Hyperprolactinemia: neuroendocrine and diagnostic aspects

Camanni, F.; Ciccarelli, Enrica; Ghigo, Ezio; Müller, Eugenio E.

doi:10.1007/bf03350030

Cited by 9 publications

(4 citation statements)

References 102 publications

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“…To conclude, we can say that the present data confirm that in patients with hyperprolactinemia PRL secretion is, at least partly, refractory to stimulation (16). Reduced lactotrope responsiveness to stimulation has also been reported in obesity (38,39).…”

Section: Discussionsupporting

confidence: 88%

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Effects of glucose load and/or arginine on insulin and growth hormone secretion in hyperprolactinemia and obesity

Maccario

Grottoli²,

Razzore³

et al. 1996

European Journal of Endocrinology

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In hyperprolactinemic patients an exaggerated glucose-induced insulin secretion has been reported, but these results have not been confirmed by other researchers. On the other hand, there are few data concerning somatotrope secretion in this condition. In order to clarify these points, in seven normal weight hyperprolactinemic female patients (HP: age 18-46 years, body mass index = 21.8 +/- 0.6 kg/m(2), basal prolactin = 91.7 +/- 16.5 micrograms/l) we studied the effects of glucose load (100 g orally) and/or arginine (0.5 g/kg infused over 30 min) on insulin glucose and growth hormone (GH) levels. These results were compared with those obtained in seven patients with simple obesity (OB: age 23-48 years, body mass index = 38.3 +/- 2.6 kg/m(2)) in whom exaggerated insulin and low GH secretion are well known. Seven normal women (NS: age 26-32 years, body mass index = 20.6 +/- 1/9 kg/m(2)) were studied as controls. The insulin response to glucose in HP (area under curve = 11,460.8 +/- 1407.5 mU x min x l(-1)) was not significantly different from NS (7743.7 +/- 882.9 mU x min x l(-1)) and OB (14,504.8 +/- 1659.9 mU x min x l(-1)). The arginine-induced insulin release in HP and OB was similar (4219.4 +/- 631.7 and 4107.3 +/- 643.2 mU x min x l(-1), respectively), both being higher (p < 0.02) than in NS (2178.1 +/- 290.9 mU x min x l(-1). Glucose and arginine had an additive effect on insulin release in HP and NS (19,769.1 +/- 3249.6 and 10,996.6 +/- 1201.0 mU x min 1(-1), respectively) and a synergistic effect in OB (28 117.3 +/- 5224.7 mU x min x l(-1)). In HP the insulin response to the combined administration of glucose and arginine was not significantly different from the one in OB, and both were higher (p < 0.05) than in NS. The increase in glucose levels after glucose administered on its own or combined with arginine was higher (p < 0.02) and longer lasting in OB than in NS and HP. After arginine in OB, the glucose levels did not show the late decrease under baseline values observed in HP and NS. Glucose inhibited GH secretion both in HP and NS (p < 0.05), while arginine stimulated it in all groups, although the GH response in HP and NS was higher (p < 0.03) than in OB. The arginine-induced GH secretion was inhibited by glucose in HP and NS but not in OB. These results demonstrate that both in hyperprolactinemic patients and in obesity there is a clear increase in insulin secretion. The insulin hyperresponsiveness in hyperprolactinemia is more clearly demonstrated by combined stimulation with glucose and arginine. In spite of similar insulin hypersecretion in hyperprolactinemic and obese patients, GH secretion is reduced only in the latter; with these data the hypothesis that somatotrope insufficiency in obesity is due to hyperinsulinism is unlikely.

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Section: Discussionsupporting

confidence: 88%

“…Interestingly, recent data in animals and in men suggest that prolactin plays a major role in /3-cell trophism, as well as on insulin synthesis and secretion (13)(14)(15). On the other hand, there are few data concerning somatotrope secretion in hyperprolactinemia (16).…”

mentioning

confidence: 99%

Effects of glucose load and/or arginine on insulin and growth hormone secretion in hyperprolactinemia and obesity

Maccario

Grottoli²,

Razzore³

et al. 1996

European Journal of Endocrinology

View full text Add to dashboard Cite

show abstract

“…In man, a slight but significant PRL increase has been demonstrated after GHRP-6 or hexarelin administration (Ilson et al, 1989;Bowers et al, 1990;Ghigo et al, 1994) while, to our knowledge, no study has yet been performed in pathological conditions. The evidence that hexarelin fails to modify high PRL levels in hyperprolactinaemic patients is in accord with the refractoriness of lactotroph cells in this condition to almost all secretagogues (Camanni et al, 1989;Muller & Nisticò, 1989). However, it has to be considered that acromegalic patients, who frequently share this refractoriness to PRL secretagogues (Camanni et al, 1982), displayed a significant PRL response to hexarelin administration.…”

Section: Discussionmentioning

confidence: 62%

“…In our HPRL patients we can exclude the possibility of hypothalamic damage, since only patients with small pituitary lesions were studied. However, it is well known that pathological hyperprolactinaemia is associated with functional hypothalamic alterations, namely the dopaminergic control of anterior pituitary function (Scanlon et al, 1981;Camanni et al, 1989;Muller & Nisticò, 1989). As somatotroph secretion is also under dopaminergic control (Muller & Nisticò, 1989) we could consider the possibility that hypothalamic alterations present in hyperprolactinaemic conditions could explain the reduced effect of hexarelin in HPRL patients.…”

Section: Discussionmentioning

confidence: 99%