目的:越来越多的证据表明,高盐摄入是肥胖的独立危险因素,但机制未知.我们新的工作假设是高盐摄入量驱动皮质醇的产生,反过来,导致肥胖.当前的研究旨在证明单次高盐餐后的急性皮质醇反应。
方法:8名参与者(年龄30.5±9.8岁[平均值±SD],50%女性),在随机交叉设计中消耗高盐(3.82g;1529mg钠)和低盐(0.02g;9mg钠)膳食。
结果:泌尿和唾液皮质醇以及血浆促肾上腺皮质激素(ACTH)显示出有序效应。当第二高盐时,尿皮质醇的峰值高于基线(26.3%),唾液皮质醇(9.4%)和血浆ACTH(4.1%),随后每种激素显着下降(治疗*时间,F[9,18]=2.641,p=0.038,部分η2=0.569;治疗*时间,F[12,24]=2.668,p=0.020,部分η2=0.572;治疗*时间,F[12,24]=2.580,p=0.023,部分η2=0.563),但不是在首先给予高盐时(全部p>0.05)。
结论:这些有趣的发现为我们的假设提供了部分支持,并支持需要进一步研究以阐明高盐摄入在皮质醇生产中的作用,反过来,在肥胖的病因中。
背景:ACTRN12623000490673;注册日期12/05/2023;回顾性注册。
OBJECTIVE: Evidence is growing that high salt intake is an independent risk factor for obesity, but the mechanisms are unknown. Our novel working hypothesis is that high salt intake drives cortisol production, which in turn, drives obesity. The current
study aimed to demonstrate an acute cortisol response following a single high salt meal.
METHODS: Eight participants (age 30.5 ± 9.8 years [mean ± SD], 50% female), consumed high salt (3.82 g; 1529 mg sodium) and low salt (0.02 g; 9 mg sodium) meals in a randomized cross-over design.
RESULTS: Urinary and salivary cortisol and plasma adrenocorticotropic hormone (ACTH) demonstrated order effects. When high salt was given second, there was a peak above baseline for urinary cortisol (26.3%), salivary cortisol (9.4%) and plasma ACTH (4.1%) followed by a significant decline in each hormone (treatment*time, F[9, 18] = 2.641, p = 0.038, partial η2 = 0.569; treatment*time, F[12, 24] = 2.668, p = 0.020, partial η2 = 0.572; treatment*time, F[12, 24] = 2.580, p = 0.023, partial η2 = 0.563, respectively), but not when high salt was given first (p > 0.05 for all).
CONCLUSIONS: These intriguing findings provide partial support for our hypothesis and support a need for further research to elucidate the role of high salt intake in cortisol production and, in turn, in the aetiology of obesity.
BACKGROUND: ACTRN12623000490673; date of registration 12/05/2023; retrospectively registered.