THE REDUCTION OF CIRCULATING GROWTH-HORMONE AND PROLACTIN IN STREPTOZOCIN-INDUCED DIABETIC MALE-RATS IS POSSIBLY CAUSED BY HYPOTHALAMIC RATHER THAN PITUITARY CHANGES

To gain further information on diabetes-related disorders in the somat otrophic and lactotrophic axes, we undertook a functional, morphometri cal and densitometrical study of the arcuate nucleus (AN), median emin ence (ME) and anterior pituitary gland of adult male rats one month af ter streptozocin-induced diabetes (STZ-D). The basal secretory activit y of somatotrophs and lactotrophs was tested by the reverse haemolytic plaque assay (RHPA) and plasma GH and prolactin (PRL) levels were det ermined by RIA. The number of GH-releasing factor (GRF)labelled axons and the amount of axonal tyrosine hydroxylase (TH)-immunoreactivity in creased in STZ-D. There were no significant differences in any of the other densitometrical measurements performed on GRF-, somatostatin-, t hyrotropin-releasing hormone- and TH-labelled ME axon cross-sections a s well as those on tuberoinfundibular-dopaminergic neurones of the AN in STZ-D compared with control rats. Plasma GH and PRL levels and meas urements on anterior pituitary GH- and PRL-labelled structures were de creased in STZ-D. However, the GH and PRL plaque areas were increased after RHPA implying that the secretory capacity of somatotrophs and la ctotrophs was not impaired. Taken together, these results suggest that the accumulated GRF in the ME is due to reduced GRF release. This cou ld account for the reduced amplitude and/or frequency of GH secretory pulses. The increased axonal TH-immunoreactivity may indicate an incre ased dopamine synthesis. If coupled to increased release this could, i n turn, be partly responsible for the reduced plasma and anterior pitu itary PRL concentration. Although a direct effect of diabetes on the a nterior pituitary cannot be ruled out, the reduction of circulating GH and PRL in STZ-D male rats seems to be caused by hypothalamic rather than anterior pituitary changes.