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Biomedical subjects

M Donnadieu

Publications and source records attributed to M Donnadieu.

At least 37 records · Page 2Linked to original sources
PubMed1986

Relationship of plasma growth hormone-releasing hormone levels to pubertal changes.

Basal plasma GH-releasing hormone (GHRH) concentrations were measured by RIA in 180 normal subjects (93 boys and 87 girls between the ages of 8 and 18 yr). Every subject was in good health and between -2 and +2 SD for height. Fourteen boys with delayed puberty also were studied. Plasma GHRH concentrations were higher during puberty than before it. At midpuberty, the mean GHRH levels in girls was 159.1 +/- 28.5 (+/- SEM) pg/ml, approximately 5-fold higher than the level in prepubertal girls (30.3 +/- 4.3 pg/ml). The mean plasma GHRH in midpubertal boys (101.4 +/- 11.5 pg/ml) was approximately 2-fold higher than the level in prepubertal boys (48.1 +/- 5.2 pg/ml). The GHRH levels in boys with delayed puberty more closely resembled those in boys at a similar pubertal stage than those in boys of similar chronological age. The dramatic rise in plasma GHRH levels during puberty suggests a role for this peptide in the adolescent growth spurt. Moreover, these data indicate that GHRH levels during adolescence may be a marker of the patient's pubertal development.

Adolescent↗
PubMed1986

Negative correlation between peripheral plasma somatostatin levels and GH responses to GH-RH stimulation tests in children.

On forty-six fasting and resting children, aged 5-17 years, with short stature (below -2 SD) a growth hormone releasing hormone (GH-RH) stimulation test (2 micrograms/kg iv bolus, Sanofi) was performed. Twenty-two children were prepubertal, of which, 13 had a constitutional short stature (CSS), nine an idiopathic growth hormone deficiency (IGHD). Twenty-four subjects were pubertal, at the stage II or III of Tanner. Among them, six had a constitutional short stature (CSS) and 18 an idiopathic delayed puberty (IDP). Blood samples were taken for determination of plasma somatostatin-like immunoreactivity (SLI) in chilled test tubes containing EDTA + aprotinin. Plasma SLI levels were measured after extraction and concentration on C18 Sep Pack columns by radioimmunoassay using an antibody against 1-14 somatostatin. The sensitivity of this assay is around 3 pg/ml. After GH-RH stimulation the peak of GH (mean +/- SEM) was in prepubertal subjects: 25.3 +/- 9.1 micrograms/l in CSS, and 18.6 +/- 10.3 micrograms/l in IGHD. In pubertal subjects GH peaks were 17.6 +/- 8.4 micrograms/l in CSS and 15.6 +/- 3.8 micrograms/l in children with IDP. No significant differences was found between basal plasma SLI levels in the four groups of subjects, being respectively (mean +/- SEM) 11.9 +/- 1.8 pg/ml in prepubertal subjects with CSS, 9.6 +/- 2.6 pg/ml in IGHD, 7.6 +/- 1.7 pg/ml in pubertal children with CSS and 6.6 +/- 1.5 pg/ml in children with IDP.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1985

Variations of plasma growth hormone (GH)-releasing factor levels during GH stimulation tests in children.

GH-releasing factor (GHRH) was measured by RIA in the plasma of 22 constitutionally short children given an ornithine infusion or an oral dose of L-dopa. After an overnight fast and 1 h of rest, plasma GHRH levels were 49.7 +/- 7.3 pg/ml (+/- SEM). In 5 children, L-dopa induced an increase in mean GH levels from 1.8 to 12 ng/ml at 60 min. Mean plasma GHRH levels increased from 47 pg/ml to a peak of 96 pg/ml at 15 min (P less than 0.02). In 4 other children, no increase in either GH or GHRH occurred after L-dopa treatment. In these 9 children, a significant correlation was found between the peak GH and GHRH concentrations (r = 0.841; P less than 0.001). On the contrary, ornithine-induced GH release was not preceded by a GHRH rise, but was followed by a GHRH decrease, from 51 to 27 pg/ml (P less than 0.02). We conclude that the 2 tests stimulate GH release in different ways, and that GH levels may be involved in the feedback control of GHRH secretion.

Adolescent↗
PubMed1984

Production of immunoreactive calcitonin and parathyroid hormone by embryonal carcinoma cells: alteration with retinoic acid-induced differentiation.

