The demonstration in the central nervous system of a group of endogenous opioid-like substances has suggested their physiological role as neurotransmitter or neuromodulator in the control of hypothalamic-pituitary function. Recent studies have described a stimulatory effect of opioid substances on PRL, GH and TSH and an inhibitory influence on LH and FSH secretion. Naloxone, a specific opiate antagonist has been reported to prevent these effects (Morley 1981). Multiple endocrine disorders are present in diabetics, mainly characterized by altered basal secretion of pituitary hormones and impaired response to provocative stimuli. Recently it was observed that administration of TRH to diabetic subjects elicits abnormal secretion of FSH and GH

Weightman and Hall 1980) in both men and women, whereas growth hormone (GH) release by the pituitary remains unmodified, at least in normal men (Sowers, McCallum, Hershman, Carlson, Sturdevant and Meyer 1976). On the other hand, the administration of MCP to hypogonadal men significantly increases GH serum levels (Cohen, Hay, Beastall and Thomson 1979). Thus blood estrogen concentrations and/or the androgen/estrogen ratio may be important for the development of this response and may play a role in the control of the GH secretory system. To test this hypothesis the effect of an acute administration of MCP on serum GH concentrations in normal women was evaluated.

These data show that in diabetic, but not in normal subjects LVP enhances the GH responsiveness to secretagogues, such as GH-RH, clonidine and arginine, which act through three different mechanisms. These findings suggest that in diabetes mellitus, vasopressin functions as a primer for various GH responses.

In order to determine whether nicotine exerts its stimulant effect on serum concentrations of growth hormone (GH) by interacting with an adrenergic pathway, we evaluated the effect of cigarette smoking on the response of GH to the administration of clonidine, a specific a-adrenoceptor agonist. In six normal volunteers, clonidine significantly increased serum levels of GH. When subjects smoked two non-filter cigarettes, GH response to the a-adrenoceptor agonist was greatly enhanced. These findings suggest that in man nicotinic cholinergic and adrenergic mechanisms might interact in the stimulation of GH secretion.

Enzyme immunoassay (EIA) and electron microscopy (EM) were utilized to investigate the presence of rotavirus in feces of 388 children with acute enteritis hospitalized at the Hospital Santa Casa de Misericórdia in Porto Alegre, Brazil. The survey covered 12 months, beginning in July 1981. There were 162 rotavirus-positive cases (41.8%). During the period of the study rotavirus was detected throughout the year, but there was a striking seasonal variation (78.1% of cases) during January 1982.

In its initial encounter with growth hormone (GH) in vitro, epididymal fat excised from GH-deficient rats responds with an insulin-like increase in glucose metabolism. Tissues freshly excised from normal rats are refractory to the insulin-like effects of GH, but become sensitive immediately after surgical stress. Reversal of refractoriness is prevented by administration of the opioid antagonist, naloxone, just prior to stress, suggesting a possible role of β-endorphin or related peptides. These experiments were undertaken to determine the source of these peptides which might equally well be released from the pituitary, adrenal medullae, or nerve endings in response to stress. Since adrenalectomy, like stress, also results in increased secretion of adrenocorticotropic hormone (ACTH) and related peptides, we studied the effects of GH on glucose oxidation in adipose tissue obtained from adrenalectomized rats and found a significant insulin-like response to GH in tissues studied 4 days after adrenalectomy. This effect was not due to GH deficiency, since plasma concentrations were only slightly reduced by adrenalectomy. Administration of naloxone (250 µg/rat), 30 or 60 min before sacrifice, or dexamethasone (100 µg/injection), 60 and 120 min before sacrifice, prevented a response to GH without affecting circulating levels of GH. The effects of adrenalectomy could not be reproduced by preincubation of adipose tissue from normal nonstressed rats with ACTH and β-endorphin, but were duplicated by preincubation of adipose tissue for 15 min in medium in which pituitary glands had previously incubated in the presence of corticotropin-releasing hormone (0.1 µM) and arginine vasopressin (0.2 µM). Addition of naloxone (250 µg/ml) blocked this effect. Neither medium, in which pituitary glands had been incubated in the absence of hypothalamic peptides, nor the hypothalamic peptides alone were effective in inducing an insulin-like response to GH in adipose tissue of normal rats. The pituitary glands used for these studies were obtained from rats that had been thyroidectomized 3–5 weeks earlier and hence were virtually devoid of GH. The data suggest that substances released along with ACTH in the adrenalectomized or stressed rat can acutely reverse the refractoriness of normal adipose tissue to the insulin-like effects of GH.

These results indicate a role for both deficiency in residual endogenous insulin secretion and duration of diabetes in the derangement of LH secretory control. The data suggest that the protective role exerted by residual beta-cell activity on LH secretion during the early years of DM diminishes with time elapsed after the onset of diabetes mellitus.

Our previous studies showed that naloxone is unable to stimulate LH secretion in elderly men, suggesting a loss in the endogenous opioid inhibitory control of LH in senescence. Methods: In the present study, we examined whether increasing age during the reproductive period in women is associated with alterations in the LH-releasing effect of naloxone. Studies were performed in younger (age 20–28 years, n = 8) and older (age 40–48 years, n = 8) subjects with normal menstrual cycles and normal gonadal steroid levels to avoid the interference of premenopause or menopause on gonadotropin secretion. The LH response to naloxone (4 mg as an i.v. bolus plus 10 mg infused in 2 h) was tested not only in normal conditions, but also after chronic dopaminergic stimulation with bromocriptine (5 mg/day for 7 days), because this treatment has been found able to restore normal LH responses to naloxone in elderly men. All tests were performed on the 22nd day of normal menstrual cycles. Results: Naloxone induced a 100% increase in plasma LH levels in the younger group. In contrast, naloxone enhanced only by 50% LH secretion in the older subjects. When experiments were repeated after bromocriptine treatment, the effect of naloxone did not change in the younger subjects, whereas it was significantly higher in the older group. In the presence of bromocriptine, naloxone-induced LH increment in the older group was indistinguishable from that observed in the younger group. These data suggest that during the reproductive period, increasing age is associated with an impairment in the endogenous opioid control of LH secretion. In addition, age-related dopaminergic alterations independent of circulating gonadal steroid levels appear to underlie the defective endogenous opioid control of LH secretion in normally cycling women.