title: The reduction of circulating growth hormone and prolactin in streptozocin-induced diabetic male rats is possibly caused by hypothalamic rather than pituitary changes.
abstract: To gain further information on diabetes-related disorders in the somatotrophic and lactotrophic axes, we undertook a functional, morphometrical and densitometrical study of the arcuate nucleus (AN), median eminence (ME) and anterior pituitary gland of adult male rats one month after streptozocin-induced diabetes (STZ-D). The basal secretory activity of somatotrophs and lactotrophs was tested by the reverse haemolytic plaque assay (RHPA) and plasma GH and prolactin (PRL) levels were determined by RIA. The number of GH-releasing factor (GRF)-labelled axons and the amount of axonal tyrosine hydroxylase (TH)-immunoreactivity increased in STZ-D. There were no significant differences in any of the other densitometrical measurements performed on GRF-, somatostatin-, thyrotropin-releasing hormone- and TH-labelled ME axon cross-sections as well as those on tuberoinfundibular-dopaminergic neurones of the AN in STZ-D compared with control rats. Plasma GH and PRL levels and measurements on anterior pituitary GH- and PRL-labelled structures were decreased in STZ-D. However, the GH and PRL plaque areas were increased after RHPA implying that the secretory capacity of somatotrophs and lactotrophs was not impaired. Taken together, these results suggest that the accumulated GRF in the ME is due to reduced GRF release. This could account for the reduced amplitude and/or frequency of GH secretory pulses. The increased axonal TH-immunoreactivity may indicate an increased dopamine synthesis. If coupled to increased release this could, in turn, be partly responsible for the reduced plasma and anterior pituitary PRL concentration.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Division of Experimental Pathology, University of Bern, Switzerland.
authors.forename: C E
authors.initials: CE
authors.lastname: Boujon
authors.forename: G E
authors.initials: GE
authors.lastname: Bestetti
authors.forename: F
authors.initials: F
authors.lastname: Abramo
authors.forename: V
authors.initials: V
authors.lastname: Locatelli
authors.forename: G L
authors.initials: GL
authors.lastname: Rossi
mesh_terms: D000818:Animals; D001369:Axons / Q000737:chemistry; D003720:Densitometry; D003921:Diabetes Mellitus, Experimental / Q000097:blood*; D013006:Growth Hormone / Q000032:analysis / Q000097:blood*; D013007:Growth Hormone-Releasing Hormone / Q000032:analysis; D007031:Hypothalamus / Q000378:metabolism*; D007150:Immunohistochemistry; D008297:Male; D008473:Median Eminence / Q000737:chemistry; D010903:Pituitary Gland, Anterior / Q000737:chemistry / Q000378:metabolism*; D011388:Prolactin / Q000032:analysis / Q000097:blood*; D051381:Rats; D017207:Rats, Sprague-Dawley; D014446:Tyrosine 3-Monooxygenase / Q000032:analysis
chemical_list: D011388:Prolactin; D013006:Growth Hormone; D013007:Growth Hormone-Releasing Hormone; D014446:Tyrosine 3-Monooxygenase