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.
Center for Health Technology and Services Research (CINTESIS), Faculty of Medicine, University of Porto, 4200-319, Porto, Portugal.
Nutr J. 2022 Oct 19;21(1):65. doi: 10.1186/s12937-022-00819-4.
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.
Nineteen women with obesity (BMI 30-34.9 kg/m) and 18 eutrophic ones (BMI 20.0-24.9 kg/m) 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.
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.
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.
NCT01692327.
已知高脂膳食（HFM）可诱导肥胖女性微血管功能障碍（MD），并加重肥胖女性的 MD。我们的目的是研究单次 HFM 摄入后观察到的 MD 是否是由内皮损伤或炎症状态增加引起的，这两者均由血液生物标志物确定。
19 名肥胖（BMI 30-34.9kg/m）和 18 名瘦素（BMI 20.0-24.9kg/m）的女性被分为两组：肥胖组（OBG）和对照组（CG）。在五个时间点采集血液样本：空腹状态（fasting state）和 HFM 摄入后 30、60、120 和 180 分钟，以确定脂肪因子（脂联素、瘦素）、非酯化脂肪酸（NEFA）、炎症[肿瘤坏死因子-α（TNF-α）、白细胞介素-6（IL-6）]和内皮损伤[可溶性 E-选择素、可溶性血管细胞黏附分子-1（sVCAM-1）、可溶性细胞间黏附分子-1（sICAM-1）、纤溶酶原激活物抑制剂-1（PAI-1）]生物标志物的水平。
在所有时间点，OBG 的可溶性 E-选择素、瘦素和 PAI-1 水平均高于 CG（P<0.05）。在空腹状态下，OBG 的 NEFA 水平高于 CG（P<0.05）。在组内分析中，两组 HFM 摄入后循环炎症和内皮损伤生物标志物水平均无显著变化。
我们的研究结果表明，与瘦素相比，肥胖女性具有更高的促炎状态和更显著的内皮损伤。然而，高脂膳食并不足以改变两组循环炎症和内皮损伤生物标志物的水平。
NCT01692327。
