最近血清渗透压增加与急性应激反应有关,随着时间的推移会导致肥胖风险增加,高血压,和其他慢性疾病。盐和果糖是可引起血清渗透压急性变化的两种主要刺激。在这里,我们研究了钠和果糖消耗的早期代谢作用,并确定钠或果糖负荷的影响是否可以通过阻断水合作用的渗透压变化来减轻。将44名没有疾病和药物的健康受试者分为四组。禁食过夜后,第1组的受试者喝了500毫升的咸汤,而第2组的人饮用500毫升无盐汤15分钟。第3组受试者在5分钟内饮用500毫升100%苹果汁,而第4组受试者在5分钟内饮用500毫升100%苹果汁和500毫升水。血压(BP),血浆钠,和葡萄糖水平测量每15分钟在前2小时。血清和尿液渗透压,血清尿酸,皮质醇,成纤维细胞生长因子21(FGF21),醛固酮,促肾上腺皮质激素(ACTH)水平,和血浆肾素活性(PRA)在基线和2小时测量。盐或果糖的急性摄入增加血清渗透压(最大〜4mOsm/L峰值在75分钟)与收缩压和舒张压血压升高相关,PRA,醛固酮,ACTH,皮质醇,血浆葡萄糖,尿酸,FGF21盐倾向于引起肾素-血管紧张素系统(RAS)的更大激活,而果糖引起葡萄糖和FGF21的更大升高。在这两种情况下,水合可以阻止渗透压并在很大程度上阻止急性应激反应。血清渗透压的急性变化可以诱导ACTH-皮质醇的显著激活,RAS,葡萄糖代谢,和对水合反应的尿酸轴。除了经典的脱水,盐,含果糖的糖可以激活这些反应。尽管暴露于糖和盐,但保持良好的水分可能会带来好处。需要更多的研究来调查水合作用是否可以阻止糖和盐对疾病的慢性影响。
Increasing serum
osmolality has recently been linked with acute stress responses, which over time can lead to increased risk for obesity, hypertension, and other chronic diseases. Salt and fructose are two major stimuli that can induce acute changes in serum
osmolality. Here we investigate the early metabolic effects of sodium and fructose consumption and determine whether the effects of sodium or fructose loading can be mitigated by blocking the change in osmolality with hydration. Forty-four healthy subjects without disease and medication were recruited into four groups. After overnight fasting, subjects in Group 1 drank 500 mL of salty soup, while those in Group 2 drank 500 mL of soup without salt for 15 min. Subjects in Group 3 drank 500 mL of 100% apple juice in 5 min, while subjects in Group 4 drank 500 mL of 100% apple juice and 500 mL of water in 5 min. Blood pressure (BP), plasma sodium, and glucose levels were measured every 15 min in the first 2 h. Serum and urine osmolarity, serum uric acid, cortisol, fibroblast growth factor 21 (FGF21), aldosterone, adrenocorticotropic hormone (ACTH) level, and plasma renin activity (PRA) were measured at the baseline and 2 h. Both acute intake of salt or fructose increased serum
osmolality (maximum ∼4 mOsm/L peaking at 75 min) associated with a rise in systolic and diastolic BP, PRA, aldosterone, ACTH, cortisol, plasma glucose, uric acid, and FGF21. Salt tended to cause greater activation of the renin-angiotensin-system (RAS), while fructose caused a greater rise in glucose and FGF21. In both cases, hydration could prevent the
osmolality and largely block the acute stress response. Acute changes in serum
osmolality can induce remarkable activation of the ACTH-cortisol, RAS, glucose metabolism, and uric acid axis that is responsive to hydration. In addition to classic dehydration, salt, and fructose-containing sugars can activate these responses. Staying well hydrated may provide benefits despite exposure to sugar and salt. More studies are needed to investigate whether hydration can block the chronic effects of sugar and salt on disease.