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Am J Physiol Endocrinol Metab 287: E263-E268, 2004. First published April 6, 2004; doi:10.1152/ajpendo.00514.2003
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Plasma hyperosmolality stimulates leptin secretion acutely by a vasopressin-adrenal mechanism

James R. Levy1,2 and Wayne Stevens1

1Section of Endocrinology and Metabolism, McGuire Veterans Administration Medical Center and 2Medical College of Virginia/Virginia Commonwealth University, Richmond, Virginia 23249

Submitted 13 November 2003 ; accepted in final form 31 March 2004

Glucose administration to rodents acutely stimulates leptin secretion. To investigate the mechanism, rats were infused intravenously with various concentrations of glucose, and plasma leptin concentrations were measured with time. The osmolality of the infusates was equalized with various concentrations of carbohydrates that are not metabolized. Hyperosmolar glucose stimulates leptin secretion in a dose-dependent manner, with peak plasma leptin concentrations occurring ~3 h after the end of the glucose infusion. Hypertonic infusions of galactose, mannitol, and sodium chloride independently stimulate leptin secretion with approximately one-half the strength of equivalent osmolar concentrations of glucose. Peak plasma leptin concentrations occur ~4 h after the end of the hypertonic solution infusion. Hypertonic solutions of mannitol do not stimulate leptin secretion in vasopressin-deficient or in adrenalectomized animals. In conclusion, intravenous infusions of hypertonic glucose and hypertonic mannitol independently stimulate leptin secretion. Hyperosmolality stimulates leptin secretion by a vasopressin-adrenal mechanism.


Address for reprint requests and other correspondence: J. R. Levy, McGuire Veterans Administration Medical Center, 111-P, 1201 Broad Rock Blvd., Richmond, VA 23249 (E-mail: James.Levy{at}med.va.gov).






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