2篇JCI改写传统认知:高盐食物,让你饿,而不是渴!
2017/04/19
我们都曾经历过:吃过咸的食物容易渴,所以我们需要补充水分。可是,一项模拟太空飞行的研究却发现事实并非如此!高盐食物不会让我们渴,相反,它们会增加饥饿感,因为需要补充更多的能量。


通常,我们认为含盐量高的食物会让我们口渴,需要补充更多的水分。但是,近期2篇发表于《Journal of Clinical Investigation》期刊的文章却表明,事实并非如此!通过模拟太空飞行,科学家们意外发现:摄取高盐食物会减少喝水量,同时,它会增加饥饿感。

我们明确的是,盐摄取量的增加会刺激我们产生更多的尿液。过去,科学家们认为,这与喝水有关联。但是,来自于德国航空航天中心(DLR)、最高德尔布吕克分子医学中心(MDC)、范德堡大学的科学家团队却在一项模拟火星的研究中,得出了不一样的结论。

高盐食物会减少喝水?!

盐与火星有什么关联?并没有,硬要牵扯的话,就是宇航员在长时间的太空飞行中需要节约每一滴水。而盐摄取量对于水分补充的关联会影响飞行之前食材、水资源的准备。但是,这项模拟试验却得出了让研究人员意外的结果。

Natalia Rakova教授带领团队招募了10名男性志愿者参与试验。研究人员将他们分成两组,安置在两个模拟宇宙飞船的密闭空间中。第一组参与者会接受试验105天,而第二组成员需要坚持超205天。两组参与者的饮食一样,除了连续几周,他们会得到3种含盐量不同的食物。这一研究提供了一个环境便于精准控制、测量一个人摄取的水、盐量。

结果证实,摄取盐量增加,其尿量也会变多,而且液体中的含盐量会增加。这一点与过去的认知一致。但是,研究人员发现:这一变化与补充水分无关!因为,高盐饮食会减少喝水量,盐会引发肾脏组织启动“节约用水”的机制。

尿素促使水分再利用

过去,体液循环中我们一直认为,盐中的钠离子、氯离子会“抓住”水分子,将其带至尿液中排出体外。但是,最新的研究却发现,盐分子会停留在尿液中,而水分子会重新流转至肝脏及身体的其他部位。

这一最新发现让埃朗根大学、范德堡大学医学中心的Jens Titze教授团队很困惑:促使水分子循环的动力是什么?

他们以小鼠为研究模型,发现尿素可能在其中发挥重要作用,尿素是控制氮元素的关键步骤。在小鼠体内,尿素在肾脏组织中富集,抵消了钠离子、氯离子对水分子的控制力。但是,合成尿素需要消耗很多能量,这一点可以解释为什么食用高盐食物的小鼠饮食量会增加。

高盐饮食并不会增加它们的渴感,相反,它们会增加饥饿感。接受模拟太空飞行的参与者们也在食用高盐食物后,表现出饥饿的症状。

这一研究修正了科学家对尿素生物功能的认知。研究人员表示:“它不再仅仅只是废物。事实上,尿素是一种非常重要的渗透剂。当身体摄入过多的盐,尿素会负责结合、运输水分子,从而确保水的再利用。”

参考资料:

Mission control: Salty diet makes you hungry, not thirsty

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  • Increased salt consumption induces body water conservation and decreases fluid intake

    BACKGROUND. The idea that increasing salt intake increases drinking and urine volume is widely accepted. We tested the hypothesis that an increase in salt intake of 6 g/d would change fluid balance in men living under ultra-long-term controlled conditions. METHODS. Over the course of 2 separate space flight simulation studies of 105 and 205 days’ duration, we exposed 10 healthy men to 3 salt intake levels (12, 9, or 6 g/d). All other nutrients were maintained constant. We studied the effect of salt-driven changes in mineralocorticoid and glucocorticoid urinary excretion on day-to-day osmolyte and water balance. RESULTS. A 6-g/d increase in salt intake increased urine osmolyte excretion, but reduced free-water clearance, indicating endogenous free water accrual by urine concentration. The resulting endogenous water surplus reduced fluid intake at the 12-g/d salt intake level. Across all 3 levels of salt intake, half-weekly and weekly rhythmical mineralocorticoid release promoted free water reabsorption via the renal concentration mechanism. Mineralocorticoid-coupled increases in free water reabsorption were counterbalanced by rhythmical glucocorticoid release, with excretion of endogenous osmolyte and water surplus by relative urine dilution. A 6-g/d increase in salt intake decreased the level of rhythmical mineralocorticoid release and elevated rhythmical glucocorticoid release. The projected effect of salt-driven hormone rhythm modulation corresponded well with the measured decrease in water intake and an increase in urine volume with surplus osmolyte excretion. CONCLUSION. Humans regulate osmolyte and water balance by rhythmical mineralocorticoid and glucocorticoid release, endogenous accrual of surplus body water, and precise surplus excretion.

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  • High salt intake reprioritizes osmolyte and energy metabolism for body fluid conservation

    Natriuretic regulation of extracellular fluid volume homeostasis includes suppression of the renin-angiotensin-aldosterone system, pressure natriuresis, and reduced renal nerve activity, actions that concomitantly increase urinary Na+ excretion and lead to increased urine volume. The resulting natriuresis-driven diuretic water loss is assumed to control the extracellular volume. Here, we have demonstrated that urine concentration, and therefore regulation of water conservation, is an important control system for urine formation and extracellular volume homeostasis in mice and humans across various levels of salt intake. We observed that the renal concentration mechanism couples natriuresis with correspondent renal water reabsorption, limits natriuretic osmotic diuresis, and results in concurrent extracellular volume conservation and concentration of salt excreted into urine. This water-conserving mechanism of dietary salt excretion relies on urea transporter–driven urea recycling by the kidneys and on urea production by liver and skeletal muscle. The energy-intense nature of hepatic and extrahepatic urea osmolyte production for renal water conservation requires reprioritization of energy and substrate metabolism in liver and skeletal muscle, resulting in hepatic ketogenesis and glucocorticoid-driven muscle catabolism, which are prevented by increasing food intake. This natriuretic-ureotelic, water-conserving principle relies on metabolism-driven extracellular volume control and is regulated by concerted liver, muscle, and renal actions.

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