Maria das Graças Coelho de Souza1, Priscila Alves Maranhão1,2, Diogo Guarnieri Panazzolo1, José Firmino Nogueira Neto3, Eliete Bouskela1,4, Luiz Guilherme Kraemer-Aguiar5,6,7. 1. Laboratory for Clinical and Experimental Research on Vascular Biology (BioVasc), Biomedical Center, State University of Rio de Janeiro (UERJ), 20550- 013, Rio de Janeiro, RJ, Brazil. 2. Center for Health Technology and Services Research (CINTESIS), Faculty of Medicine, University of Porto, 4200-319, Porto, Portugal. 3. Lipids Laboratory (Lablip), State University of Rio de Janeiro (UERJ), Policlínica Piquet Carneiro, 20550-003, Rio de Janeiro, RJ, Brazil. 4. Obesity Unit, Centro de Pesquisa Clínica Multiusuário (CePeM), Hospital Universitário Pedro Ernesto (HUPE), State University of Rio de Janeiro, Rio de Janeiro (UERJ), 20551-030, Rio de Janeiro, RJ, Brazil. 5. Laboratory for Clinical and Experimental Research on Vascular Biology (BioVasc), Biomedical Center, State University of Rio de Janeiro (UERJ), 20550- 013, Rio de Janeiro, RJ, Brazil. lgkraemeraguiar@gmail.com. 6. Department of Internal Medicine, Faculty of Medical Sciences, State University of Rio de Janeiro (UERJ), 20551-170, Rio de Janeiro, RJ, Brazil. lgkraemeraguiar@gmail.com. 7. Obesity Unit, Centro de Pesquisa Clínica Multiusuário (CePeM), Hospital Universitário Pedro Ernesto (HUPE), State University of Rio de Janeiro, Rio de Janeiro (UERJ), 20551-030, Rio de Janeiro, RJ, Brazil. lgkraemeraguiar@gmail.com.
Abstract
BACKGROUND: It is known that consuming a high-fat meal (HFM) induces microvascular dysfunction (MD) in eutrophic women and aggravates it in those with obesity. Our purpose was to investigate if the MD observed after a single HFM intake is caused by endothelial damage or increased inflammatory state, both determined by blood biomarkers. METHODS: Nineteen women with obesity (BMI 30-34.9 kg/m2) and 18 eutrophic ones (BMI 20.0-24.9 kg/m2) were enrolled into two groups: Obese (OBG) and Control (CG), respectively. Blood samples were collected at five-time points: before (fasting state) and 30, 60, 120, and 180 min after HFM intake to determine levels of adipokines (adiponectin, leptin), non-esterified fatty acid (NEFA), inflammatory [tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6)] and endothelium damage [soluble E-selectin, soluble vascular cell adhesion molecule-1 (sVCAM-1), soluble intercellular adhesion molecule-1 (sICAM-1), plasminogen activator inhibitor-1 (PAI-1)] biomarkers. RESULTS: Levels of soluble E-selectin, leptin, and PAI-1 were higher in OBG at all-time points (P < 0.05) compared to CG. In the fasting state, OBG had higher levels of NEFA compared to CG (P < 0.05). In intra-group analysis, no significant change in the levels of circulating inflammatory and endothelial injury biomarkers was observed after HFM intake, independently of the group. CONCLUSION: Our findings suggest that women with obesity have an increased pro-inflammatory state and more significant endothelial injury compared to eutrophic ones. However, the consumption of a HFM was not sufficient to change circulating levels of inflammatory and endothelial injury biomarkers in either group. REGISTRATION NUMBER FOR CLINICAL TRIALS: NCT01692327.
BACKGROUND: It is known that consuming a high-fat meal (HFM) induces microvascular dysfunction (MD) in eutrophic women and aggravates it in those with obesity. Our purpose was to investigate if the MD observed after a single HFM intake is caused by endothelial damage or increased inflammatory state, both determined by blood biomarkers. METHODS: Nineteen women with obesity (BMI 30-34.9 kg/m2) and 18 eutrophic ones (BMI 20.0-24.9 kg/m2) were enrolled into two groups: Obese (OBG) and Control (CG), respectively. Blood samples were collected at five-time points: before (fasting state) and 30, 60, 120, and 180 min after HFM intake to determine levels of adipokines (adiponectin, leptin), non-esterified fatty acid (NEFA), inflammatory [tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6)] and endothelium damage [soluble E-selectin, soluble vascular cell adhesion molecule-1 (sVCAM-1), soluble intercellular adhesion molecule-1 (sICAM-1), plasminogen activator inhibitor-1 (PAI-1)] biomarkers. RESULTS: Levels of soluble E-selectin, leptin, and PAI-1 were higher in OBG at all-time points (P < 0.05) compared to CG. In the fasting state, OBG had higher levels of NEFA compared to CG (P < 0.05). In intra-group analysis, no significant change in the levels of circulating inflammatory and endothelial injury biomarkers was observed after HFM intake, independently of the group. CONCLUSION: Our findings suggest that women with obesity have an increased pro-inflammatory state and more significant endothelial injury compared to eutrophic ones. However, the consumption of a HFM was not sufficient to change circulating levels of inflammatory and endothelial injury biomarkers in either group. REGISTRATION NUMBER FOR CLINICAL TRIALS: NCT01692327.
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