Investigation of possible underlying mechanisms behind water-induced glucose reduction in adults with high copeptin
Elevated copeptin, a surrogate marker of vasopressin, is linked to low water intake and increased diabetes risk.
The study investigates possible underlying mechanisms behind the water-induced glucose reduction in adults with high copeptin. Elevated copeptin, a surrogate marker of vasopressin, is linked to low water intake and increased diabetes risk. Water supplementation in habitual low-drinkers with high copeptin significantly lowers both fasting plasma copeptin and glucose. Thirty-one healthy adults with high copeptin (> 10.7 pmol·L−1 (men), > 6.1 pmol−1 (women)) and a 24-h urine volume of < 1.5 L and osmolality of > 600 mOsm·kg−1 were included. The intervention consisted of adding 1.5 L water daily for 6 weeks. However, the study found no significant effect on fasting-adrenocorticotropic hormone (ACTH), cortisol, or insulin levels. Notably, decreased copeptin was significantly associated with changes in ACTH and glucagon levels. When participants were divided according to baseline copeptin, a reduction in ACTH was observed in those with higher baseline copeptin levels. The glucose-lowering effect from water may partly be attributable to the decrease in hypothalamic–pituitary–adrenal axis activity.