Inhibition of glucose-induced insulin release by xylazine.
The effects of xylazine, a sedative that is extensively used in veterinary medicine, on glucose-stimulated insulin release have been studied using isolated perifused rat pancreatic islets. Xylazine had no effect on insulin release under basal conditions. Glucose-stimulated insulin release was inhibited in a concentration-dependent manner over the range of 10(-9)-10(-6) M. Maximum inhibition even with 10(-5) M xylazine was around 80%, which suggested that xylazine is only a partial agonist at its receptor. The inhibitory effect could be completely eliminated by yohimbine, an alpha 2-adrenergic antagonist, and was unaffected by prazosin, an alpha 1-adrenergic antagonist. That xylazine is a partial agonist was verified by the fact that when present in excess, it could stimulate insulin release which had already been inhibited to 100% by epinephrine. It is concluded that xylazine is a potent partial alpha 2-adrenergic agonist and that this mechanism is responsible, at least in part, for the hyperglycemia and insulinopenia associated with its use.[1]References
- Inhibition of glucose-induced insulin release by xylazine. Abdel el Motal, S.M., Sharp, G.W. Endocrinology (1985) [Pubmed]
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