G. Bambini

Effects of continuous light and dark exposure on hypothalamic thyrotropin-releasing hormone in rats

The thyrotropin-releasing hormone (TRH) content in whole hypothalamus was measured by specific radioimmunoassay in rats exposed to a daily light-dark cycle (06:00–18:00 light, 18:00–06:00 dark) and in animals exposed to constant light or constant darkness for 12 days. A nyctohemeral variation of hypothalamic TRH was observed in light-dark exposed animals, while this variation was abolished by exposure either to constant light or constant darkness. These data indicate that any study involving hypothalamic TRH determination should be carried out taking into account the diurnal variation and the effect of environmental light exposure.

Effects of gonadotropin-releasing hormone (GnRH) on gastric secretion and gastrin release in the dog

The effects of GnRH on gastric secretion and gastrin release from dogs provided with gastric fistulae and Heidenhain pouches have been investigated. A transient yet significant inhibition of pentagastrin-stimulated secretion from gastric fistulae was observed, while secretion from Heidenhain pouches was unchanged. The maximal inhibitory effect of GnRH on both acid and pepsin secretion stimulated by 2-deoxy-D-glucose was obtained from gastric fistulae. On the contrary, GnRH failed to affect either acid secretion stimulated by bethanechol or acid secretion and gastrin release induced by bombesin. The present results indicate that GnRH possesses an inhibitory action on gastric secretion from the vagally innervated stomach of the dog. The most likely inhibitory mechanism seems to be represented by a decrease of the vagal activity.

Serum tissue polypeptide antigen (TPA) in thyroid cancer

Serum tissue polypeptide antigen, (TPA), carcinoembryonic antigen (CEA), calcitonin (CT) and thyroglobulin (Tg) have been measured by specific radioimmunoassays in 174 patients with various types of thyroid cancer previously submitted to thyroidectomy. Elevated serum TPA concentrations were found in 12 of 13 patients with local invasion or distant metastases from undifferentiated thyroid cancer or thyroid lymphosarcoma, while serum Tg and CEA values were normal or undetectable. In 123 patients with well differentiated thyroid cancer serum TPA was usually normal regardless of the presence or absence of functioning metastases. On the contrary, 14 of 15 patients with “dedifferentiated” metastases from previously differentiated thyroid cancer had elevated serum TPA values, while serum CEA was normal and serum Tg variable. Serum CT was confirmed as the most sensitive marker of metastatic medullary thyroid carcinoma, but elevated serum TPA values were also found in most of these cases. The present data indicate that serum TPA provides a new humoral marker in the follow-up of undifferentiated and “dedifferentiated” thyroid carcinoma and may also be usefully employed as an additional marker for medullary thyroid carcinoma.

Effect of 2-deoxy-D-glucose on hypothalamic-pituitary-thyroid axis in rats

The intraperitoneal administration to rats of 500 mg/kg body weight of 2-deoxy-D-glucose, an analog of glucose which produces intracellular glucopenia with rise in extracellular fluid glucose concentration, is followed by a significant though transient reduction of hypothalamic TRH content, observed at 15 and 25 minutes after drug administration. A subsequent increase in serum thyrotropin followed by that of triiodothyronine concentration was also observed. These findings indicate that the neuroglucopenia induced by 2-deoxy-D-glucose may play a role in the regulating the hypothalamic-pituitary-thyroid axis.

Ontogeny of Pancreatic TRH Occurs Independently of Brain Development

TRH was first isolated from the hypothalamus and considered to specifically regulate thyroid-stimulating hormone (TSH) secretion. The presence, however, of TRH has been subsequently demonstrated also in other areas of the central nervous system, as well as in other tissues, including the p a n ~ r e a s . ~ ~ We have previously described the ontogenetic development of pancreatic TRH in human fetuses and in infants, showing a progressive increase in pancreatic TRH up to the 34th week of gestation, with a progressive decline thereafter.ln These results have then been confirmed by Leduque et al.” The aim of this study was to evaluate whether defective brain development can affect pancreatic TRH content. Human pancreata were obtained from three anencephalic fetuses after pregnancy interruption for medical reasons or accidental events. Six fetuses matched for gestational age and with normal brain development were evaluated as controls. TRH and insulin contents of pancreatic methanolic extracts were measured by a specific radioimmunoassay.In As illustrated in TABLE 1 , the presence of TRH and insulin could be demonstrated in the pancreata of anencephalic and control fetuses, with no differences between the two groups. In addition, both TRH and insulin contents increased with gestational age. The identity between synthetic and pancreatic TRH was assessed by gel filtration, immunoreactivity , and susceptibility to serum inactivation (data not shown). These results confirm previous reports by t h i ~ ~ ~ ! ~ and other laboratories,6%J J , 2 which showed the presence of TRH in the pancreas and its progressive increase with gestational age. The finding that no differences in pancreatic TRH content were found between anencephalic and control fetuses clearly indicate that the occurrence of TRH in the pancreas in human fetuses is independent of brain development.

Ontogeny of Human Pancreatic Thyrotropin-Releasing Hormone

It is known that thyrotropin-releasing hormone (TRH) is present in hypothalami, as well as in other cerebral areas and in other tissues including the gastrointestinal tract and, particularly, the pancreas (1–7). In rats, the islets of Langerhans are the main source of pancreatic TRH (6) and it has been shown immunohistochemically that TRH is localized especially in marginal islet cells (8,9). The role of pancreatic TRH is not well established (10), but it has been shown to enhance arginine-induced glucagon release in the adult dog (11). Ontogenetic studies in rats have demonstrated that pancreatic TRH content is higher in the neonatal period and progressively declines after the first weeks of life (5,12–14). No data are available on the ontogeny of pancreatic TRH in humans and this represents the aim of the present study.