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R. Ziegler and G. Delling

ABSTRACT

In 20 intact and 20 parathyroidectomized female Sprague-Dawley rats, holes with a diameter of 1.8 mm were bored into the proximal third of the tibia. Half the animals served as controls and received the vehicle, the remainder received daily subcutaneous injections of 100 MRCmU calcitonin in 5 % gelatin. Tetracycline labelling was performed weekly. 5 animals from each group were sacrificed after 3 weeks, the other 5 after 6 weeks. Nondecalcified ground sections through the center of the holes were evaluated with an integration ocular; the surface of the newly formed bone was compared with the original size of the defect. The course of the regeneration for the control animals was in agreement with previous data in the literature. Calcitonin treatment produced a distinct acceleration of the healing process. Presumably, the hormone does not only act via inhibition of bone resorption, but also by stimulating the activity of osteoblasts and by increasing the mineralization of the osteoid seams.

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R. Ziegler and G. Delling

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J Pfeilschifter and R Ziegler

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K. FRANK, P. VECSEI and R. ZIEGLER

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K. FRANK, S. KORTH-SCHÜTZ and R. ZIEGLER

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H. Minne, S. Bellwinkel and R. Ziegler

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R. M. Altorfer, W. H. Ziegler and E. R. Froesch

Abstract.

Insulin tolerance tests were carried out in normal subjects and in adrenalectomized (ADX) patients in order to better understand the importance of counter regulatory hormones for the recovery from hypoglycaemia.

Compared to normal subjects recovery of plasma glucose and of free fatty acid levels in adrenalectomized patients is retarded. The levels of glucagon are significantly higher in ADX patients during rest than in normal subjects. As expected, epinephrine and norepinephrine levels did not increase in ADX patients and, accordingly, blood pressure did not change. Growth hormone levels were the same in both groups of subjects. Interestingly, there was no clear-cut difference with regard to subjective symptoms of hypoglycaemia.

It would appear that epinephrine is important for the rapid initial recovery from hypoglycaemia, whereas other hormones play a more important role later on.

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T Seck, I Diel, H Bismar, R Ziegler and J Pfeilschifter

OBJECTIVE: Osteoprotegerin (OPG) and its ligand 'receptor activator of NF-kB ligand' (RANKL) are important regulators of bone metabolism. RANKL, expressed in osteoblasts, activates osteoclast differentiation and osteoclast function by binding the 'receptor activator of NF-kB' (RANK), expressed in ostoclast precursors and mature osteoclasts. The effect is prevented by OPG, a soluble receptor of RANKL. In vitro studies have suggested that estrogen stimulates OPG, whereas parathyroid hormone (PTH) inhibits OPG expression and stimulates the expression of RANKL. DESIGN: In the present study, we examined the relationship between the menopause, serum PTH and the expression of OPG and RANKL in human bone tissue in vivo. METHODS: To address this question, we established a 5'-nuclease assay to quantify the mRNA copies of human OPG and RANKL, normalized to the number of copies of beta-actin mRNA in 169 women (mean age: 52.4+/-11.6 years), who underwent surgery for early breast cancer. Intact serum PTH was measured by chemoluminescence in 61 women. RESULTS: We found no significant difference in the expression of OPG and RANKL between postmenopausal women and premenopausal women. Also, the ratio of RANKL to OPG was unchanged in relation to the menopausal status. Serum PTH was negatively associated with the expression of OPG (r=-0.33, P=0.01), but also, surprisingly, with the expression of RANKL (r=-0.28, P=0.03). CONCLUSION: We failed to observe the expected changes in the expression of OPG and RANKL in human bone samples at menopause. High in vivo levels of circulating PTH are accompanied by low levels of expression of the two transcripts in human bone tissue.