Mass spectrometry data from a quantitative analysis of protein expression in gills of immuno-challenged blue mussels (Mytilus edulis).

Here, we provide the dataset associated with our research article on the potential effects of ocean acidification on antimicrobial peptide (AMP) activity in the gills of Mytilus edulis, "Impact of ocean acidification on antimicrobial activity in gills of the blue mussel (Mytilus edulis)" [1]. Blue mussels were stimulated with lipopolysaccharides and samples were collected at different time points post injection. Protein extracts were prepared from the gills, digested using trypsin and a full in-depth proteome investigation was performed using liquid chromatography coupled to tandem mass spectrometry (LC-MS/MS). Protein identification and quantification was performed using the MaxQuant 1.5.1.2 software, "MaxQuant enables high peptide identification rates, individualized p.p.b.-range mass accuracies and proteome-wide protein quantification" [2].

Impact of ocean acidification on antimicrobial activity in gills of the blue mussel (Mytilus edulis).

Here, we aimed to investigate potential effects of ocean acidification on antimicrobial peptide (AMP) activity in the gills of Mytilus edulis, as gills are directly facing seawater and the changing pH (predicted to be reduced from ∼8.1 to ∼7.7 by 2100). The AMP activity of gill and haemocyte extracts was compared at pH 6.0, 7.7 and 8.1, with a radial diffusion assay against Escherichia coli. The activity of the gill extracts was not affected by pH, while it was significantly reduced with increasing pH in the haemocyte extracts. Gill extracts were also tested against different species of Vibrio (V. parahaemolyticus, V. tubiashii, V. splendidus, V. alginolyticus) at pH 7.7 and 8.1. The metabolic activity of the bacteria decreased by ∼65-90%, depending on species of bacteria, but was, as in the radial diffusion assay, not affected by pH. The results indicated that AMPs from gills are efficient in a broad pH-range. However, when mussels were pre-exposed for pH 7.7 for four month the gill extracts presented significantly lower inhibit of bacterial growth. A full in-depth proteome investigation of gill extracts, using LC-Orbitrap MS/MS technique, showed that among previously described AMPs from haemocytes of Mytilus, myticin A was found up-regulated in response to lipopolysaccharide, 3 h post injection. Sporadic occurrence of other immune related peptides/proteins also pointed to a rapid response (0.5-3 h p.i.). Altogether, our results indicate that the gills of blue mussels constitute an important first line defence adapted to act at the pH of seawater. The antimicrobial activity of the gills is however modulated when mussels are under the pressure of ocean acidification, which may give future advantages for invading pathogens.

Acute effects of an oral calcium load on markers of bone metabolism during endurance cycling exercise in male athletes.

Although sport and physical activity are generally considered as positive factors for bone metabolism some endurance trainings such as running and bicycling have few or no beneficial or even deleterious effects on bone mineral density. The present study was designed to investigate the acute effect of an intensive endurance cycling exercise on biochemical bone markers. Furthermore, the effect of the oral intake of 1 g calcium load, by drinking high-calcium mineral water, just prior to and during the exercise was checked. Twelve well-trained elite male triathletes aged 23-37 years were explored. The serum concentrations of calcium, phosphate, PTH, bone alkaline phosphatase (BALP) and C-terminal cross-linking telopeptide of type 1 collagen (CTX) were measured before, during and after a 60 min 80% VO2max cycle ergometer exercise. Since cycling exercise was accompanied by a reduction in plasma volume the total amount of biochemical bone markers was calculated. When the exercise was performed without calcium load both serum concentrations and total amount of CTX began to increase progressively 30 min after the start of the exercise and were still significantly elevated, by 45-50%, 2h after the end of the exercise. Ingestion of high-calcium mineral water completely suppressed the CTX response. By contrast serum concentrations and total amount of BALP fluctuated and showed no significant difference with or without calcium load. The present study demonstrates that the burst of osteoclastic activity acutely induced by an endurance cycling exercise can be suppressed by the previous intake of a calcium load afforded by drinking high-calcium mineral water.

Wintertime vitamin D deficiency in male adolescents: effect on parathyroid function and response to vitamin D3 supplements.

