Efectos de la hiperprolactinemia sobre el metabolismo hidrocarbonado / Effects of hyperprolactinemia on the carbohidrate metabolism

Con el objetivo de evaluar el efecto de la hiperprolactinemia sobre el metabolismo hidrocarbonado, se estudiaron, antes de iniciar el tratamiento con bromocriptina, 21 pacientes con hiperprolactinemia de causa idiopática, normopesos y sin antecedentes de otras enfermedades y una muestra de 48 mujeres sanas, con normopeso y edades similares a las del grupo de estudio. Se realizó una prueba de tolerancia a la glucosa oral (PTG-o) para medir glucemia e insulinemia después de una sobrecarga oral de 75 g de glucosa. Se calculó el índice insulinogénico inicial (IIo-30) y el de resistencia a la insulina (RI) para cada mujer. El grupo con hiperprolactinemia se dividió en 2 subgrupos según los valores de la prolactina plasmática (Prl), uno con Prl< 2 500 mU/L (subgrupo 1a) y otro con Prl > 2 500 mU/L (subgrupo 1b). Los valores de la glucemia plasmática en respuesta a la sobrecarga de la glucosa oral, en todos los momentos de la PTG, fueron superiores significativamente en el grupo de las mujeres híperprolactinémicas en relación con el grupo control, con la mayor diferencia (p < 0,01) a los 30 min (mediana = 5,8 mmol/L y 4,1 mmol/L, respectivamente). El subgrupo 1a, no presentó diferencias significativas con el grupo control en ningún momento de la PTG-o, mientras que el subgrupo 1b, mantuvo cifras superiores al control, y de manera significativa a los 30, 90 y 120 min (p < 0,05). No hubo diferencias en ningún momento de la PTG-o ni en el área bajo la curva de insulina entre el grupo hiperprolactinémico y el control. Los índices (II0-30 y de RI) fueron similares en ambos grupos. En conclusión, hubo menor tolerancia a la glucosa oral en las mujeres con hiperprolactinemia, en especial aquéllas con los valores más altos de PRL; esta diferencia no se asoció a un estado de hiperinsulinismo ni de resistencia a la insulina(AU)

21 patients with hyperprolactinemia of idiopathic cause, with normal weight and no history of other diseases, and a sample of 48 sound women with normal weight and ages similar to those of the study group were studied aimed at evaluating the effect of hyperprolactinemia on the carbohidrate metabolism before beginning the treatment with bromocriptine. Glucose tolerance test was made to determine glucaemia and insulinaemia after an overload of 75 g of glucose. The initial insulinogenic index (II0-30) and that of insulin resistance (IR) were calculated for each woman. The group with hyperprolactinemia was divided into subgroups according to the values of plasmatic prolactin (Prl), one with Prl<2 500 mU/L (subgroup 1a) and the other with Prl ?_2 500 mU/L (subgroup 1b). The values of plasmatic glucaemia in response to the overload of oral glucose during the GTT were always significantly higher in the group of hyperprolactinemic women compared with the control group. The highest difference (p<0.01) was observed at the 30 minutes (mean = 5.8 mmol/L and 4.1 mmol/L, respectively). In the subgroup 1a there were not marked differences in comparison with the control group at any moment of the GTT; however, in subgroup 1b there were figures over those of the control group that were significant at the 30, 90 and 120 minutes (p < 0.05). There were no differences either during the GTT or in the area under the insulin curve between the hyperprolactinemic group and the control group. The indexes (II0-30 and IR) were similar in both groups. To conclude, oral glucose tolerance was lower in women with hyperprolactinemia, specially in those with the highest values of Prl. This difference was not associated either with a state of hyperinsulinism or with insulin resistance(AU)

Chronic effect of antidopaminergic drugs or estrogen on male Wistar rat lactotrophs and somatotrophs

The aim of the present study was to evaluate the effect of antidopaminergic agents on the somatotrophs in the presence of hyperprolactinemia. Adult male Wistar rats were divided into 6 groups: a control group and five groups chronically treated (60 days) with haloperidol, fluphenazine, sulpiride, metoclopramide or estrogen. Somatotrophs and lactotrophs were identified by immunohistochemistry and the data are reported as percent of total anterior pituitary cells counted. The drugs significantly increased the percentage of lactotrophs: control (mean + or - SD) 21.3 + or - 4.4, haloperidol 27.8 + or - 2.2, fluphenazine 34.5 + or - 3.6, sulpiride 32.7 + or - 3.5, metoclopramide 33.4 + or - 5.5 and estrogen 42.4 + or - 2.8. A significant reduction in somatotrophs was observed in animals treated with haloperidol (23.1 + or - 3.0), fluphenazine (22.1 + or - 1.1) and metoclopramide (24.2 + or - 3.0) compared to control (27.3 + or - 3.8), whereas no difference was observed in the groups treated with sulpiride (25.0 + or - 2.2) and estrogen (27.1 + or - 2.8). In the groups in which a reduction occurred, this may have simply been due to dilution, secondary to lactotroph hyperplasia. In view of the duplication of the percentage of prolactin-secreting cells, when estrogen was applied, the absence of a reduction in the percent of somatotrophs suggests a replication effect on this cell population. These data provide additional information about the direct or indirect effect of drugs which, in addition to interfering with the dopaminergic system, may act on other pituitary cells as well as on the lactotrophs.

