[Simultaneous evaluation of the effects that change values of the thyreoliberin test in psychiatric patients].
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Biomedical subjects
Publications and source records attributed to C Höschl.
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The authors have studied the effect of calcitonin on glucose metabolism. Ten healthy volunteers were investigated. Calcitonin administered intramuscularly in one single dose inhibited the physiological decrease of blood glucose levels during the forenoon fast. Salmon calcitonin administered in an intravenous infusion in the dose of 0.15 U MRC/kg of body weight impaired the glucose tolerance test with the increase of blood glucose levels. The greatest difference was in the 120th minute after the administration of 100 gm of glucose. Calcitonin failed to produce any significant inhibition of immunoreactive insulin release following the glucose stimulus. However, further studies will be necessary to show whether this lack of the inhibitory beta cytotropic action of calcitonin was due to the low dose of calcitonin.
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Alterations in calcium homeostasis might be implicated in the neuropathology of Alzheimer's disease (AD). To date it is not clear whether changes in cytosolic calcium level ([Ca2+ ]i) are the result or the cause of pathogenic effects. In platelets of patients with early stages of AD, the basal values of [Ca2+]i in the absence of extracellular Ca2+ were significantly lower in comparison with age-matched and young controls. After the addition of 1 mM calcium into the incubation medium the [Ca2+]i markedly increased in platelets of AD patients whereas the increase only to a smaller extent was observed in control age-matched and young subjects. The present study proposes that calcium dysregulation during the whole disease period could not be uniform and according to our results the [Ca2+]i is reduced in the first stages of AD. We suggest that the disturbed calcium homeostasis in AD is an "early defect."