The first part of this study consisted of an 18 month follow-up of the vitamin D status and parathyroid function in a group of 54 French male adolescents, aged from 13 to 16 years old and all pupils of a jockey training school. During the 18 month period four samplings were made, one every 6 months. The first was during September of the first year, the second and third during March and October of the second year, and the last in March of the third year. Therefore we had two main periods: summer and winter. The summer 25-hydroxyvitamin D (25(OH)D) concentrations were higher (71.6 +/- 19.9 and 52.4 +/- 16.5 nmol/l) than the winter ones (20.4 +/- 6.9 and 21.4 +/- 6.1 nmol/l). Conversely, the winter intact parathyroid hormone (iPTH) serum levels (4.18 +/- 1.18 and 4.11 +/- 1.35 pmol/l) were higher than the summer ones (2.44 +/- 0.82 and 2.71 +/- 0.71 pmol/l). At the two winter time points the 25(OH)D concentrations were lower than 25 nmol/l (10 ng/ml) in 72% (2nd year) and 68% (3rd year) of the adolescents. In the second part of the study we tried a vitamin D3 supplementation procedure designed to maintain the 25(OH)D and iPTH postsummer serum levels throughout the winter. Pairs of male adolescents matched for height, weight and Tanner pubertal stage were randomly assigned to either vitamin D3 supplementation (2.5 mg, i.e., 100,000 IU) administered orally at three specific periods (end of September, November and January) or no vitamin D3 treatment (control subjects). Blood was collected just before the first intake of vitamin D3 and 2 months after the last intake (March). The control subjects had blood drawn at the same time points. In the vitamin D3-treated subjects, the concentrations of 25 (OH)D (55.3 +/- 11.5 nmol/l) and of iPTH (3.09 +/- 1.16 pmol/l) in March and September (53.8 +/- 12.3 nmol/l and 2.75 +/- 1.26 pmol/l) were not significantly different. In the control subjects, March 25(OH)D levels (21.0 +/- nmol/l were low, with values below 25 nmol/l in 78% of subjects, and iPTH concentrations (3.97 +/- 1.08 pmol/l) were significantly (p<0.001) higher than in September (2.91 +/- 0.81 pmol/l). The constant vitamin D wintertime deficiency and wintertime rise in iPTH in adolescent French males throughout puberty has been demonstrated. In adolescents with low dairy calcium intakes, the vitamin D3 treatment was sufficient to maintain 25(OH)D concentrations at their summer levels throughout winter and to prevent an excessive wintertime rise in iPTH levels.

Mineral water as a source of dietary calcium: acute effects on parathyroid function and bone resorption in young men.

BACKGROUND: Calcium is a major component of mineralized tissues and is required for normal growth and maintenance of bone. Epidemiologic studies showed that a large percentage of the population fails to meet the currently recommended guidelines for optimal calcium intake. OBJECTIVE: The present study was designed to determine whether high-calcium mineral water is an efficient additional source of dietary calcium. DESIGN: Twelve healthy young men (mean +/- SD age: 21.1 +/- 1.2 y) ingested in a randomized order either 0.5 L of a mineral water containing 344 mg Ca/L or 0.5 L of a mineral water with a very low concentration of calcium (<10 mg/L) as a control. Blood samples were drawn before and 1, 2, 3, and 4 h after intake of the water. Urine was collected for 2 h before and every 2 h for 4 h after ingestion of the water. Serum concentrations of intact parathyroid hormone (iPTH) and serum concentrations and urinary excretion of a recently developed biochemical marker of bone resorption, type 1 collagen cross-linked C-telopeptide (CTx), were measured. RESULTS: Serum iPTH was significantly (P < 0.002) lower after ingestion of high-calcium water than after ingestion of the control. There was a significant (P = 0.01) progressive decrease in urinary CTx after ingestion of the high-calcium water, whereas after ingestion of low-calcium water the changes were modest and not significant. The fall in serum CTx concentrations was 34.7% 3 h after ingestion of high-calcium water, compared with 17.6% with the control. The decreases in serum CTx concentrations were significantly (P < 0.05) lower 1, 2, 3, and 4 h after ingestion of high-calcium water than after ingestion of the control. CONCLUSION: The present study showed that one oral intake of water containing a very moderate dose of calcium (172 mg) acutely inhibited iPTH secretion and bone resorption.

