Biomedical subjects

M Prelot

Publications and source records attributed to M Prelot.

10 recordsLinked to original sources

PubMed1991

[In vitro effects of 24R,25-dihydroxyvitamin D3 on alkaline phosphatase and gamma-glutamyltransferase in the kidney of hypophysectomized rats].

The effects of 24R,25-dihydroxyvitamin D3 (24,25-(OH)2D3 on alkaline phosphatase (PAL), gamma-glutamyltransferase (GGT) and acid phosphatase (PAC) activities were investigated on renal cortex slices of hypophysectomized rats. Indeed after hypophysectomy renal 24,25-(OH)2D3 production was increased and renal PAL and GGT activities were decreased. After 5h incubation with physiological concentrations (0.1-10 nM) of 24,25-(OH)2D3 significant increases of PAL and GGT activities were produced. The maximum stimulation obtained with 1 nM was +23% for PAL and +26% for GGT as compared to controls. PAC was not modified. The time course of these effects was studied from 45 min to 8 h. In the presence of 24,25-(OH)2D3 (1 nM), delayed (3h) stimulation of PAL and GGT appeared. It reached the maximal value after 6h, +37% for PAL and +30% for GGT and persisted again at 8h. Cycloheximide added to incubation medium with steroid inhibited the stimulating effect on PAL only. Actinomycin D suppressed the induction of both enzymes, indicating that the observed actions of 24,25-(OH)2D3 depend on protein synthesis whose responsible mechanisms were different. These protein synthesis inhibitors did not modified enzymatic activities. Physiological significance of these renal effects is to be clarified.

24,25-Dihydroxyvitamin D 3↗

PubMed1990

[In vitro effects of 1,25-dihydroxycholecalciferol on alkaline phosphatase and gamma-glutamyltransferase activity in hypophysectomized rats].

Effects in vitro of 1,25-dihydroxycholecalciferol (1,25-(OH)2D3) on alkaline phosphatase (PAL), gamma-glutamyltransferase (gamma-GT) and acid phosphatase (PAC) activities were investigated on renal cortex from hypophysectomized rats. In these animals the biosynthesis of 1,25-(OH)2D3 and the specific activities of kidney PAL and gamma-GT were decreased. The course of these effects was determined from 45 min to 8 h. In the presence of 1,25-(OH)2D3 (2 x 10(-6) M) a delayed (5h) but simultaneous stimulation of the three enzymes was observed. It reached a maximum at 6h and disappeared at 8h. The dose-response relation was studied at 6h. In the presence of 1,25-(OH)2D3 (5 x 10(-7) M), the three enzymes were activated. The effect was maximal at 10(-6) M; it was +22% for PAL, +17% and +15% respectively for gamma-GT and PAC compared with controls. Cycloheximide suppressed the induction of PAL but not of gamma-GT activity. The effects of the secosteroid on renal enzymes seems to be a pharmacological more than a physiological one.

Acid Phosphatase↗

PubMed1989

[In vitro stimulation of alkaline phosphatase and gamma- glutamyltransferase in the kidney of hypophysectomized rat by the mixture of 1,25 and 24,25 dihydroxycholecalciferols].

The present study was undertaken to investigate the in vitro effects of two cholecalciferol metabolites 1,25(OH)2CC and 24,25(OH)2CC on the renal cortex alkaline phosphatase (ALP), gamma-glutamyltransferase (GGT) and acid phosphatase (ACP) activities in hypophysectomized rats. We found that both 1,25-CC and 24,25-CC stimulated ALP and GGT. An additive effect was obtained on ALP and GGT after incubation with one with the other metabolites. When 1,25-CC was used alone, it increased ACP; in presence of 24,25-CC, this stimulating effect disappeared. In the rat, together 1,25-CC and 24,25-CC correct in vitro ALP and GGT activities decreased by hypophysectomy. Physiological signification of these effects remains again unknown.

24,25-Dihydroxyvitamin D 3↗

PubMed1985

Thyroidectomy abolishes pulsatile growth hormone secretion without affecting hypothalamic somatostatin.

The effects of thyroid hormone deprivation and of subsequent replacement therapy on growth hormone (GH) secretion were investigated in unrestrained unanesthetized rats. Male rats were thyroparathyroidectomized (TPTX) 5 weeks prior to plasma sampling for GH assay, or to decapitation for evaluation of hypothalamic somatostatin (SRIF) content and in vitro SRIF and GH release. Thyroid hormone deprivation suppressed pulsatile GH secretion as well as GH release induced by clonidine (150 micrograms/kg). Treatment of TPTX rats with small doses of triiodothyronine (T3) restored an episodic pattern of GH secretion, but with lower peak values than controls, as well as the GH response to clonidine. Thyroid deprivation induced a 92-fold decrease in GH release from the pituitary; however, the ratio between GH release and GH content was similar in TPTX and normal rats, and human pancreatic growth hormone-releasing factor (GRF) (3 X 10(-8) M) was still able to stimulate residual GH release by hemipituitaries from TPTX rats in a manner similar to that in euthyroid controls (295 and 254% stimulation, respectively). Thyroid deprivation or T3 replacement did not modify SRIF content in the hypothalamus or other brain structures tested. The capacity of K+ depolarization to release SRIF in vitro from the hypothalamus was not modified by TPTX. These findings indicate that thyroid hormones are necessary to maintain both pulsatile and induced GH secretion in unanesthetized rats. In addition they suggest that impairment of GH secretion in thyroidectomized rats does not depend upon changes in the hypothalamic SRIF regulation of the hormone but could be dependent on a defect in GRF release and/or, most probably, GH synthesis directly at the pituitary level.

Animals↗

PubMed1972