Background: Mean daily water intake from fluids (WATER-FL) has proven to be difficult to measure because of a range of nonvalidated data collection t

The purpose of this investigation was to quantify the effects of storage temperature, duration, and the urinary sediment on urinary hydration markers. Thirty-six human urine samples were analyzed fresh and then the remaining sample was separated into 24 separate vials, six in each of the following four temperatures: 22 °C, 7 °C, -20 °C, and -80 °C. Two of each sample stored in any given temperature, were analyzed after 1, 2, and 7 days either following vortexing or centrifugation. Each urine sample was analyzed for osmolality (UOsm), urine specific gravity (USG), and urine color (UC). UOsm was stable at 22 °C, for 1 day (+5–9 mmol∙kg-1, p > .05) and at 7 °C, UOsm up to 7 days (+8–8 mmol∙kg-1, p > .05). At -20 and -80 °C, UOsm decreased after 1, 2, and 7 days (9–61 mmol∙kg-1, p < .05). Vortexing the sample before analysis further decreased only UOsm in the -20 °C and -80 °C storage. USG remained stable up to 7 days when samples were stored in 22 °C or 7 °C (p > .05) but declined significantly when stored in -20 °C, and -80 °C (p < .001). UC was not stable in any of the storing conditions for 1, 2, and 7 days. In conclusion, these data indicate that urine specimens analyzed for UOsm or USG remained stable in refrigerated (7 °C) environment for up to 7 days, and in room temperature for 1 day. However, freezing (-20 and -80 °C) samples significantly decreased the values of hydration markers.

Epidemiological studies in humans show increased concentrations of copeptin, a surrogate marker of arginine vasopressin (AVP), to be associated with increased risk for type 2 diabetes. To examine the acute and independent effect of osmotically stimulated AVP, measured via the surrogate marker copeptin, on glucose regulation in healthy adults. Sixty subjects (30 females) participated in this crossover design study. On 2 trial days, separated by ≥7 d (males) or 1 menstrual cycle (females), subjects were infused for 120 min with either 0.9% NaCl [isotonic (ISO)] or 3.0% NaCl [hypertonic (HYPER)]. Postinfusion, a 240-min oral-glucose-tolerance test (OGTT; 75 g) was administered. During HYPER, plasma osmolality and copeptin increased (P < 0.05) and remained elevated during the entire 6-h protocol, whereas renin-angiotensin-aldosterone system hormones were within the lower normal physiological range at the beginning of the protocol and declined following infusion. Fasting plasma glucose did not differ between trials (P > 0.05) at baseline and during the 120 min of infusion. During the OGTT the incremental AUC for glucose from postinfusion baseline (positive integer) was greater during HYPER (401.5 ± 190.5 mmol/L·min) compared with the ISO trial (354.0 ± 205.8 mmol/L·min; P < 0.05). The positive integer of the AUC for insulin during OGTT did not differ between trials (HYPER 55,850 ± 36,488 pmol/L·min compared with ISO 57,205 ± 31,119 pmol/L·min). Baseline values of serum glucagon were not different between the 2 trials; however, the AUC of glucagon during the OGTT was also significantly greater in HYPER (19,303 ± 3939 ng/L·min) compared with the ISO trial (18,600 ± 3755 ng/L·min; P < 0.05). The present data indicate that acute osmotic stimulation of copeptin induced greater hyperglycemic responses during the oral glucose challenge, possibly due to greater glucagon concentrations.This study was registered at clinicaltrials.gov as NCT02761434.