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Updated: Jun 17, 2026

Experimental Approach to Examine Leptin Signaling in the Carotid Bodies and its Effects on Control of Breathing
Published on: October 25, 2019
Physiologic hyperleptinemia in obesity does not affect vasopressin secretion in acute hypo- or hyperosmolality
Minneke J Coenraad1, Marijke Frölich, A E Meinders
1Department of Internal Medicine, Leiden University Medical Center, 2300RC Leiden The Netherlands. m.j.coenraad@lumc.nl
Purpose:
Abnormal water excretion after ingestion of a water load has been described in obesity. We hypothesized that AVP secretion is abnormal in obese subjects in acute hypo- and hyperosmolality and that the hormone leptin is partly responsible for this.
Methods:
We studied the relation between leptin, AVP and serum osmolality in two separate tests: (1) after ingestion of a water load (20 ml/kg lean body mass plus 5 ml /kg of adipose tissue) and (2) after iv hypertonic saline (5% NaCl) at a rate of 0.1 ml/kg lean body mass/minute for 120 min in ten subjects of normal weight (BMI > 20 and < 25 kg/m2; controls) and ten obese females (BMI > 30 kg/m2). Obese subjects were tested before (98.6 +/- 9.3 kg) and after weight loss (90.2 +/- 8.5 kg).
Results:
In the water load experiment, obese subjects excreted a smaller percentage of the water load than controls. Weight loss restored the ability to excrete the water load in the obese. In the water load and hypertonic saline infusion experiment, plasma AVP concentrations and the area under the curve (AUC) for AVP concentration were not different in obese from normal weight women. Baseline leptin concentration was not correlated with baseline AVP or the change in AVP during the experiment in any of the groups. Weight loss did not change AVP responses in obese subjects.
Conclusion:
AVP secretion in response to acute hypo- and hyperosmolality is not different in normal weight and obese subjects. There is no correlation between leptin and AVP in normal weight or obese subjects.
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