Department of Internal Medicine, University of Pisa School of Medicine, Via Roma, 67, I-56100 Pisa, Italy.
Br J Nutr. 2011 Aug;106(3):364-8. doi: 10.1017/S0007114511000286. Epub 2011 Mar 9.
A family history of type 2 diabetes (T2D) confers a high risk of developing the disease, independent of that due to other common risk factors. Postprandial state is a pro-inflammatory condition associated with a transiently impaired endothelial function; an increased oxidative stress is considered as a mediator of such effects in T2D. We evaluated the short-term effect of a lipid meal on markers of early vascular damage in subjects at risk of developing T2D. A total of thirty-two healthy volunteers, divided according to the presence (FHD+) or absence (FHD - ) of a family history of T2D, underwent a fatty meal test. We measured the monocyte mRNA expressions of IL-6, IL-8 and IL-1β, and IL-6, soluble CD40 ligand (sCD40L), vascular cellular adhesion molecule-1 (VCAM-1), intracellular adhesion molecule-1 (ICAM-1) and nitrotyrosine plasma concentrations at baseline and in the post-meal phase, relating them to the lipid profile and other biochemical parameters. The basal expression of the cytokines did not differ in FHD - and FHD+ subjects; neither was it modified by the meal ingestion. IL-6 and sCD40L plasma levels, similar in the two groups in the fasting state, did not vary after the meal. VCAM-1 and ICAM-1 increased in FHD+ subjects but not in FHD - subjects. Nitrotyrosine, similar between the FHD - and FHD+ subjects at baseline, increased more in FHD+ subjects than in FHD - subjects after the meal. In conclusion, the presence of a familial history of T2D confers an abnormal endothelial activation after an oral lipid meal, coupled with an increased oxidative stress, supporting the hypothesis of an early endothelial dysfunction already present in healthy individuals prone to develop T2D.
家族性 2 型糖尿病(T2D)病史会增加患病风险,且独立于其他常见风险因素。餐后状态是一种促炎状态,与内皮功能短暂受损有关;氧化应激增加被认为是 T2D 中这种作用的介导者。我们评估了脂质餐对易患 T2D 人群早期血管损伤标志物的短期影响。共有 32 名健康志愿者,根据是否存在(FHD+)或不存在(FHD-)T2D 家族史进行分组,进行了脂肪餐测试。我们测量了单核细胞 IL-6、IL-8 和 IL-1β,以及 IL-6、可溶性 CD40 配体(sCD40L)、血管细胞黏附分子-1(VCAM-1)、细胞间黏附分子-1(ICAM-1)和硝基酪氨酸的血浆浓度,在基线和餐后阶段进行测量,并将其与血脂谱和其他生化参数相关联。在 FHD-和 FHD+组中,细胞因子的基础表达没有差异;饮食摄入也没有改变。在空腹状态下,两组的 IL-6 和 sCD40L 血浆水平相似,餐后没有变化。VCAM-1 和 ICAM-1 在 FHD+组中增加,但在 FHD-组中没有增加。在基线时,FHD-和 FHD+组之间的硝基酪氨酸相似,餐后 FHD+组比 FHD-组增加更多。总之,T2D 家族史的存在会导致口服脂质餐后内皮激活异常,同时伴有氧化应激增加,支持了在易患 T2D 的健康个体中已经存在早期内皮功能障碍的假说。