Neuroleptic-mediated hypothalamic deregulation of central insulin and peripheral glucose metabolism in tardive dyskinesia: a hypothesis.
In the following communication we discuss evidence that impaired peripheral and central glucose and insulin metabolism may be significant in the pathophysiology of neuroleptic-induced tardive dyskinesia. Such an association between alterations in glucose metabolism and pathophysiology of tardive dyskinesia may open new avenues in the prevention and pharmacological management of this often therapy-resistant chronic neurological disorder.
D000818:Animals; D014150:Antipsychotic Agents / Q000494:pharmacology*; D001921:Brain / Q000378:metabolism*; D004409:Dyskinesia, Drug-Induced / Q000378:metabolism*; D005947:Glucose / Q000378:metabolism*; D006801:Humans; D007031:Hypothalamus / Q000502:physiology*; D007328:Insulin / Q000378:metabolism*; D008962:Models, Theoretical
D014150:Antipsychotic Agents; D007328:Insulin; D005947:Glucose