Acute effects of oral calcium load on parathyroid function and on bone resorption in young men.

AIM: The aim of the present study was to check whether a calcium oral load was able to inhibit bone resorption as assessed by urinary excretion of a new bone marker, type 1 collagen cross-linked C-telopeptide (CrossLaps(TM)), in healthy young male adults. METHODS: Twenty healthy young male adults (age 22 +/- 2 years) were studied. In one series of assays, an oral calcium load of 1 g of elemental calcium as calcium citrate dissolved in 200 ml of low-calcium water was ingested, while in another series of assays the subjects ingested 200 ml of water alone. Blood samples were collected before and 1, 2, 3 and 4 h after the intake of calcium. Urine was collected at 2-hour intervals, i.e. before and for 4 h after the intake of calcium. Serum ionized calcium, phosphate and intact parathormone (iPTH) were measured at each time point. Urinary calcium, phosphate, creatinine and CrossLaps (as a ratio to creatinine) were measured in each urine sample. RESULTS: Calcium intake was associated with very significant (ANOVA, p < 0.001) increases in serum ionized calcium and decreases in PTH. After calcium intake, measurements of urinary CrossLaps showed a progressive statistically significant (ANOVA, p < 0.001) decrease (-20% at 2 h and -55% at 4 h), whereas after ingestion of water, the changes were modest and not statistically significant. CONCLUSIONS: The present results show that bone resorption as assessed by urinary excretion of CrossLaps can be significantly suppressed by the ingestion of a 1-gram calcium load and attest that calcium supplementation has an acute effect on bone metabolism.

Vitamin D status during puberty in French healthy male adolescents.

The vitamin D status was determined on one to four occasions either after summer (September-October) or after winter (March-April) in 175 male adolescents (13-17 years), resulting in 394 measurements of serum 25-hydroxyvitamin D (25(OH)D) and intact parathyroid hormone (iPTH). The subjects lived in a rural area to the north of Paris (49 degrees N). After summer the 25(OH)D concentration was 58.5 +/- 18.0 nmol/l (mean +/- SD), while after winter it had fallen to 20.6 +/-6.0 nmol/l (p = 0.0001). Meanwhile the iPTH concentration was 2.76 +/- 0.97 pmol/l (mean +/- SD) after summer and increased to 4.20 +/- 1.21 pmol/l after winter (p = 0. 0001). All the results were pooled and a nonlinear population model with random parameters was used to describe the relationship between serum iPTH and 25(OH)D. When the concentration of 25(OH)D was higher than 83 nmol/l, an iPTH mean 'plateau' level at 2.48 pmol/l was reached. When 25(OH)D concentrations fell below 83 nmol/l, the increase in iPTH concentration accelerates, and when the mean 25(OH)D concentration was equal to or lower than 10 nmol/l the mean iPTH level (4.97 pmol/l) was twice as high as the 'plateau' value.

[Vitamin D status in the adolescent: seasonal variations and effects of winter supplementation with vitamin D3]. / Statut vitaminique D de l'adolescent: variations saisonnières et effets d'une supplémentation hivernale par la vitamine D3.

