Currently, the conceptualization of thirst is based nearly entirely on osmoregulation, with some acknowledgment of anticipatory-thirst, though with no testable mechanism. Such a model of thirst is unable to explain many thirst-related phenomena, such as why drinking can occur with hypoosmolality or how quantity of intake at a drinking occasion is regulated.This model aimed to unify various lines of thinking from different disciplines surrounding thirst by presenting a 4-compartment model comprising true-thirst (primarily osmo-regulated), contextual-thirst (e.g., mouth-breathing), pharmacological-thirst (induced from drugs), and impulsive-thirst (everyday spontaneous drinking). Within this framework, xerostomia (dry mouth) is the primary regulator of drinking, with a further differentiation between a literal dry mouth ("true-xerostomia," hyposalivation) and the sensation of dry mouth ("sensational-xerostomia," a typically nonoverwhelming desire to drink based on a feeling of dry mouth without hyposalivation). Based on pharmacological-thirst mechanisms, the cholinergic system is proposed to initiate impulsive-thirst by triggering a (sensation of) dry mouth in everyday life. Food-appetite constructs that are centrally regulated (sensory-specific satiety, palatability, and pleasantness) are applied to thirst to explain everyday drinking patterns.This model helps to explain some anomalies that are thus far unexplained by true-thirst, though there are several other factors which may need to be included after further exploration in the future.
To examine whether calcium type and co-ingestion with protein alter gut hormone availability.Healthy adults aged 26 ± 7 years (mean ± SD) completed three randomized, double-blind, crossover studies. In all studies, arterialized blood was sampled postprandially over 120 min to determine GLP-1, GIP and PYY responses, alongside appetite ratings, energy expenditure and blood pressure. In study 1 (n = 20), three treatments matched for total calcium content (1058 mg) were compared: calcium citrate (CALCITR); milk minerals rich in calcium (MILK MINERALS); and milk minerals rich in calcium plus co-ingestion of 50 g whey protein hydrolysate (MILK MINERALS + PROTEIN). In study 2 (n = 6), 50 g whey protein hydrolysate (PROTEIN) was compared to MILK MINERALS + PROTEIN. In study 3 (n = 6), MILK MINERALS was compared to the vehicle of ingestion (water plus sucralose; CONTROL).MILK MINERALS + PROTEIN increased GLP-1 incremental area under the curve (iAUC) by ~ ninefold (43.7 ± 11.1 pmol L-1 120 min; p < 0.001) versus both CALCITR and MILK MINERALS, with no difference detected between CALCITR (6.6 ± 3.7 pmol L-1 120 min) and MILK MINERALS (5.3 ± 3.5 pmol L-1 120 min; p > 0.999). MILK MINERALS + PROTEIN produced a GLP-1 iAUC ~ 25% greater than PROTEIN (p = 0.024; mean difference: 9.1 ± 6.9 pmol L-1 120 min), whereas the difference between MILK MINERALS versus CONTROL was small and non-significant (p = 0.098; mean difference: 4.2 ± 5.1 pmol L-1 120 min).When ingested alone, milk minerals rich in calcium do not increase GLP-1 secretion compared to calcium citrate. Co-ingesting high-dose whey protein hydrolysate with milk minerals rich in calcium increases postprandial GLP-1 concentrations to some of the highest physiological levels ever reported. Registered at ClinicalTrials.gov: NCT03232034, NCT03370484, NCT03370497.
Publication bias is prevalent within the scientific literature. Whilst there are multiple ideas on how to reduce publication bias, only a minority of journals have made substantive changes to address the problem. We aimed to explore the perceived feasibility of strategies to reduce publication bias by gauging opinions of journal editors (n = 73) and other academics/researchers (n = 160) regarding nine methods of publishing and peer-reviewing research: mandatory publication, negative results journals/articles, open reviewing, peer-review training and accreditation, post-publication review, pre-study publication of methodology, published rejection lists, research registration, and two-stage review. Participants completed a questionnaire asking both quantitative (multiple choice or Likert scales) and qualitative (open-ended) questions regarding the barriers to implementing each suggestion, and their strengths and limitations. Participants were asked to rate the nine suggestions, then choose the method they felt was most effective. Mandatory publication was most popularly selected as the 'most effective' method of reducing publication bias for editors (25%), and was the third most popular choice for academics/researchers (14%). The most common selection for academics/researchers was two-stage review (26%), but fewer editors prioritised this (11%). Negative results journals/articles were the second and third most common choices for academics/researchers (21%) and editors (16%), respectively. Editors more commonly chose research registration as 'most effective' (21%), which was favoured by only 6% of academics/researchers. Whilst mandatory publication was generally favoured by respondents, it is infeasible to trial at a journal level. Where suggestions have already been implemented (e.g. negative results journals/articles, trial registration), efforts should be made to objectively assess their efficacy. Two-stage review should be further trialled as its popularity amongst academics/researchers suggests it may be well received, though editors may be less receptive. Several underlying barriers to change also emerged, including scientific culture, impact factors, and researcher training; these should be further explored to reduce publication bias.
