance, and autonomic nervous system function.
  • Analysis of experimental and clinical studies investigating the bidirectional relationship between adipose tissue and the ANS.
  • Synthesis of evidence linking genetic, epigenetic, gut microbiota, and autonomic factors to VAS.

Main Results:

  • Expansion of visceral adipose tissue promotes inflammation and insulin resistance.
  • Insulin resistance in various tissues (adipose, liver, vasculature, kidney) contributes to the VAS phenotype.
  • Autonomic nervous system activity, particularly sympathetic/parasympathetic balance and adrenergic receptor function, significantly modulates visceral adipose tissue and insulin sensitivity.

Conclusions:

  • Visceral adiposity syndrome is a complex condition influenced by multiple factors including genetics, environment, gut microbiota, and autonomic dysfunction.
  • Abnormal autonomic activity, specifically an imbalance in sympathetic and parasympathetic tone, is a critical regulator of visceral adipose tissue and insulin sensitivity.
  • Adipose tissue plays a complex, dynamic role in VAS, with autonomic nervous system input being a key regulatory mechanism.