BACKGROUND: Recently, 25 hydroxyvitamin D (25 OHD) blood concentrations measured in adolescents during or at the end of winter were found very low. A concomitant stimulation of parathyroid function was observed. The aim of the present study was to test the biological effects of a treatment with vitamin D3 during winter. POPULATIONS AND METHODS: The effects of vitamin D3 supplementation (100,000 IU, twice, at the end of November and of January) were assessed in 24 male Caucasian adolescents (mean age +/- SD: 14 y 6 m +/- 9 m). They were pupils in a lad-jockeys training center located in the countryside near Chantilly (49 degrees northern latitude). Blood concentrations of 25 OHD, calcium and intact parathormone (PTH) were measured three times: before each oral intake of vitamin D3 and 2 months after the last intake (March). A group of 32 male adolescents (mean age +/- SD: 14 y 9 m +/- 6 m), pupils in the same center, receiving no vitamin D and sampled in November and in March, served as controls. RESULTS: In March, mean concentrations of 25 OHD (8.36 +/- 2.73 micrograms/L) were very low in vitamin D-not supplemented adolescents since 34% had levels less than 6 micrograms/L. In March, PTH concentrations (40.5 +/- 12.2 ng/L) were significantly (P = 0.0001) higher than in November (28.8 +/- 9.9 ng/L). In boys receiving vitamin D3 25 OHD serum concentrations measured in January (17.5 +/- 3.2 micrograms/L) and in March (18.7 +/- 4.0 micrograms/L) remained at a level not very different from that measured in November (16.6 +/- 3.8 micrograms/L). During the same period, calcium and PTH concentrations (32.2 +/- 11.7 ng/L in November; 32.4 +/- 14.3 in January and 32.9 +/- 13.5 ng/L in March) remained at their basal level as well. CONCLUSIONS: The observation that, after winter, a relatively large number of adolescents presented low concentrations of 25 OHD suggests that, during winter, usual dietary intakes and/or vitamin D stores are not sufficient to provide for their needs. Administration of two oral doses of 100,000 IU of vitamin D3 could maintain the vitamin D status at its initial level. The efficiency of such a prophylactic treatment is also assessed by its effect on parathyroid function.

Acute PTH response to oral calcium load and seasonal variation of vitamin D status in healthy young adult subjects.

OBJECTIVE: The aim of the present study was to check the relationship between seasonal variations of vitamin D status and parathyroid function explored both in basal conditions and after oral calcium load. DESIGN: The calcium and parathyroid hormone response to the intake of calcium load was studied at two different seasons, before winter (November) and after winter (March-April), corresponding to different vitamin D status. SUBJECTS: Eighteen healthy young male adults (age: 25 +/- 3 y) were studied. All were medical students who were selected as having no disorders known to affect calcium metabolism. INTERVENTION: At each period an oral calcium load (1 g of elemental calcium as calcium carbonate) was administered. Blood samples were collected before and 1 h, 2 h, 3 h and 4 h after the intake of calcium. Serum ionized calcium (Ca2+) and intact parathormone (PTH1-84) were measured at each time point and 25-hydroxyvitamin D (25(OH)D) was measured before each calcium test. RESULTS: After winter, basal 25(OH)D concentrations were decreased (from 16.4 +/- 6.6 to 11.5 +/- 4.4 micrograms/l) and basal PTH concentrations were increased (from 24.1 +/- 6.5 to 31.7 +/- 9.1 pg/ ml), and the difference between pre- and post-winter basal concentrations were statistically significant for both variables (P < 0.001). A statistically significant negative correlation between PTH and 25(OH)D was obtained both before (r = -0.63; P = 0.005) and after (r = -0.64; P = 0.004) winter. The maximum decrement in PTH (delta PTHmax) was not different before (13.92 +/- 4.58 pg/ml) and after (14.14 +/- 7.79 pg/ml) winter, but as a consequence of post-winter higher basal levels of PTH, at all time points after oral calcium load, concentrations of PTH after winter were significantly higher than before. CONCLUSIONS: The present results show that PTH concentrations are physiologically linked to 25(OH)D concentrations, and emphasize the need of taking into account the vitamin D status of each subject to predict the effect of an oral calcium load on absolute concentrations of PTH.

Vitamin D-dependent seasonal variation of PTH in growing male adolescents.

