Effects of hydration on plasma copeptin, glycemia and gluco-regulatory hormones: a water intervention in humans

Abstract

Purpose High plasma copeptin, a marker of vasopressin, predicts diabetes mellitus. We tested if copeptin could be suppressed by increased water intake in healthy individuals, and if a water-induced change in copeptin was accompanied by altered concentrations of glucose, insulin or glucagon. Methods Thirty-nine healthy individuals underwent, in random order, 1 week of high water intake (3 L/day on top of habitual intake) and 1 week of normal (habitual) fluid intake (control). Fasting plasma concentrations of copeptin, glucose, insulin and glucagon were compared between the ends of both periods. Furthermore, acute copeptin kinetics were mapped for 4 h after ingestion of 1 L of water. Results After acute intake of 1 L water, copeptin was significantly reduced within 30 min, and reached maximum reduction within 90 min with on average 39% reduction (95% confidence interval (95 CI) 34-45) (p < 0.001) and remained low the entire test period (4 h). One week of increased water intake led to a 15% reduction (95 CI 5-25) (p = 0.003) of copeptin compared to control week. The greatest reduction occurred among subjects with habitually high copeptin and concentrated urine ("water-responders"). Water-responders had significant water-induced reduction of glucagon, but glucose and insulin were unaffected. Conclusions Both acute and 1 week extra water intake potently reduced copeptin concentration. In those with the greatest decline (water-responders), who are typically low drinkers with high baseline copeptin, water induced a reduction in fasting glucagon. Long-term trials assessing the effect of water on glucometabolic traits should focus on low-water drinkers with high copeptin concentration.

Plasma copeptin and chronic kidney disease risk in 3 European cohorts from the general population

“…In the present investigation in cohorts from the general population, associations with severe kidney outcomes (eGFR slope steeper than -5 ml/min/1.73 m 2 or ESRD) could not be assessed, as their prevalence or incidence during follow-up was far too low as to be studied as endpoints. A few short-term pilot studies showed that increased water intake can lead to a significant decrease in plasma copeptin concentration in healthy individuals (34,35), especially in those with high plasma copeptin at baseline (34), as well as in stage 3 CKD patients (36). However, data on kidney outcomes from intervention studies modifying vasopressin secretion or action are scarce.…”

Measuring Human Water Needs

“…Urinary biomarkers of hydration status change throughout the day as they reflect water intake and outputs. When human water intake is experimentally manipulated either through extra water provision or water restriction, urinary biomarkers reflect those changes either through more dilute or more concentrated urine (Enhörning et al, ; Perrier et al, ). These biomarkers stabilize within 24 hours to reflect the current water intake state.…”

Elevated copeptin, arterial stiffness, and elevated albumin excretion in adolescents with type 1 diabetes

“…Recent short-term clinical trials have shown that increased water intake can reduce concentrations of plasma copeptin, fasting blood glucose and glucagon in healthy participants. 13,49 Another study also found that increased water consumption resulted in decreased copeptin concentrations in participants with chronic kidney disease, however, no differences in rates of eGFR decline were observed in participants with or without increased water intake. 50 Mechanisms leading to increased AVP, and thus copeptin, in diabetes are also incompletely elucidated.…”