This study demonstrates that unopposed oestrogen replacement therapy during 2 months in postmenopausal women slightly, but significantly, increases total serum leptin levels. This observation suggests a role for oestrogens in the regulation of leptin.
Calcium uptake from the gut is increased by GH effects on vitamin D metabolism or action. Bone metabolism is stimulated by many factors, of which GH and insulin-like growth factor I (IGF-I) are only two examples. From various animal and human data, it can be shown that GH and IGF-I seem to influence bone formation more than bone resorption. However, GH excess, as seen in acromegaly, does not result in increased bone mass. GH was used to treat osteoporosis in a few clinical trials. In only one, in combination with calcitonin, an increase in bone mass was observed. In GH-defïcient adult patients, substitution therapy resulted in a temporary increase in serum calcium levels. Effects on bone mineral mass were only found in a pilot study performed by us in a group of 8 GH-deficient adult patients. The mean increase of bone mineral mass was 0.04 g hydroxypatite/cm2, p < 0.05. These data indicate that GH substitution can result in increased bone mass.
Circulating concentrations of 1,25-dihydroxyvitamin D, 24,25-dihydroxyvitamin D and 25-hydroxyvitamin D were measured in 21 anephric subjects. 13 subjects had no therapy with vitamin D, dihydrotachysterol or lα-hydroxyvitamin D3. In 7 subjects of this group 1,25-dihydroxyvitamin D was undetectable ( < 5 pmol/l). In the other 6 patients concentrations ranged from 10 to 43 pmol/l (reference value 111 ± 33 pmol/l). All subjects taking high doses of vitamin D showed detectable 1,25-dihydroxyvitamin D concentrations in the same range. Dihydrotachysterol therapy caused spuriously high ‘1,25-dihydroxyvitamin D’ values, probably by interference of a metabolite of dihydrotachysterol in our assay. In subjects on vitamin D or dihydrotachysterol therapy 25-hydroxyvitamin D concentrations were significantly elevated (314 ± 146 nmol/l and 98 ± 19 nmol/l, respectively; reference value 52 ± 22 nmol/l). Concentrations of 24,25-dihydroxyvitamin D were only measured in subjects without vitamin D2 intake. In general very low but detectable concentrations were found. One subject on a high dose of vitamin D3 showed a 24,25-dihydroxyvitamin D3 concentration of 10.2 nmol/l (reference value 4.4 ± 2.9 nmol/l). Our results therefore confirm earlier reports on extrarenal synthesis of 24,25-dihydroxyvitamin D and suggest that there may be extrarenal production of 1,25-dihydroxyvitamin D as well.
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