多喝水能预防和缓解代谢综合征？ | 热心肠日报

10.1172/jci.insight.140848

12-15, Article

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Subjects with obesity frequently have elevated serum vasopressin levels, noted by the stable analog, copeptin. Vasopressin acts primarily to reabsorb water via urinary concentration. However, fat is also a source of metabolic water, raising the possibility that vasopressin might have a role in fat accumulation. Fructose has also been reported to stimulate vasopressin. Here we tested the hypothesis that fructose induced metabolic syndrome is mediated by vasopressin. Orally administered fructose, glucose or high fructose corn syrup increased vasopressin (copeptin) concentrations and was mediated by fructokinase, an enzyme specific for fructose metabolism. Suppressing vasopressin with hydration both prevented and ameliorated fructose-induced metabolic syndrome. The vasopressin effects were mediated by the Vasopressin 1b receptor, as Vasopressin 1b receptor knockout mice were completely protected while V1a knockout paradoxically showed worse metabolic syndrome. The mechanism is likely mediated in part by de novo expression of V1b in the liver that amplifies fructokinase expression in response to fructose. Thus, our studies document a new role for vasopressin in water conservation via the accumulation of fat as a source of metabolic water. Clinically, it also suggests that increased water intake may be a beneficial way to both prevent or treat metabolic syndrome.

First Authors:
Ana Andres-Hernando,Thomas J Jensen,Masanari Kuwabara

Correspondence Authors:
Miguel Lanaspa

All Authors:
Ana Andres-Hernando,Thomas J Jensen,Masanari Kuwabara,David J Orlicky,Christina Cicerchi,Nanxing Li,Carlos A Roncal-Jimenez,Gabriela E Garcia,Takuji Ishimoto,Paul S MacLean,Petter Bjornstad,Laura Gabriela Sanchez-Lozada,Mehmet Kanbay,Takahiko Nakagawa,Richard Johnson,Miguel Lanaspa