Send to

Choose Destination
Neuroendocrinology. 1993 Mar;57(3):525-31.

Effects of streptozotocin-induced diabetes on neuroendocrine responses to ovariectomy and estrogen replacement in female rats.

Author information

Department of Physiology, Southern Illinois University School of Medicine, Carbondale 62901.


The effects of streptozotocin-induced (STZ) diabetes on the negative feedback regulation of LH and FSH were evaluated in adult female rats. Rats were injected with STZ (50 mg/kg) or vehicle and ovariectomized 10 days later. Estrogen (EB; 100 micrograms/kg) or oil injections were given on alternate days, starting on the day of ovariectomy. Blood samples for LH, FSH and PRL assay were taken on days 10, 13, 15 and 17. The rats were decapitated on day 17. One hour prior to sacrifice, one half of the animals were injected with alpha-methyl-p-tyrosine for determination of catecholamine turnover rates. Pituitaries were incubated to determine basal secretion rates. Rats treated with STZ exhibited the expected weight loss and elevation of plasma glucose levels. At the time of ovariectomy, FSH, but not LH or PRL, was depressed in the diabetic rats. The postovariectomy rise in LH and FSH was severely attenuated in the diabetic rats. EB treatment was more effective in lowering LH and FSH levels in the diabetic as compared to the control rats. Median eminence (ME) norepinephrine (NE) and dopamine (DA) turnover was higher in the oil-treated diabetic rats than oil-treated controls. EB also caused a greater decrease in ME NE and DA turnover in the diabetic rats. EB was more effective in decreasing in vitro LH secretion and increasing in vitro PRL secretion from pituitaries of control as compared to STZ-treated animals. These results demonstrated that STZ-induced diabetes leads to an attenuation of LH and FSH release after ovariectomy and potentiates the negative feedback effects of EB.(ABSTRACT TRUNCATED AT 250 WORDS).

[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for S. Karger AG, Basel, Switzerland
Loading ...
Support Center