Loss of Visceral Fat is Associated with a Reduction in Inflammatory Status in Patients with Metabolic Syndrome

Identificador:  imarina:9287015

Handle: https://hdl.handle.net/20.500.11797/imarina9287015

Autors:  Castro-Barquero, Sara; Casas, Rosa; Rimm, Eric B; Tresserra-Rimbau, Anna; Romaguera, Dora; Martinez, J Alfredo; Salas-Salvado, Jordi; Martinez-Gonzalez, Miguel A; Vidal, Josep; Ruiz-Canela, Miguel; Konieczna, Jadwiga; Sacanella, Emilio; Garcia-Gavilan, Jesus Francisco; Fito, Montse; Garcia-Arellano, Ana; Estruch, Ramon

Resum:
Excessive visceral adipose tissue (VAT) is associated with higher secretion of pro-inflammatory molecules, contributing to systemic inflammation and obesity-related metabolic disturbances.This prospective analysis includes 117 overweight/obese adults (55-75 years) from the PREDIMED-Plus study. Fourteen inflammatory markers and adipokines were measured using a Bio-Plex assay with multiplex technology: insulin, glucagon, IL-6, visfatin, ghrelin, GLP-1, TNF-α, MCP-1, PAI-1, resistin, C-peptide, leptin, adipsin and adiponectin. Participants were categorized into tertiles according to changes in VAT after 1-year of follow-up, determined by dual-energy X-Ray absorptiometry. Participants allocated in tertile 3, which represent an increase of VAT content after 1-year of follow-up compared to tertile 1, showed significant differences in insulin (T3 versus T1, fully adjusted model: p = 0.037, p for trend 0.042), PAI-1 (fully adjusted model: p = 0.05, p for trend 0.06), c-peptide (fully adjusted model: p = 0.037, p for trend 0.042), and TNF-α (fully adjusted model p = 0.037, p for trend 0.042).Our results evidenced that a reduction in VAT was associated with clinical improvements in several inflammatory and adiposity markers, mainly in insulin, c-peptide, and PAI-1 levels, and these improvements may contribute to a reduction in cardiometabolic disturbances observed in obesity. This article is protected by copyright. All rights reserved.This article is protected by copyright. All rights reserved.