Twenty-eight young male adolescents (age from 13 years 6 months to 15 years 9 months) from a horseback-riding school were studied. They were studied at the end of summer (September of 1993) and, six months later, at the end of winter (March of 1994). At each timepoint their height and weight were measured and their pubertal status determined. Blood was collected and 25-hydroxyvitamin D [25(OH)D], intact parathyroid hormone (PTH1-84), and 1,25-dihydroxy-vitamin D [1,25(OH)2D] were measured. After winter, weight and height had increased by a mean of 2.9 +/- 1.3 kg and of 3.3 +/- 1.2 cm, respectively. 25(OH)D concentrations which were 29.96 +/- 7.46 micrograms/L in September had significantly (p = 0.0001) fallen by a mean of 23.31 +/- 6.6 micrograms/L in March (6.61 +/- 2.04 micrograms/L). March and September concentrations of 25(OH)D were significantly correlated (r = 0.536, p = 0.0039). March values were negatively correlated with the pubertal status (r = 0.41; p = 0.03). In the meantime, PTH had significantly (p = 0.0001) increased by a mean of 8.59 +/- 8.53 ng/L (22.8 +/- 7.44 ng/L in September vs. 30.33 +/- 8.05 ng/L in March). A statistically significant correlation between PTH and 25(OH)D concentrations (r = 0.493; p = 0.0001) was obtained. Serum 1,25(OH)2D concentrations measured in September (37.7 +/- 12.94 ng/L) and in March (38.2 +/- 7.8 ng/L) were not different. March values were positively correlated with pubertal status (r = 0.49; p = 0.008). Modulation of PTH secretion by vitamin D appears to be a physiological mechanism occurring during adolescence. In spite of a marked depletion of vitamin D stores after winter, PTH values remained within normal range. Nevertheless, we cannot exclude that a more prolonged vitamin D deficiency could adversely affect bone metabolism during this critical period of life characterized by an increased need of vitamin D.

Age-related effect of a single oral dose of calcium on parathyroid function: relationship with vitamin D status.

The parathyroid response to the administration of a single oral dose of 0.5 g Cal was studied in 71 normal subjects of both sexes (34 males, 37 females) aged 20-88 y. Serum 25-hydroxyvitamin D [25(OH)D] and 1,25-dihydroxyvitamin D [1,25(OH)2D] were measured before the intake of calcium. Serum ionized calcium (Ca++) and intact parathormone (PTH1-84) were measured before and 1, 2, and 3 h after the intake of calcium. The Ca++ maximal response (delta Ca++max), which significantly decreased with age (P = 0.0001), was correlated with both 25(OH)D (r = 0.375, P < 0.01) and 1,25(OH)2D (r = 0.284, P < 0.02). The maximal PTH1-84 suppressive response expressed as a function of basal values (delta PTH%) decreased with age. Basal PTH1-84 values were significantly increased with age (P = 0.0002) and were negatively correlated with 25(OH)D concentrations (r = 0.414, P < 0.002) which were low in elderly people. These results suggest that correction of vitamin D deficiency should improve delta Ca++max, lower basal PTH1-84, and consequently make the oral intake of calcium more efficient to decrease PTH1-84 concentrations.

Comparison of the suppressive effect of two doses (500 mg vs 1500 mg) of oral calcium on parathyroid hormone secretion and on urinary cyclic AMP.

The respective effects of the ingestion of two different doses of calcium (500 and 1500 mg) on serum ionized calcium, intact parathyroid hormone (PTH 1-84), and the urinary excretion of 3',5'-cyclic adenosine monophosphate (cyclic AMP) were evaluated in 15 young male adults. Ionized serum calcium and PTH 1-84 were measured before and 1 hour, 2 hours and 3 hours (P1, P2, and P3) after the oral intake of calcium. Cyclic AMP was measured in 2-hour urine samples collected before and during 4 hours after the ingestion of calcium. Similar increments in serum ionized calcium (delta Ca2+) were observed except at P3 where the delta Ca2+ was significantly (P < 0.02) higher after 1500 mg (0.088 mmol/liter) than after 500 mg of (0.062 mmol/liter). In the same way, the comparison of the PTH 1-84 concentrations showed no statistical difference except at P3 (P < 0.002). When expressed as a percentage of P0, the P1 and P2 PTH 1-84 values were more suppressed after 1500 mg than after 500 mg of calcium (P1: -69% vs -59%; P < 0.02; P2: -66% vs -50%; P < 0.02). However, the simultaneous cyclic AMP responses (-24% vs -19%) were not significantly different. The results show that the respective maximal effects on PTH secretion and on urinary cyclic AMP of two very different oral doses of calcium are only slightly different.

