Vasopressin mediates fructose-induced metabolic syndrome by activating the V1b receptor

Subjects with obesity frequently have elevated serum vasopressin levels, noted by measuring the stable analog, copeptin. Vasopressin acts primarily to reabsorb water via urinary concentration. However, fat is also a source of metabolic water, raising possibility that might role in accumulation. Fructose has been reported stimulate vasopressin. Here, we tested hypothesis fructose-induced syndrome mediated Orally administered fructose, glucose, or high-fructose corn syrup increased (copeptin) concentrations and was fructokinase, an enzyme specific for fructose metabolism. Suppressing hydration both prevented ameliorated syndrome. The effects were 1b receptor (V1bR), as V1bR-KO mice completely protected, whereas V1a-KO paradoxically showed worse mechanism likely part de novo expression V1bR liver amplifies fructokinase response fructose. Thus, our studies document conservation accumulation water. Clinically, they suggest intake may be beneficial way prevent treat