• F M Reis, A Ribeiro-de-Oliveira, R M Guerra, A M Reis, and C C Coimbra.
• Department of Physiology and Biophysics, Institute of Biological Sciences, Federal University of Minas Gerais, Belo Horizonte, Brazil.
• Life Sci. 1996 Jan 1; 58 (2): 155-61.

AbstractThe effects of chronic hyperprolactinemia on plasma prolactin (PRL) and glucose were investigated in male rats submitted to two different types of stress: restraint (60 min in a plastic tube) or surgery (laparotomy under ether anesthesia). Hyperprolactinemia was induced by grafting one homologous pituitary gland under the kidney capsule. Restraint stress induced a marked increase of plasma PRL of control rats with a peak at 15 min (increase of 403%), but did not change the PRL levels of hyperprolactinemic rats. Plasma glucose levels of both groups were elevated by restraint stress at 5 min (control, 26%; grafted, 63%), and remained above basal levels during the whole experimental period. However, at 15 min the hyperglycemic response of the grafted rats was higher than that of control rats (p<0.05). Surgical stress induced a 204% increase of plasma PRL at 5 min in the control group, but failed to induce alterations of PRL in the hyperprolactinemic group. Plasma glucose was remarkably elevated at 15 min both in control (138%) and grafted (124%) rats after surgery, producing a hyperglycemic response much more intense than that induced by restraint. Grafted rats presented hyperglycemia during all the experimental period, whereas control rats showed glycemia similar to basal levels by the end of the experiment. In conclusion, different responses are induced depending on the type of stress: more intense PRL secretion is induced by restraint and higher hyperglycemia by surgery. Chronic hyperprolactinemia induced a higher (restraint) or longer lasting (surgery) hyperglycemic response in the rat, adding new evidence for a diabetogenic effect of PRL.

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