Release of human neurophysin I during insulin-induced hypoglycemia in depressed patients is abolished after recovery with clomipramine treatment.
Release of human neurophysin I (hNp I) and neurophysin II (hNp II) during insulin-induced hypoglycemia was studied in 10 unipolar depressed women before and after 4-5 weeks of standard antidepressant drug treatment with daily intravenous infusions of clomipramine. Before treatment, a significant increase of hNp I but not of hNp II serum levels in response to hypoglycemia was observed. At retest during clomipramine administration, a marked clinical amelioration occurred in all patients as determined with the Hamilton Rating Scale for Depression; the hNp I response to insulin was abolished, but no effect on hNp II concentration could be demonstrated. No correlation was found between the degree of the depression score decrease and the amplitude of the inhibition of hNp I release or serum levels of clomipramine or its metabolite, desmethylclomipramine. The meaning of this difference in reactivity of the neurohypophyseal system in the course of depressive illness, based on the pharmacological and biochemical profiles of clomipramine action, is discussed.
D001786:Blood Glucose / Q000032:analysis; D002997:Clomipramine / Q000031:analogs & derivatives / Q000097:blood / Q000627:therapeutic use*; D003866:Depressive Disorder / Q000188:drug therapy / Q000503:physiopathology*; D005260:Female; D006801:Humans; D007328:Insulin; D008875:Middle Aged; D009481:Neurophysins / Q000378:metabolism*; D010904:Pituitary Gland, Posterior / Q000503:physiopathology*
D001786:Blood Glucose; D007328:Insulin; D009481:Neurophysins; C012273:desmethylclomipramine; D002997:Clomipramine