The response of ACTH, beta-endorphin and cortisol to calcitonin administration was investigated in 8 subjects with recent fractures of the vertebrae due to postmenopausal or senile osteoporosis (Ost) and in seven normal healthy controls (NC). A significant increase of the three hormones was observed in 13 subjects. The maximum increase was observed between 15 and 60 min.: the cortisol level (microgram/100 ml) rose from 14.3 +/- 1.9 to 24.8 +/- 3.2 (P less than 0.05) in Ost and from 7.7 +/- 0.6 to 21.7 +/- 1.7 (P less than 0.001) in NC, the beta-endorphin (pmol/l) from 5.8 +/- 0.6 and to 21.2 +/- 1.3 in OST (P less than 0.001) and from 5.9 +/- 0.4 to 21.9 +/- 4.5 (P less than 0.01) in NC and the ACTH levels (pg/ml) from 21.3 +/- 5.7 to 61.7 +/- 3.6 (P less than 0.001) in OST and from 30.0 +/- 6.2 to 58.8 +/- 7.5 (P less than 0.05) in NC. The results indicate a possible role of calcitonin in modulating the anterior pituitary function. It also suggests that the analgesic effect of calcitonin might be mediated by the increase of beta-endorphin. The possibility that this analgesic effect of calcitonin is due to its direct binding to the opiate receptors was excluded in the present study by in vitro binding assay.
Carotenemia with its yellowish-red tint is found in diabetes. The frequency of this phenomenon is unknown and the relationship between skin colour and blood carotenoid level is controversial. Frequently the suspicion of diabetes arising from inspection of the skin colour is in fact confirmed by the usual laboratory tests. We decided to examine skin colour, blood carotenoids, cholesterol and total blood lipid levels in 51 overt diabetics, 42 latent diabetics and 25 healthy subjects as well as 14 patients who had recently suffered an acute myocardial infarction. The healthy subjects showed blood carotenoid levels slightly higher than the patients. As is known, in cases of increased intake of carotenoid-rich fruit and vegetables the yellowish-red skin colour is marked. Diabetic patients however show this phenomenon even though they may not follow such a diet. This finding, although diagnostically useful, does not usually parallel a high carotenoid blood level. From this point of view overt and latent diabetes are similar.
In a previous study we observed that calcitonin increases beta-endorphin, ACTH, and cortisol secretion. We assumed that calcitonin might have a modulatory role on the pituitary function. The present study was initiated to clarify whether this effect is due to a direct pituitary stimulation or to an indirect stimulation through CRF (corticotropin releasing factor). Fourteen healthy subjects, aged 30-60 years were investigated. All the subjects received 100 IU Salmon calcitonin Sandoz i.v. at 8 a.m. (time 0). Plasma beta-endorphin, ACTH and cortisol were estimated every 30 min from -30 to 120 min by specific radioimmunoassay. The same parameters were estimated a second time, at the same intervals, when cyproheptadine 8 mg (7 subjects) and 40 mg propranolol (7 subjects) were given per os at -30 min and calcitonin i.v. at time 0. beta-endorphin, ACTH and cortisol levels (Mean +/- SEM) rose significantly after calcitonin (peak value at 30-90 min) from 5.2 +/- 0.7 to 15.1 +/- 2.6 pmol/l; from 43.0 +/- 2.7 to 70.7 +/- 4.1 pg/ml and from 10.6 +/- 1.5 to 19.6 +/- 2.1 micrograms/100 ml respectively (p less than 0.0001 by analysis of variance and covariance and repeated measures). Propranolol 40 mg (per os) administered at time -30 did not alter the response of beta-endorphin, ACTH and cortisol to calcitonin (infused at time 0). Cyproheptadine, the antiserotonergic substance that inhibits the synthesis and release of CRF completely inhibited the stimulatory effect of calcitonin. We conclude that probably calcitonin has a modulatory role on the hypothalamo-pituitary adrenal axis and that it acts at the hypothalamic level probably by stimulating CRF secretion.
The effect of short-term treatment with diphenylhydantoin (DPH) on the insulin secretion patterns during OGTT and on the daily insulin profile was studied in obese patients. DPH treatment for 3 days with a dose of 300 mg/die (100 mg, 3 times daily) significantly decreased the insulin release after glucose ingestion, but did not alter the basal insulin level. No effect on the fasting glucose concentration as well as on the glucose profiles during OGTT was observed after short-term DPH treatment. A smaller decrease of plasma free fatty acid concentration during OGTT performed after DPH administration confirmed the inhibitory effect of the drug on insulin release. Short-term DPH treatment was also shown to decrease markedly the postpradial insulin release in obese patients. No difference was noted between plasma 11-OHCS and serum HGH concentrations during OGTT before and after DPH treatment. The possible therapeutic role of DPH in obesity is discussed.
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