Departamento de Bioquímica e Imunologia, Universidade Federal de Minas Gerais, Minas Gerais, Brazil.
Department of Medicine, University of California San Diego, San Diego, California, United States.
Nutrition. 2020 Jul-Aug;75-76:110658. doi: 10.1016/j.nut.2019.110658. Epub 2019 Nov 27.
Atherosclerosis is an underlying cause of cardiovascular disease, and obesity is one of the risk factors for atherogenesis. Although a gluten-free diet (GFD) has gained popularity as a strategy for weight loss, little is known about the effects of gluten on obesity. We have previously shown a negative effect of gluten on obesity in mice. However, its effects on atherogenesis are still unknown. Therefore, the aim of this study was to determine the effects of gluten on atherosclerosis progression during obesity.
Atherosclerosis-susceptible ApoE knockout mice were subjected to an obesogenic GFD or a diet with 4.5% gluten (GD) for 10 wk.
Results from the study found that food intake and lipid profile were similar between the groups. However, GD promoted an increase in weight gain, adiposity, and plasma glucose. Pro-inflammatory factors such as tumor necrosis factor, interleukin-6, chemokine ligand-2, and matrix metalloproteinase-2 and -9 also were increased in the adipose tissue of gluten-fed mice. This inflammatory profile was associated with reduced phosphorylation of Akt, and consequently with the intensification of insulin resistance. The GD-enhanced vascular inflammation contributed to the worsening of atherosclerosis in the aorta and aortic root. Inflammatory cells, such as monocyte/macrophage and natural killer cells, and oxidative stress markers, such as superoxide and nitrotyrosine, were increased in atherosclerotic lesions of the GD group. Furthermore, the lesions presented higher necrotic core and lower collagen content, characterizing the less stable plaques.
The gluten-containing high-fat diet was associated with a more severe proatherogenic profile than the gluten-free high-fat diet owing to increased inflammatory and oxidative status at atherosclerotic lesions in obese mice.
动脉粥样硬化是心血管疾病的根本原因，而肥胖是动脉粥样硬化形成的危险因素之一。尽管无麸质饮食（GFD）已作为减肥策略而流行，但人们对麸质对肥胖的影响知之甚少。我们之前已经证明了麸质对肥胖小鼠的负面影响。然而，其对动脉粥样硬化形成的影响仍不清楚。因此，本研究旨在确定麸质在肥胖期间对动脉粥样硬化进展的影响。
易患动脉粥样硬化的载脂蛋白 E 基因敲除小鼠接受致肥胖的无麸质饮食或含 4.5%麸质的饮食（GD）10 周。
研究结果发现，各组的食物摄入量和血脂谱相似。然而，GD 促进了体重增加、肥胖和血浆葡萄糖的增加。促炎因子，如肿瘤坏死因子、白细胞介素-6、趋化因子配体-2 和基质金属蛋白酶-2 和 -9，也在麸质喂养小鼠的脂肪组织中增加。这种炎症表型与 Akt 磷酸化减少有关，进而与胰岛素抵抗加剧有关。GD 增强的血管炎症导致主动脉和主动脉根部的动脉粥样硬化恶化。炎症细胞，如单核细胞/巨噬细胞和自然杀伤细胞，以及氧化应激标志物，如超氧阴离子和硝基酪氨酸，在 GD 组的动脉粥样硬化病变中增加。此外，病变部位的坏死核心更高，胶原含量更低，特征为更不稳定的斑块。
与无麸质高脂肪饮食相比，含麸质的高脂肪饮食与肥胖小鼠动脉粥样硬化病变中炎症和氧化应激状态增加有关，导致更严重的促动脉粥样硬化表型。
