Preuss H G, Zein M, MacArthy P, Dipette D, Sabnis S, Knapka J
Department of Medicine, Georgetown University Medical Center, Washington, DC 20007, USA.
J Am Coll Nutr. 1998 Feb;17(1):36-47. doi: 10.1080/07315724.1998.10720453.
Since the majority of studies concerned with sugar-induced blood pressure elevation have principally been short-term, the present investigation followed the effects of heavy sucrose ingestion on systolic blood pressure (SBP) and related parameters over the lifespan of three substrains of Wistar rats.
Two hundred twenty-five rats (75 spontaneously hypertensive rats (SHR), 75 Wistar Kyoto rats (WKY), 75 Munich Wistar rats (WAM) were given one of five diets. The baseline diet in terms of calories derived 32% from sucrose, 33% from protein, and 35% from fat. The remaining four diets derived their calories as follows: a high sugar-low protein diet--52% of calories from sucrose, 15% from protein, and 33% from fat; a high sugar-low fat diet--53% of calories from sucrose, 37% from protein, and 10% from fat; a low sugar-high protein diet--11% calories from sucrose, 56% from protein, and 33% from fat, and a low sugar-high fat--13% of calories from sucrose, 32% from protein, and 55% from fat.
All substrains showed the highest systolic blood pressure when ingesting the two diets highest in sucrose. The highest sugar-induced SBP elevation, which remained over the lifespan of all substrains, was found in SHR. WKY had an intermediate elevation. WAM showed the lowest responses, although the average elevation of 6-8 mm Hg was statistically significant. The following parameters could not be correlated with long-term elevation of SBP; body weight, catecholamine excretion, renal function, and plasma renin activity. Only insulin concentrations correlated: insulin concentrations were consistently higher in the two groups of WKY and WAM consuming the high sucrose diets.
High dietary sucrose can chronically increase SBP in three substrains of Wistar rats. Increased concentrations of circulating insulin were found in WKY and WAM suggesting that the glucose/insulin system was involved, at least in these two substrains, in the maintenance of high SBP levels during chronic, heavy sugar ingestion.
由于大多数关于糖诱导血压升高的研究主要是短期的，本研究追踪了大量摄入蔗糖对三种Wistar大鼠亚系整个生命周期内收缩压（SBP）及相关参数的影响。
225只大鼠（75只自发性高血压大鼠（SHR）、75只Wistar Kyoto大鼠（WKY）、75只慕尼黑Wistar大鼠（WAM））被给予五种饮食中的一种。基线饮食的热量来源为32%来自蔗糖、33%来自蛋白质、35%来自脂肪。其余四种饮食的热量来源如下：高糖低蛋白饮食——52%的热量来自蔗糖、15%来自蛋白质、33%来自脂肪；高糖低脂饮食——53%的热量来自蔗糖、37%来自蛋白质、10%来自脂肪；低糖高蛋白饮食——11%的热量来自蔗糖、56%来自蛋白质、33%来自脂肪，以及低糖高脂肪饮食——13%的热量来自蔗糖、32%来自蛋白质、55%来自脂肪。
所有亚系在摄入蔗糖含量最高的两种饮食时收缩压最高。在SHR中发现了最高的糖诱导SBP升高，且在所有亚系的整个生命周期内都持续存在。WKY的升高程度居中。WAM的反应最低，尽管平均升高6 - 8 mmHg具有统计学意义。以下参数与SBP的长期升高无关；体重、儿茶酚胺排泄、肾功能和血浆肾素活性。只有胰岛素浓度相关：在食用高蔗糖饮食的两组WKY和WAM中，胰岛素浓度一直较高。
高糖饮食可使三种Wistar大鼠亚系的SBP长期升高。在WKY和WAM中发现循环胰岛素浓度升高，这表明葡萄糖/胰岛素系统至少在这两个亚系中参与了长期大量摄入糖期间高SBP水平的维持。
