Lipids and Atherosclerosis Unit, IMIBIC/Reina Sofia University Hospital, University of Cordoba and CIBER Fisiopatología Obesidad y Nutrición, Instituto de Salud Carlos III, Cordoba, Spain.
Mol Nutr Food Res. 2011 Dec;55(12):1759-70. doi: 10.1002/mnfr.201100200.
Dysfunctional adipose tissue may be an important trigger of molecular inflammatory pathways that cause cardiovascular diseases. Our aim was to determine whether the specific quality and quantity of dietary fat produce differential postprandial inflammatory responses in adipose tissue from metabolic syndrome (MetS) patients.
A randomized, controlled trial conducted within the LIPGENE study assigned MetS patients to 1 of 4 diets: (i) high-saturated fatty acid (HSFA), (ii) high-monounsaturated fatty acid (HMUFA), (iii) low-fat, high-complex carbohydrate diet supplemented with n-3 polyunsaturated fatty acids (PUFA) (LFHCC n-3), and (iv) low-fat, high-complex carbohydrate diet supplemented with placebo (LFHCC), for 12 wk each. A fat challenge reflecting the fatty acid composition as the original diets was conducted post-intervention. We found that p65 gene expression is induced in adipose tissue (p=0.003) at the postprandial state. In addition, IκBα (p<0.001), MCP-1 (p<0.001) and IL-1β (p<0.001) gene expression was equally induced in the postprandial state, regardless of the quality and quantity of the dietary fat. Notably, IL-6 transcripts were only detected in the postprandial state.
Our results indicate that individuals with MetS typically exhibit exacerbated adipose tissue postprandial inflammatory responses, which seem to be independent of the quality and quantity of dietary fat.
功能失调的脂肪组织可能是引发心血管疾病的分子炎症途径的重要触发因素。我们的目的是确定饮食中脂肪的特定质量和数量是否会在代谢综合征（MetS）患者的脂肪组织中产生不同的餐后炎症反应。
在 LIPGENE 研究中进行的一项随机对照试验将 MetS 患者分配到 4 种饮食中的 1 种：（i）高饱和脂肪酸（HSFA），（ii）高单不饱和脂肪酸（HMUFA），（iii）低脂肪、高复合碳水化合物饮食补充 n-3 多不饱和脂肪酸（PUFA）（LFHCC n-3），和（iv）低脂肪、高复合碳水化合物饮食补充安慰剂（LFHCC），每种饮食持续 12 周。干预后进行了反映原始饮食脂肪酸组成的脂肪挑战。我们发现，p65 基因在脂肪餐后在脂肪组织中被诱导（p=0.003）。此外，IκBα（p<0.001）、MCP-1（p<0.001）和 IL-1β（p<0.001）的基因表达在脂肪餐后同样被诱导，而与饮食脂肪的质量和数量无关。值得注意的是，IL-6 转录物仅在脂肪餐后被检测到。
我们的结果表明，患有 MetS 的个体通常表现出加剧的脂肪组织餐后炎症反应，这似乎与饮食脂肪的质量和数量无关。