Glycemic responses are commonly measured in both research and clinical practice. Factors such as prior food intake and physical exertion are often controlled for, yet water intake and hydration status are typically uncontrolled and may impact results. PURPOSE: To investigate the effects of hydration status on glycemic control and to inform future study design. METHODS: In a randomized-crossover design, five healthy individuals (80 % male) aged 28 ± 4 y, were dehydrated in a sauna (55–85°C) for 45 minutes between 1700–1900 hours, before either remaining dehydrated (consuming maximum 200 mL) or rehydrating with 150 % of individual weight losses throughout the evening. Participants then arrived at the laboratory the next morning in a fasted state at 0800 hours and provided a urine sample to verify hydration status based on urine osmolality, before commencing an oral glucose tolerance test (75 g glucose solution in 89 mL water). Venous blood samples were drawn at baseline and every 15 minutes for 120 minutes. Trials were separated by seven days, with diet and physical activities replicated for 24 h prior to each. Data were analysed via visual checking of trends and calculating the incremental area under the curve (iAUC). RESULTS: Body mass was reduced by 1.2 ± 0.8 kg. The following week, participants matched this weight loss or remained in the sauna for 45 minutes (whichever came first). Urine osmolality was significantly higher when dehydrated than rehydrated (1069 ± 67 and 606 ± 292 mOsm). The iAUC for blood glucose was higher in the dehydrated trial than the rehydrated trial (72.9 ± 45.5 vs. 66.6 ± 49.1 mmol*120min/L. This was reflective of a similar time-course of initial response but then an attenuated concentration in the hydrated trial from 45 minutes onwards. Blood lactate concentrations were also lower in the rehydrated group, although the differences in the time-course of the initial response were only apparent from 75 minutes. CONCLUSIONS: Hydration status may be an important factor to consider when measuring glycaemic response. The trend in the lactate data suggest the effect is beyond that of hemodilution alone. This pilot will inform future research design to further explore the effects of hydration on glycemic control and the mechanisms involved.
Abstract Purpose Plasma copeptin (a surrogate marker of arginine vasopressin) is increasingly being used as a marker of stress in several research and clinical contexts. However, the response to an acute physical stressor in healthy adults has not yet been tested meaning it is unclear whether copeptin reflects dynamic changes in stress or whether this is moderated by different basal copeptin concentrations and how this relates to other stress hormones. Methods Secondary data analysis in a subsample of participants (n = 7; n = 1 woman) who opted-in for muscle biopsies in a randomised crossover study investigating the effects of acute hypohydration (HYPO) versus rehydration (RE) on metabolism. Results Plasma copeptin responded to the muscle biopsy stress stimulus, with a similar magnitude of difference according to basal concentrations during HYPO and RE; however, the peak was higher and concentrations typically took longer to return to baseline during HYPO. Despite large differences in copeptin concentrations, adrenocorticotropin hormone (ACTH) and cortisol showed a similar trends in response to the biopsies, regardless of hydration status. Conclusion Copeptin responded dynamically to an acute physical stressor (muscle biopsy). HYPO induced higher basal copeptin concentrations compared to RE, and resulted in a higher and prolonged copeptin response. Further research should investigate the mechanisms underlying the lack of differences in ACTH and cortisol according to hydration status.
