TY - JOUR
T1 - The effect of hydration status on plasma fgf21 concentrations in humans
T2 - A subanalysis of a randomised crossover trial
AU - Carroll, Harriet A.
AU - Chen, Yung Chih
AU - Templeman, Iain
AU - James, Lewis J.
AU - Betts, James A.
AU - Trim, William V.
N1 - Publisher Copyright:
© 2020 Carroll et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
PY - 2020/8
Y1 - 2020/8
N2 - Aim Fibroblast growth factor 21 (FGF21) has recently been implicated in thirst in rodent models. The mechanisms for this are currently uncertain, and it is unclear whether hydration status can alter FGF21 concentrations, potentially providing an additional mechanism by which hypohydration induces thirst. The aim of this study is therefore to understand whether hydration status can alter circulating FGF21 in humans. Methods Using a heat tent and fluid restriction, we induced hypohydration (1.9% body mass loss) in 16 healthy participants (n = 8 men), and compared their glycaemic regulation to a rehydration protocol (heat tent and fluid replacement) in a randomised crossover design. Results After the hypohydration procedure, urine specific gravity, urine and serum osmolality, and plasma copeptin (as a marker for arginine vasopressin) increased as expected, with no change after the rehydration protocol. In the fasted state, the median paired difference in plasma FGF21 concentrations from the rehydrated to hypohydrated trial arm was -37 (interquartile range -125, 10) pg.mL-1(P = 0.278), with average concentrations being 458 ± 462 pg.mL-1 after hypohydration and 467 ± 438 pg.mL-1 after rehydration; mean difference -9 ± 173 pg.mL-1. Conclusion To our knowledge, these are the first causal data in humans investigating hydration and FGF21, demonstrating that an acute bout of hypohydration does not impact fasted plasma FGF21 concentrations. These data may suggest that whilst previous research has found FGF21 administration can induce thirst and drinking behaviours, a physiological state implicated in increased thirst (hypohydration) does not appear to impact plasma FGF21 concentrations in humans.
AB - Aim Fibroblast growth factor 21 (FGF21) has recently been implicated in thirst in rodent models. The mechanisms for this are currently uncertain, and it is unclear whether hydration status can alter FGF21 concentrations, potentially providing an additional mechanism by which hypohydration induces thirst. The aim of this study is therefore to understand whether hydration status can alter circulating FGF21 in humans. Methods Using a heat tent and fluid restriction, we induced hypohydration (1.9% body mass loss) in 16 healthy participants (n = 8 men), and compared their glycaemic regulation to a rehydration protocol (heat tent and fluid replacement) in a randomised crossover design. Results After the hypohydration procedure, urine specific gravity, urine and serum osmolality, and plasma copeptin (as a marker for arginine vasopressin) increased as expected, with no change after the rehydration protocol. In the fasted state, the median paired difference in plasma FGF21 concentrations from the rehydrated to hypohydrated trial arm was -37 (interquartile range -125, 10) pg.mL-1(P = 0.278), with average concentrations being 458 ± 462 pg.mL-1 after hypohydration and 467 ± 438 pg.mL-1 after rehydration; mean difference -9 ± 173 pg.mL-1. Conclusion To our knowledge, these are the first causal data in humans investigating hydration and FGF21, demonstrating that an acute bout of hypohydration does not impact fasted plasma FGF21 concentrations. These data may suggest that whilst previous research has found FGF21 administration can induce thirst and drinking behaviours, a physiological state implicated in increased thirst (hypohydration) does not appear to impact plasma FGF21 concentrations in humans.
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U2 - 10.1371/journal.pone.0235557
DO - 10.1371/journal.pone.0235557
M3 - Article
C2 - 32756564
AN - SCOPUS:85089170475
SN - 1932-6203
VL - 15
JO - PloS one
JF - PloS one
IS - 8 August 2020
M1 - e0235557
ER -