Cargando…

Visceral adiposity syndrome

The association of anthropometric (waist circumference) and hemodynamic (blood pressure) changes with abnormalities in glucose and lipid metabolism has been motivation for a lot of discussions in the last 30 years. Nowadays, blood pressure, body mass index/abdominal circumference, glycemia, triglyce...

Descripción completa

Detalles Bibliográficos
Autores principales: Lopes, Heno F., Corrêa-Giannella, Maria Lúcia, Consolim-Colombo, Fernanda M., Egan, Brent M.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4950710/
https://www.ncbi.nlm.nih.gov/pubmed/27437032
http://dx.doi.org/10.1186/s13098-016-0156-2
_version_ 1782443595746246656
author Lopes, Heno F.
Corrêa-Giannella, Maria Lúcia
Consolim-Colombo, Fernanda M.
Egan, Brent M.
author_facet Lopes, Heno F.
Corrêa-Giannella, Maria Lúcia
Consolim-Colombo, Fernanda M.
Egan, Brent M.
author_sort Lopes, Heno F.
collection PubMed
description The association of anthropometric (waist circumference) and hemodynamic (blood pressure) changes with abnormalities in glucose and lipid metabolism has been motivation for a lot of discussions in the last 30 years. Nowadays, blood pressure, body mass index/abdominal circumference, glycemia, triglyceridemia, and HDL-cholesterol concentrations are considered in the definition of Metabolic syndrome, referred as Visceral adiposity syndrome (VAS) in the present review. However, more than 250 years ago an association between visceral and mediastinal obesity with hypertension, gout, and obstructive apnea had already been recognized. Expansion of visceral adipose tissue secondary to chronic over-consumption of calories stimulates the recruitment of macrophages, which assume an inflammatory phenotype and produce cytokines that directly interfere with insulin signaling, resulting in insulin resistance. In turn, insulin resistance (IR) manifests itself in various tissues, contributing to the overall phenotype of VAS. For example, in white adipose tissue, IR results in lipolysis, increased free fatty acids release and worsening of inflammation, since fatty acids can bind to Toll-like receptors. In the liver, IR results in increased hepatic glucose production, contributing to hyperglycemia; in the vascular endothelium and kidney, IR results in vasoconstriction, sodium retention and, consequently, arterial hypertension. Other players have been recognized in the development of VAS, such as genetic predisposition, epigenetic factors associated with exposure to an unfavourable intrauterine environment and the gut microbiota. More recently, experimental and clinical studies have shown the autonomic nervous system participates in modulating visceral adipose tissue. The sympathetic nervous system is related to adipose tissue function and differentiation through beta(1), beta(2), beta(3), alpha(1), and alpha(2) adrenergic receptors. The relation is bidirectional: sympathetic denervation of adipose tissue blocks lipolysis to a variety of lipolytic stimuli and adipose tissue send inputs to the brain. An imbalance of sympathetic/parasympathetic and alpha(2) adrenergic/beta(3) receptor is related to visceral adipose tissue storage and insulin sensitivity. Thus, in addition to the well-known factors classically associated with VAS, abnormal autonomic activity also emerges as an important factor regulating white adipose tissue, which highlights complex role of adipose tissue in the VAS.
format Online
Article
Text
id pubmed-4950710
institution National Center for Biotechnology Information
language English
publishDate 2016
publisher BioMed Central
record_format MEDLINE/PubMed
spelling pubmed-49507102016-07-20 Visceral adiposity syndrome Lopes, Heno F. Corrêa-Giannella, Maria Lúcia Consolim-Colombo, Fernanda M. Egan, Brent M. Diabetol Metab Syndr Review The association of anthropometric (waist circumference) and hemodynamic (blood pressure) changes with abnormalities in glucose and lipid metabolism has been motivation for a lot of discussions in the last 30 years. Nowadays, blood pressure, body mass index/abdominal circumference, glycemia, triglyceridemia, and HDL-cholesterol concentrations are considered in the definition of Metabolic syndrome, referred as Visceral adiposity syndrome (VAS) in the present review. However, more than 250 years ago an association between visceral and mediastinal obesity with hypertension, gout, and obstructive apnea had already been recognized. Expansion of visceral adipose tissue secondary to chronic over-consumption of calories stimulates the recruitment of macrophages, which assume an inflammatory phenotype and produce cytokines that directly interfere with insulin signaling, resulting in insulin resistance. In turn, insulin resistance (IR) manifests itself in various tissues, contributing to the overall phenotype of VAS. For example, in white adipose tissue, IR results in lipolysis, increased free fatty acids release and worsening of inflammation, since fatty acids can bind to Toll-like receptors. In the liver, IR results in increased hepatic glucose production, contributing to hyperglycemia; in the vascular endothelium and kidney, IR results in vasoconstriction, sodium retention and, consequently, arterial hypertension. Other players have been recognized in the development of VAS, such as genetic predisposition, epigenetic factors associated with exposure to an unfavourable intrauterine environment and the gut microbiota. More recently, experimental and clinical studies have shown the autonomic nervous system participates in modulating visceral adipose tissue. The sympathetic nervous system is related to adipose tissue function and differentiation through beta(1), beta(2), beta(3), alpha(1), and alpha(2) adrenergic receptors. The relation is bidirectional: sympathetic denervation of adipose tissue blocks lipolysis to a variety of lipolytic stimuli and adipose tissue send inputs to the brain. An imbalance of sympathetic/parasympathetic and alpha(2) adrenergic/beta(3) receptor is related to visceral adipose tissue storage and insulin sensitivity. Thus, in addition to the well-known factors classically associated with VAS, abnormal autonomic activity also emerges as an important factor regulating white adipose tissue, which highlights complex role of adipose tissue in the VAS. BioMed Central 2016-07-19 /pmc/articles/PMC4950710/ /pubmed/27437032 http://dx.doi.org/10.1186/s13098-016-0156-2 Text en © The Author(s) 2016 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Review
Lopes, Heno F.
Corrêa-Giannella, Maria Lúcia
Consolim-Colombo, Fernanda M.
Egan, Brent M.
Visceral adiposity syndrome
title Visceral adiposity syndrome
title_full Visceral adiposity syndrome
title_fullStr Visceral adiposity syndrome
title_full_unstemmed Visceral adiposity syndrome
title_short Visceral adiposity syndrome
title_sort visceral adiposity syndrome
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4950710/
https://www.ncbi.nlm.nih.gov/pubmed/27437032
http://dx.doi.org/10.1186/s13098-016-0156-2
work_keys_str_mv AT lopeshenof visceraladipositysyndrome
AT correagiannellamarialucia visceraladipositysyndrome
AT consolimcolombofernandam visceraladipositysyndrome
AT eganbrentm visceraladipositysyndrome