The aim of this study was to investigate the acute effect of hydration status on glycemic regulation in healthy adults and explore underlying mechanisms. In this randomized crossover trial, 16 healthy adults (8 men, 8 women) underwent an oral glucose tolerance test (OGTT) when hypohydrated and rehydrated after 4 days of pretrial standardization. One day before OGTT, participants were dehydrated for 1 h in a heat tent with subsequent fluid restriction (HYPO) or replacement (RE). The following day, an OGTT was performed with metabolic rate measurements and pre- and post-OGTT muscle biopsies. Peripheral quantitative computer tomography thigh scans were taken before and after intervention to infer changes in cell volume. HYPO (but not RE) induced 1.9% (SD 1.2) body mass loss, 2.9% (SD 2.7) cell volume reduction, and increased urinary hydration markers, serum osmolality, and plasma copeptin concentration (all P ≤ 0.007). Fasted serum glucose [HYPO 5.10 mmol/l (SD 0.42), RE 5.02 mmol/l (SD 0.40); P = 0.327] and insulin [HYPO 27.1 pmol/l (SD 9.7), RE 27.6 pmol/l (SD 9.2); P = 0.809] concentrations were similar between HYPO and RE. Hydration status did not alter the serum glucose ( P = 0.627) or insulin ( P = 0.200) responses during the OGTT. Muscle water content was lower before OGTT after HYPO compared with RE [761 g/kg wet wt (SD 13) vs. 772 g/kg wet wt (SD 18) RE] but similar after OGTT [HYPO 779 g/kg wet wt (SD 15) vs. RE 780 g/kg wet wt (SD 20); time P = 0.011; trial × time P = 0.055]. Resting energy expenditure was similar between hydration states (stable between −1.21 and 5.94 kJ·kg −1 ·day −1 ; trial P = 0.904). Overall, despite acute mild hypohydration increasing plasma copeptin concentrations and decreasing fasted cell volume and muscle water, we found no effect on glycemic regulation. NEW & NOTEWORTHY We demonstrated for the first time that an acute bout of hypohydration does not impact blood sugar control in healthy adults. Physiological responses to mild hypohydration (<2% body mass loss) caused an elevation in copeptin concentrations similar to that seen in those with diabetes as well as reducing cell volume by ~3%; both of these changes had been hypothesized to cause a higher blood sugar response.
PURPOSE: Skeletal dysplasia refers to restricted bone growth, culminating in disproportionate short stature and increased risk of obesity and related chronic diseases. For those with skeletal dysplasia, neither metabolic requirements nor the extent of adiposity that poses health risks have been established. METHODS: Thirty-seven adult men and women with skeletal dysplasia (Age 43 ± 15 y, Height 1.30 ± 0.09 m; Body Mass 61.4 ± 18.6 kg; Mean ± SD) presented in an overnight fasted state for assessments of anthropometry, resting metabolic rate (COSMED K4), and venous blood samples. Reference data (from our published research) are presented as a control sample (n = 138) of broadly age-matched (38 ± 16 y) men and women without skeletal dysplasia (Height 1.74 ± 0.13 m, Body Mass 81.3 ± 17 kg; Mean ± SD). RESULTS: Resting metabolic rate was similar between those with and without skeletal dysplasia (1561 ± 407 vs. 1626 ± 334 kcal·d-1, respectively) and underestimated by common predictive equations (e.g., Schofield, Harris Benedict and Mifflin St Jeor) in those with skeletal dysplasia. Fasted plasma markers of metabolic health for individuals with skeletal dysplasia were within the healthy population range (i.e., total cholesterol 4.54 ± 0.85 mmol·L-1; HDL 1.41 ± 0.31 mmol·L-1, TAG 0.84 ± 0.37 mmol·L-1; glucose 5.55 ± 0.73 mmol·L-1; insulin 36.4 ± 19.9 pmol·L-1; CRP 2.53 ± 2.66 mg·L-1; leptin 36.4 ± 41.3 ng·mL-1; free thyroxine 22.9 ± 3.6 pmol·L-1). The elevated leptin concentrations of those with skeletal dysplasia are consistent with overweight individuals in the general population and were moderately positively correlated within the present sample with key non-height-dependent measures of central adiposity: waist circumference (86.3 ± 16.2 cm) and sagittal abdominal diameter (21.5 ± 5.0 cm). CONCLUSION: Adults with skeletal dysplasia exhibit higher resting energy expenditure rates than demographic or anthropometric predictions, similar to the measured metabolic requirements of larger individuals without skeletal dysplasia. Metabolite and hormone plasma concentrations were within reference ranges and clinical thresholds, so did not indicate impaired metabolic health. Supported by grants from the Rare Disease Foundation.
'%3e%3cpath fill='%23012169' d='M0 0v30h60V0z'/%3e%3cpath stroke='%23fff' stroke-width='6' d='m0 0 60 30m0-30L0 30'/%3e%3cpath stroke='%23C8102E' stroke-width='4' d='m0 0 60 30m0-30L0 30' clip-path='url(%23b)'/%3e%3cpath stroke='%23fff' stroke-width='10' d='M30 0v30M0 15h60'/%3e%3cpath stroke='%23C8102E' stroke-width='6' d='M30 0v30M0 15h60'/%3e%3c/g%3e%3c/svg%3e)
