A. Banchini

Possible interaction of PGF2 alpha with hypothalamus-pituitary-thyroid axis in man.

The possible interactions of PGF2 alpha on the hypothalamus-pituitary-thyroid axis are the object of this study. Firstly a significant direct effect of PGF2 alpha infusion (mg2,5/270 min) on TSH,PRL,LH,FSH and GH pituitary secretion was excluded. Thereafter the possible PGF2 alpha on PRL and TSH pituitary response to TRH was considered: in only two cases PGF2 alpha was able to increase the TSH response. Finally the Authors studied T3 response to endogenous TSH rise induced by TRH: if they consider the mean peak responses of T3 the increase is significant only when PGF2 alpha infusion is performed.

The role of overweight and glucose tolerance in the impaired pituitary-gonadal axis of obese males

SummaryIn a group of 30 obese male patients (160.2% of ideal body weight), an impaired function of the pituitary-gonadal axis has been demonstrated. Decreased testosterone and increased estradiol basal levels, increased LH and FHS responsiveness to gonadotropin-releasing hormone. and increased basal prolactin (PRL) levels are the most significant findings. The overweight factor seems to account for the documented decreased testosterone and increased estrogen levels through a modulation of peripheral steroid metabolism. These peripheral steroid patterns might affect gonadotropin and PRL secretions as well; nevertheless an interference with the metabolism of cerebral neurotransmitters, perhaps related to a nutritional component (impaired glucose tolerance), cannot be completely excluded.

Effects of an Acetylcholine Precursor on GH Secretion in Elderly Subjects

GH secretion is under complex neurotransmitter and hormonal control. GH releasing hormone (GHRH) is released from the hypothalamus into the hypothalamic-hypophyseal circulation, stimulating pulsatile GH secretion. Hypothalamic somatostatin, on the other hand, inhibits GH release. GH stimulates the synthesis of insulin-like growth factor I in several peripheral tissues, which mediates some, but not all, of GH hormone action. Completing the feedback-loop paradigm, IGF-I directly interacts with specific IGF receptors on somatotropes, inhibiting further GH secretion. Moreover, IGF receptors are present in brain, and there is evidence that locally synthesized IGF-I can inhibit GHRH release and stimulate somatostatin secretion, thereby suppressing GH secretion (1). Finally, GH inhibits its own secretion at the level of the hypothalamus.

ACTH 1–17 stimulates GH pituitary secretion in humans

Nineteen normal subjects (12 men and 7 women) were injected with 100 μg of ACTH 1–17. Additionally 6 male subjects were studied twice at 3-day intervals with random infusions of ACTH 1–17 and saline. A clear GH response to ACTH 1–17 infusions (GH peak higher than 5 ng/ml) was documented in 10 out of 12 males and in 6 out of 7 women. In the 6 male subjects studied twice, clear-cut GH increments were observed only after peptide administration. PRL levels decreased throughout the study period both in male and female subjects; however, when the PRL percentage decline was evaluated in the same group of subjects after saline and ACTH 1–17, the more obvious decrease of PRL levels after the peptide infusion was not statistically significant. No variation of LH, FSH and TSH levels was documented. With the exception of the specific increase of cortisol levels, no significant change in peripheral steroid pattern (Te, E2, DHEA-S) was observed. In this experiment the effect on GH secretion was quite evident in both sexes. This effect was obtained using the lowest dosage of ACTH preparation documented in the literature.

Dissociated effect of buserelin on luteinizing hormone (LH) and alpha subunit in men

Chronic treatment with LHRH analogs is known to depress testosterone (T) values to castration levels. In contrast to results from animal experiments, studies in humans indicate that a pituitary-dependent mechanism predominates in the suppression of plasma T. However, this reduction in T levels may occur when LH values are within or below the normal range. One explanation for this result has been that while absolute values of LH in serum may not change, the bioactivity of LH is reduced. The present study has been performed to determine whether this discrepancy between LH and T values is obscured by the hypersecretion of the α-subunit which is devoid of any biological activity but crossreacts in most RIAs with LH. Following 2 days of blood collection to establish basal serum hormone levels, six men with prostatic cancer were treated with the LHRH agonist, Buserelin (500 μg sc, daily injection) for 15 days. The most significant endocrine responses at the end of this treatment were as follows: 1) T levels were depressed to the castration range; 2) no change was seen in the LH values with a conventional RIA procedure which crossreacted with the α-subunit; 3) a significant decrease was found in the LH values evaluated with an immunoradiometric (IRMA) method, which shows no cross-reactivity with the α-subunit; 4) there was a significant increase in the α-subunit levels; and 5) serum FSH levels were significantly decreased. In addition, when the chromatographic profiles of immunoreactive LH and α-subunit were compared from a patient at the beginning and at the end of the study, there was a shift in the elution position of the LH molecule but no change in the elution profile of the α-subunit. On the basis of these results, it appears that the pituitary LH secretion is depressed by chronic treatment with Buserelin and this reduction is responsible for the suppression of T. In addition, it appears that Buserelin therapy may bring about an alteration in the molecular form of LH which is secreted into blood.Taken together, these findings demostrate that the pituitary is the major site of action of Buserelin and that the discrepancy between the LH and T levels and between LH bioactivity and immunoreactivity values may be attributed both to the crossreactivity of the α-subunit in the LH RIA and to some change in the molecular form of LH which is secreted into the blood.

Thyrotropin and prolactin in patients with hypothalmus-pituitary diseases

SummarySeventy patients with hypothalamus-pituitary diseases were studied; 13 of them were studied before surgical treatment and then 15–20 days and 6 months later. A comparison was made with 59 controls. In all these subjects PRL and TSH were studied under basal conditions and after TRH stimulation. As for TSH the highest percentage of abnormal responses was found in the group of patients with chromophobe adenoma and parasellar dysplasias. This area of the pituitary appears relatively undamaged in acromegalic patients. In clinically hypothyroid patients, normal or high TSH responses to TRH were often found. As for PRL, a hyperprolactinaemia was mostly found in the group of patients with chromophobe adenoma, parasellar dysplasias and craniopharyngioma, although there was a different pattern in the TSH responses. No correlation was found between the basal PRL levels and the TSH responses to TRH. There was no significant difference in the TSH responses of the patients with PRL secreting and non-secreting chromophobe adenomas. The hypothesis of two autonomous systems is supported by the finding of differences in the functional recovery of the two pituitary areas studied at different times after surgical treatment.