Insulin-, glucagon- and calcitonin-induced early decrease in serum calcium.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to K Steczek.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Analysis of calcium tolerance in suggested to represent a valuable diagnostic aid in osteoporosis, particulary in the menopause. The serum calcium level was found to exceed 11.0 mg/dl 60 min after the intravenous injection of 3.6 mg per kg body weight of Ca++ in all patients with osteoporosis, while the level was normal at that point of time in every subject without osteoporosis, including patients with bone disease other than osteoporosis. Administration of norandrosterone decanoate or dehydroepinandrosterone to patients with menopausal osteoporosis resulted in normalization of the post-load hypercalcaemia. Calcium tolerance of menopausal patients without osteoporosis was not affected by dehydroepiandrosterone.
The effect of calcium on glibenclamide-induced insulin release was studied in 14 diabetic patients. Two mg glibenclamide was given intravenously and calcium, blood glucose and IRI were determined in venous blood samples at predetermined intervals. The test was repeated 3-4 days later with the patients simultaneously receiving a calcium infusion into a contralateral vein. The decrease in blood glucose and the rise in IRI level were both significantly greater in the combined glibenclamide-calcium test. It is concluded that calcium may temporarily improve carbohydrate tolerance in diabetic patients by potentiating the glibenclamide-stimulated insulin secretion.
Explore the source record for details and available documents.
Rats deprived of adrenal and gonadel sex hormones are more sensitive than normal rats to the hypercalcaemic (osteolytic) effect of parathormone and toxic doses of vitamin D3. It is suggested that sex hormone deficiency and the consecutive decrease of calcitonin sensitivity in postmenopausal osteoporosis makes the patients unprotected against factors inducing increased bone resorption, and this leads over the years of osteoporosis.