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Hyperammonaemia in V1a vasopressin receptor knockout mice caused by the promoted proteolysis and reduced intrahepatic blood volume

An analysis of arginine‐vasopressin (AVP) V1a receptor‐deficient (V1aR−/−) mice revealed that glucose homeostasis and lipid metabolism were altered in the mutant mice. Here, we used V1aR−/− mice to investigate whether the deficiency of the V1a receptor, which led to altered insulin sensitivity, affected protein metabolism. The serum 3‐methylhistidine levels were increased in V1aR−/− mice under feeding conditions, indicating that proteolysis was enhanced in muscle tissue from V1aR−/− mice. Furthermore, serum amino acid profiling revealed that the amino acid levels, including glycogenic and branched‐chain amino acids, were reduced in V1aR−/− mice. In addition, an alanine‐loading test showed that gluconeogenesis was enhanced in V1aR−/− mice. Blood ammonia, which is a by‐product of amino acid catabolism, was two times higher in V1aR−/− mice without hepatopathy under the feeding and fasting conditions than in wild‐type mice. Amino acid profiling also revealed that the amino acid pattern was not typical of a urea‐cycle enzymatic disorder. An ammonia tolerance test and an indocyanine green elimination test showed that V1aR−/− mice had lower ammonia clearance due to a decreased intrahepatic circulating blood volume. Metabolic acidosis, including lactic‐ and keto‐acidosis, was not observed in V1aR−/− mice. These results provide evidence that proteolysis promotes the production of glucose in the muscles of V1aR−/− mice and that hyperammonaemia is caused by promoted protein catabolism and reduced intrahepatic blood volume. Thus, our study with V1aR−/− mice indicates that AVP plays a physiological role via the V1a receptor in regulating both protein catabolism and glucose homeostasis.