Alterations in plasma prolactin and glucose levels induced by surgical stress in hyperprolactinemic female rats

The effects of hyperprolactinemia on plasma prolactin (PRL) and glucose were investigated in female rats submitted to surgical stress (laparotomy under ether anesthesia). Wistar rats weighing 250-280g received pituitary grafs under the kidney capsule three weeks before the experiments (N = 15) while a control group underwent sham transplantation (N = 14). The sham-operated rats presented a threefold increase of PRL levels as early as after 5 min of surgical stress (P<0.01); the PRL levels reached a peak at about 15 min and returned to baseline at 40 min. The PRL levels of the grafted rats were increased 3.5-fold compared to the sham-operated controls before stress (20.2 + 5.6 ng/ml vs 5.8 + 0.9 ng/ml, respectively; P<0.05), but did not change significantly during the experimental period. Plasma glucose was already significantly increased at 5 min in sham-operated control and grafted rats (P<0.01) and reached maximal concentrations at about 15 min. The grafted rats presented higher glucose levels than sham-operated controls before stress (122.2 + 3.3 vs 100.5 + 4.2 mg/dl; P<0.01) and at 40 min (182.6 + 13.6 vs 146.7 + 8.4 mg/dl; P<0.05). The hyperprolactinemic rats showed impaired surgical stress-induced PRL release and higher glucose levels both at rest and during the first postoperative hour. These results indicate that chronic hyperprolactinemia inhibited PRL secretion and enhanced the hyperglycemic stress response in the female rat.

Comparacao dos perfis hipofisario, esteroidiano e lipoproteico em pacientes com galactorreia normoprolactinemica e galactorreia hiperprolactinemica / Comparison of pituitary, steroid and lipoprotein profile in patients with hyperprolactinemic and normoprolactinemic galactorrhea

Objetivos: Avaliar o comportamento dos perfis hipofisario, esteroidiano e lipoproteico em pacientes com galactorreia hiperprolactinemica e galactorreia normoprolactinemica. Desenho: Foram estudadas 39 pacientes: 18 com galactorreia hiperprolactinemica e 21 com galactorreia normoprolactinemica. A avaliacao laboratorial constou das dosagens de PRL, FSH, LH e TSH (perfil hipofisario); estradiol, testosterona, androstenediona, deidroepiandrosterona e seu sulfato, 17-alfa-hidroxiprogesterona (perfil lipoproteico). O tratamento estatistico foi realizado atraves da comparacao das medias e dos respectivos desvios padrao. Resultados: O perfil hipofisario nao diferiu entre os dois grupos exceto em relacao a prolactina...

Hyperprolactinemia induced by long-term domperidone treatment does not alter the sensitivity of strial dopamine receptors

We investigated the effect of hyperprolactinemia by long-term domperidone treatment (10.0 mg/kg, single daily dose, ip) on striatal dopamine (DA) receptor sensitivity in male Wistar rats weighing 250-300 g(N=8). Domperidone treatment for days continued to produce an increased in serum concentration of prolactin (PRL) form 17.3 ñ 2.2 to 33.1 ñ 7.3 and from 16.8 ñ 2.3 to 21.9 ñ 2.1, 2 and 72 h after domperidone withdrawal, respectively. Hyperprolactinemia induced by long-term domperidone treatment did not change binding sites (B max) and dissociation constant (Kd) of [3***H]-spiroperidol binding when compared to controls. These results show that byperprolactinemia induced by long-term domperidone treatment does not effect the sensitivity of striatal DA receptors presumably because the effect of neuroleptic drugs is due to their interaction with the receptors and not to the concomitant hyperprolactinemia

Maturation events of epididymis in albino rats during puberal transition under hypo and hyperprolactinemia.

Hypoprolactinemia inhibited epididymal energy metabolism and steroidogenesis and retarded growth of epididymal structure. Hyperprolactinemia promoted the above parameters. Bromocriptine had no direct effect on epididymis, while prolactin directly influenced the tissue metabolism. The epididymal maturation seems to be dependent on the circulating levels of prolactin.