Water intake, thirst, and copeptin responses to two dehydrating stimuli in lean men and men with obesity
Objective Physiological systems responsible for water homeostasis and energy metabolism are interconnected. This study hypothesized altered responses to dehydration including thirst, ad libitum water intake, and copeptin in men with obesity. Methods Forty‐two men (22 lean and 20 with obesity) were s...
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Published in: | Obesity (Silver Spring, Md.) Vol. 30; no. 9; pp. 1806 - 1817 |
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Main Authors: | , , , , , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
01-09-2022
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Online Access: | Get full text |
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Summary: | Objective
Physiological systems responsible for water homeostasis and energy metabolism are interconnected. This study hypothesized altered responses to dehydration including thirst, ad libitum water intake, and copeptin in men with obesity.
Methods
Forty‐two men (22 lean and 20 with obesity) were stimulated by a 2‐hour hypertonic saline infusion and a 24‐hour water deprivation. In each dehydrating condition, thirst, ad libitum water intake after dehydration, and urinary and hormonal responses including copeptin were assessed.
Results
After each dehydration condition, ad libitum water intake was similar between both groups (p > 0.05); however, those with obesity reported feeling less thirsty (p < 0.05) and had decreased copeptin response and higher urinary sodium concentrations when stressed (p < 0.05). Angiotensin II, aldosterone, atrial and brain natriuretic peptides, and apelin concentrations did not differ by adiposity group and did not explain the different thirst or copeptin responses in men with obesity. However, leptin was associated with copeptin response in lean individuals during the hypertonic saline infusion (p < 0.05), but the relationship was diminished in those with obesity.
Conclusions
Diminished thirst and copeptin responses are part of the obesity phenotype and may be influenced by leptin. Adiposity may impact pathways regulating thirst and vasopressin release, warranting further investigation. |
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Bibliography: | Funding information National Institute of Diabetes and Digestive and Kidney Diseases, Grant/Award Number: DK069091‐12 ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Author Contributions: The authors’ responsibilities were as follows: DCC, AP, JCB, MEG, and JK designed research; DCC, AP, JCB, SAK, EP, MW, and JK conducted research; DCC, EJS, PP, and JK analyzed data; DCC, EJS, MEG, and JK wrote the paper; DCC had primary responsibility for final content. |
ISSN: | 1930-7381 1930-739X |
DOI: | 10.1002/oby.23520 |