Lefèbvre P J, Scheen A J
Department of Medicine, University of Liège, Belgium.
Diabet Med. 1998;15 Suppl 4:S63-8. doi: 10.1002/(sici)1096-9136(1998120)15:4+<s63::aid-dia737>3.3.co;2-z.
Metabolism in man is regulated by complex hormonal signals and substrate interactions, and for many years the clinical focus has centred on the metabolic and hormonal picture after an overnight fast. More recently, the postprandial state, i.e. 'the period that comprises and follows a meal', has received more attention. The oral glucose tolerance test (OGTT), although highly non-physiological, has been used largely as a model of the postprandial state. Epidemiological studies have shown that, when 'impaired', oral glucose tolerance is associated with an increased risk of cardiovascular disease. Postprandial hyperlipidaemia has been investigated more recently in epidemiological, mechanistical and intervention studies, most of which indicate that high postprandial triglyceride levels, and particularly postprandial rich triglyceride remnants, constitute an increased risk for cardiovascular disease. Recent studies have shown that excessive postprandial glucose excursions are accompanied by oxidative stress and, less well known, activation of blood coagulation (increase in circulating D-dimers and prothrombin fragments). The mechanisms through which increased postprandial glucose levels and lipid concentrations may damage endothelial cells on blood vessel walls appear to be complex. These mechanisms include the activation of protein kinase C, increased expression of adhesion molecules, increased adhesion and uptake of leucocytes, increased production of proliferative substances such as endothelin, increased proliferation of endothelial cells, increased synthesis of collagen IV and fibronectin, and decreased production of nitric oxide (NO). In conclusion, the 'postprandial state' cumulatively covers almost half of the nycthemeral period, and its physiology involves numerous finely regulated motor, secretory, hormonal and metabolic events. Epidemiological and mechanistical studies have suggested that perturbations of the postprandial state are involved in cardiovascular disease. Correcting the abnormalities of the postprandial state must form part of the strategy for the prevention and management of cardiovascular diseases, particularly those that are associated with diabetes mellitus.
人体新陈代谢受复杂的激素信号和底物相互作用调节，多年来临床关注的焦点一直是空腹过夜后的代谢和激素状况。最近，餐后状态，即“进食期间及进食后的时间段”，受到了更多关注。口服葡萄糖耐量试验（OGTT）虽然极不符合生理情况，但在很大程度上一直被用作餐后状态的模型。流行病学研究表明，口服葡萄糖耐量“受损”时，心血管疾病风险会增加。最近在流行病学、机制和干预研究中对餐后高脂血症进行了调查，其中大多数研究表明，餐后高甘油三酯水平，尤其是餐后富含甘油三酯的残粒，会增加心血管疾病风险。最近的研究表明，餐后血糖过度波动伴随着氧化应激，以及鲜为人知的凝血激活（循环D - 二聚体和凝血酶原片段增加）。餐后血糖水平和脂质浓度升高可能损害血管壁内皮细胞的机制似乎很复杂。这些机制包括蛋白激酶C的激活、黏附分子表达增加、白细胞黏附和摄取增加、内皮素等增殖物质产生增加、内皮细胞增殖增加、IV型胶原和纤连蛋白合成增加以及一氧化氮（NO）产生减少。总之，“餐后状态”累计覆盖了几乎一半的昼夜周期，其生理学涉及众多精细调节的运动、分泌、激素和代谢事件。流行病学和机制研究表明，餐后状态的紊乱与心血管疾病有关。纠正餐后状态异常必须成为心血管疾病预防和管理策略的一部分，尤其是那些与糖尿病相关的疾病。