Modification by phosphate of PTH-dependent renal cyclic AMP response.

The PTH response and the renal cAMP response obtained after oral administration of either tricalcium phosphate or calcium gluconolactate were compared in 12 young adult males. Each subject was studied during a control period of two hours before and during an experimental period of four hours after ingestion of a single oral dose of calcium salt. The respective dosages (1.2 g of calcium plus 0.6 g phosphorus for tricalcium phosphate; 0.5 g of calcium for gluconolactate calcium) were chosen to provide similar significant (p = 0.0001) increases in serum ionized calcium (from 1.23 to 1.29 mmol/l vs from 1.23 to 1.28 mmol/l). After tricalcium phosphate a modest (10%) but significant (p < 0.001) rise in serum phosphate was observed. In both series of experiments similar inhibitory effects on PTH circulating levels were obtained (from 22.6 to 12.4 pg/ml after tricalcium phosphate and from 24.1 to 10.6 pg/ml after calcium gluconolactate). After ingestion of calcium gluconolactate the renal secretion of cAMP fell from 12.68 to 8.64 nmol/l GF (p < 0.001), whereas no significant alterations of the mean values of nephrogenous cAMP were detected after ingestion of tricalcium phosphate. In accordance with the role of cAMP as a second messenger, after calcium gluconolactate we obtained a significant increase in tubular maximal reabsorption of phosphate (p < 0.0001) contrasting with the absence of significant effect after tricalcium phosphate. The present results confirm that suppression of PTH secretion only depends on the rise of serum ionized calcium and suggest that additional phosphate administration could have a decoupling effect between PTH and renal cAMP secretion.

[Effects of phosphate therapy on parathyroid gland reactivity]. / Effets d'un traitement par le phosphate sur la réactivité parathyroïdienne.

The effects of a single oral dose of phosphate (780 mg of elemental phosphorus as 100 drops of Phosphoneurol 120 from DOMS-Adrian Laboratories) on parathyroid function and on calcium and phosphate metabolism were studied in 10 young adults. The parathyroid response was checked by measurement of PTH 1-84 and of nephrogenous cAMP before and after a 10 days therapy by phosphate (780 mg of elemental phosphorus twice daily). Before treatment a 16 per cent increase in PTH 1-84 (p less than 0.05) and a 34 per cent increase in nephrogenous cAMP (p less than 0.02) was obtained. After treatment the increases were respectively 34 per cent for PTH 1-84 (p less than 0.001) and 67 per cent for nephrogenous cAMP (p less than 0.001). The responses in PTH 1-84 and in nephrogenous cAMP were significantly (p less than 0.05 and p less than 0.01) higher after than before treatment by phosphate.

[Exploration of the parathyroid gland function by intake or oral calcium and phosphate (only oral intake and sequential treatment with calcium-phosphate)]. / Exploration de la fonction parathyroïdienne par prise orale de calcium et de phosphate (prise orale unique et traitement séquentiel calcium-phosphate).

The parathyroid hormone response to the oral intake of either calcium or phosphate was explored in 10 young adults (23-28 years). First, the subjects were investigated during free running diet. They ingested a single oral dose of 500 mg of calcium (as a bag of Sandocal) and 10 days later a single oral dose of phosphate (750 mg of phosphorus as a tablet of Phosphore Sandoz Forte). Samples of blood and urine were collected before and during the 4 hours following the ingestion of either calcium or phosphate. After intake of calcium an acute response was obtained with a 58% decrease in PTH 1-84 at 1 hr (p less than 0.001) and a 33% decrease in nephrogenous cAMP (p less than 0.001). After ingestion of phosphate the response was delayed and less constant with a 25% increase in PTH 1-84 at 3 hr (p less than 0.01) and a 27% increase in nephrogenous cAMP (p less than 0.001). Then, the effects of a calcium therapy (3 daily doses of 500 mg each for 20 days) and of a subsequent phosphate therapy (2 daily doses of 750 mg each for 10 days) on the parathyroid hormone response to the administration of a single dose of phosphate were studied. On days 10, 21 and 31 baseline blood and urine samples were obtained prior to calcium and phosphate administration for measuring PTH 1-84 and nephrogenous cAMP. No significant variation was found. On days 21 (after calcium therapy) and 31 (after phosphate therapy) an oral load of phosphate was administered according to the procedure described above.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects on calcium and phosphate metabolism and on parathyroid function of acute administration of tricalcium phosphate.

