Motton Deborah D, Keim Nancy L, Tenorio Fatima A, Horn William F, Rutledge John C
Division of Endocrinology, Clinical Nutrition, and Vascular Medicine, Department of Internal Medicine, University of California, Davis, CA 95616, USA.
Am J Clin Nutr. 2007 Jan;85(1):60-5. doi: 10.1093/ajcn/85.1.60.
Recent data show that atherosclerosis is initiated and perpetuated by inflammatory events. Activation of immune cells such as monocytes initiates inflammation, a key step in atherosclerosis.
We hypothesize that a high-glycemic load meal activates inflammatory cells, and that this is mediated by elevated circulating triacylglycerol-rich lipoproteins.
Sixteen women [body mass index (in kg/m2): 25.7-29.6], aged 20-48 y, consumed meals with a high or a low glycemic load in a crossover fashion. Blood samples were collected before and up to 8 h after the meals. Samples were measured for glucose, insulin, triacylglycerols, and circulating cytokines, and expression of tumor necrosis factor alpha (TNF-alpha) and interleukin 1beta (IL-1beta) was measured by flow cytometry.
At 3.5 h after the test meals, we observed a significant increase in monocytes expressing TNF-alpha with both high-and low-glycemic load meals. Also, expression of IL-1beta in monocytes tended to increase, but the change was not significant. The glycemic load of the meal did not influence circulating cytokines and had only a minimal effect on postprandial triacylglycerol concentrations despite marked postprandial changes in glycemia and circulating insulin concentrations.
In the postprandial state, monocytes can be activated by both high-and low-glycemic load meals. The glycemic load of a single meal did not have a significant effect on the degree of activation of the monocytes in women who displayed only a modest increase in circulating triacylglycerols in response to test meals. Future studies should examine the effect of glycemic load in subjects who have a hyperlipemic response to dietary carbohydrate.
近期数据表明,动脉粥样硬化由炎症事件引发并持续存在。免疫细胞(如单核细胞)的激活引发炎症,这是动脉粥样硬化的关键步骤。
我们假设高糖负荷餐会激活炎症细胞,且这一过程由循环中富含三酰甘油的脂蛋白升高介导。
16名年龄在20 - 48岁的女性[体重指数(kg/m²):25.7 - 29.6],以交叉方式进食高糖负荷或低糖负荷餐。在进餐前及进餐后长达8小时采集血样。检测样本中的葡萄糖、胰岛素、三酰甘油和循环细胞因子,并通过流式细胞术检测肿瘤坏死因子α(TNF-α)和白细胞介素1β(IL-1β)的表达。
在测试餐后3.5小时,我们观察到高糖负荷餐和低糖负荷餐都会使表达TNF-α的单核细胞显著增加。此外,单核细胞中IL-1β的表达也有增加趋势,但变化不显著。尽管餐后血糖和循环胰岛素浓度有明显变化,但餐食的糖负荷并未影响循环细胞因子,对餐后三酰甘油浓度的影响也微乎其微。
在餐后状态下,高糖负荷餐和低糖负荷餐均可激活单核细胞。对于进食测试餐后循环三酰甘油仅适度增加的女性,单餐的糖负荷对单核细胞的激活程度无显著影响。未来研究应考察糖负荷对饮食碳水化合物有高脂血症反应的受试者的影响。