Both V(1A) and V(1B) vasopressin receptors deficiency result in impaired glucose tolerance.

摘要: [Arg8]-vasopressin (AVP) is involved in the regulation of glucose homeostasis via vasopressin V1A and V1B receptor. Our previous studies have demonstrated that receptor deficient (V1AR−/−) mice exhibited hyperglycemia, (V1BR−/−) mice, contrast, hypoglycemia with hypoinsulinemia. These findings indicate deficiency results decreased insulin sensitivity, whereas increased sensitivity. In our present studies, we used tolerance test to investigate mutant lacking either vasopressinV1A receptor, or both receptors, were kept on a high-fat diet. Glucose levels lower V1BR−/− than wild type (WT) when groups fed diet, which indicates sensitivity was enhanced. V1AR−/− other hand, overt obesity, along an impaired tolerance, while WT diet did not. Next, order assess effect development intolerance caused by deficiency, generated for (V1ABR−/−), them examined their tolerances using test. V1ABR−/− suggesting effects could not influence hyperglycemia promoted blockade receptors lead tolerance.