The effects of the ingestion of tricalcium phosphate on calcium and phosphate metabolism and on parathyroid function were evaluated in 10 young adults. Each subject was studied during a control period of two hours before and during an experimental period of four hours after ingestion of a single oral dose of tricalcium phosphate containing 1500 mg of calcium and 770 mg of phosphorus. Serum and urinary calcium and phosphate and the nephrogenous cAMP fraction were measured. Significant rises in serum (from 2.32 +/- 0.05 to 2.44 +/- 0.08 mmol/l) and urinary (from 1.08 +/- 0.65 to 3.43 +/- 1.38 mumols/l GF) calcium and in serum phosphate (from 1.05 +/- 0.18 to 1.28 +/- 0.14 mmol/l) occurred. Unexpectedly, the acute supply of calcium in the form of tricalcium phosphate did not provoke significant alteration of nephrogenous cAMP level. In order to assess the respective effects of calcium and of phosphate, similar tests with ingestion of similar amounts either of calcium (as a glucoheptogluconate salt) or of phosphate were subsequently performed in the same subjects. Significant increases in serum total calcium were observed after calcium glucoheptogluconate as after tricalcium phosphate. However, the effects on parathyroid function differed, since a significant (p less than 0.001) decrease in nephrogenous cAMP followed the ingestion of calcium glucoheptogluconate. Otherwise, a stimulating effect of phosphate on parathyroid function was observed. These findings suggest that the respective effects of calcium and of phosphate are counterbalanced when administered as tricalcium phosphate, resulting in the absence of parathyroid suppression.

Effect of vitamin D3 administration on serum 25-hydroxyvitamin D3, 1,25-dihydroxyvitamin D3 and osteocalcin in vitamin D-deficient elderly people.

In elderly institutionalized people, confined to bedroom and receiving no vitamin D supplementation, the frequency of vitamin D deficiency is found very high. Systematic administration of vitamin D has, therefore, been proposed to correct vitamin D deficiency. Within this context, we studied 40 elderly institutionalized subjects (mean age 80.5 + 7.2 yr) with low 25(OH)D3 concentrations (4.4 + 1.8 micrograms/l). Sixteen of them (Group I) had low serum calcium concentrations (less than 2.3 mmol/l) and 24 (Group II) had normal serum calcium concentrations (from 2.3 to 2.6 mmol/l). As hypocalcemia has been shown to regulate 1,25(OH)D3 production independent of PTH in animals and in humans, we compared their respective responses to the administration of vitamin D3. Subjects received a total dose of 15 mg (600,000 IU) of vitamin D3 divided into 3 i.m. injections at one month intervals and were explored before therapy and one and 6 months after the last dose of vitamin D3. The treatment induced a similar marked rise in 25(OH)D3 levels (from 4.1 + 1.7 to 24.4 + 8.7 micrograms/l for group I and from 5.1 + 1.8 to 27.2 + 8.0 micrograms/l for group II) in both groups but increased the 1,25(OH)2D3 concentrations only in group I (from 22.9 + 6.9 to 32.6 + 11.3 ng/l). Meanwhile serum calcium concentrations rose in group I (to low normal range i.e. 2.31 + 0.07 mmol/l) and were unaffected in group II. These results suggest that hypocalcemia is a potent stimulator of renal 1-hydroxylase in elderly people. Furthermore, a transient significant (P less than 0.01) increase in serum osteocalcin (from 10.6 + 4.1 to 14.1 + 5.9 micrograms/l) could be observed in group I which demonstrates for the first time that the osteocalcin response of osteoblasts to stimulation by 1,25(OH)2D3 is retained in very old people.