To determine possible ectopic production of, and altered responsiveness to, specific hormones and growth factors which may be involved in mediating embryonic differentiation and development embryonal carcinoma cells in culture have been employed to serve as an in vitro system of embryogenesis. Exposure of F9 embryonal carcinoma cells to all-trans-retinoic acid previously has been shown to induce differentiation of these undifferentiated stem cells to parietal endoderm and to markedly alter the ability of calcitonin and parathyroid hormone to stimulate adenylate cyclase activity. Evidence is presented that F9 cells secrete immunoreactive calcitonin into the culture medium (200 pg/12 hr/10(7) cells) while parietal yolk sac (PYS) cells secrete immunoreactive parathyroid hormone (800 pg/12 hr/10(7) cells). Retinoic-induced differentiation of F9 cells to endoderm results in a progressive reduction in immunoreactive calcitonin production, while there is an increase in the level of immunoreactive parathyroid hormone found in the conditioned medium. After exposure of F9 cells to retinoic acid for 5 days, little calcitonin is detectable in 12-hr conditioned medium. Changes in the intracellular levels of immunoreactive calcitonin and PTH follow a pattern similar to that noted for changes in the amount of secreted hormones. Thus, immunoreactive calcitonin is produced by undifferentiated F9 cells which possess a calcitonin responsive adenylate cyclase system, while parathyroid hormone is produced by parietal endoderm cells which respond to parathyroid hormone with increased cyclic AMP synthesis. Sephadex G50 gel filtration of F9-conditioned medium shows two peaks of immunoreactive calcitonin with Mr of 3500 and 20,000. Immunoprecipitation of calcitonin from 35S-labeled F9 cells reveals a specific band of 20,000 Mr. Likewise, two peaks of parathyroid hormone immunoreactive material of Mr 8000 and 39,000 are noted after gel filtration of PYS cell-conditioned medium, whereas parathyroid hormone immunoprecipitation from the same cells reveals a specific band of 39,000 Mr. These results raise the possibility that embryo production of these two hormones at specific stages in development may contribute to the regulation of subsequent steps of differentiation.

Animals↗
PubMed1984

Insulin-specific binding to erythrocytes in 6 girls with acanthosis nigricans.

6 girls, aged 4-16 years, with acanthosis nigricans and hirsutism were studied. Fasting and postglucose hyperinsulinism was present in the 5 older girls. In the youngest, a transitory diabetes with hyperinsulinism was induced by a cortisone therapy for hepatitis. Insulin resistance, suggested by the failure to significantly decrease blood glucose after insulin injection (0.1 U/kg), was demonstrated in three steps: (1) Patient plasma failed to bind 125I-insulin after a 5-day incubation followed by precipitation by antihuman globulin serum. (2) Specific 125I-insulin binding to rat liver membranes was identical in the presence of patient plasma and control plasma. (3) Specific 125I-insulin binding to the erythrocytes of the 6 patients (3.5-7.0%) was significantly lower (p less than 0.01) than in controls (4.5-19.5%). Moreover, the significant correlation present in controls between total binding and reticulocyte counts (r = 0.824, p less than 0.001) was absent in the patients. These data demonstrate further that, in the juvenile type of acanthosis nigricans, insulin resistance which may precede hyperinsulinism is not related to anti-insulin antibodies nor to antireceptor antibodies, but results from a primary defect of insulin receptors.

Acanthosis Nigricans↗
PubMed1982

Simultaneous study of somatotrophic and corticotrophic pituitary secretions during ornithine infusion test.

An ornithine infusion test was performed in fifty-four children with constitutional short stature. The ornithine infusion induced an elevated level of GH at 45 min (mean value = 873 pmol/l) and a similar rise of cortisol levels (mean value = 544 nmol/l). An important peak of ACTH appeared 15 min before the increase of cortisol. In three panhypopituitary dwarfs studied, no elevation of GH or cortisol was observed. The well tolerated ornithine infusion test allows the simultaneous study of the somatotropic and corticotropic pituitary secretions in children with delayed growth.

Adolescent↗
PubMed1981

Somatomedin activity measured as sulphation factor in culture media from normal human liver and connective tissues explants. Effects of human growth hormone.

Normal human explants from liver and from connective tissues (aponeurosis or skin) incubated in vitro released sulphation activity measurable in chick embryo cartilage. Addition of human Growth Hormone (hGH) at physiological levels (10 ng/ml) increased the sulphation activity after 6 hours incubation time. Higher doses failed to increase the sulphation activity produced by connective tissues and decreased the sulphation activity produced by the liver.

Animals↗
PubMed1981

[Serum somatomedin activity in children after surgery for craniopharyngioma (authors transl)].

Serum somatomedin activity was measured in 43 sera from 22 children aged 5 to 15 years operated on for a craniopharyngioma. All had a complete growth hormone deficiency and none received growth hormone therapy. At the time of the study, hydrocortisone therapy was given 29 times and thyroid powder 33 times. In these conditions, a highly significant correlation was found (r = 0.652, p less than 0.001) between somatomedin activity and growth velocity during the past three months. A negative correlation was also found with serum cortisol in patients who did not receive hydrocortisone (r = 0.654, P less than 0,05) and a positive correlation with serum concentrations of T4 (r = 0.640, p less than 0.05) and %3 (r = 0.956, p less than 0.001) in patients who did not receive thyroid powder. In contrast, no correlation was found with serum prolactin and insulin concentrations. These data establish than in children operated for craniopharyngioma, growth is related to a generation of somatomedin independent of growth hormone secretion, and closely controlled by endogenous secretions of cortisol and thyroid hormones.

Adolescent↗
PubMed1980

Serum branched-chain amino acids in the diagnosis of hyperinsulinism in infancy.

Fasting values of branched-chain amino acids (valine, leucine, and isoleucine) were measured by column chromatography in the sera of 27 normal infants and children, 15 days to 9 years of age, 14 children with documented ketotic hypoglycemia one to 7 years of age, and in 14 sera from six infants, 15 days to 2 years of age, with documented hyperinsulinism. In normal children and those with ketotic hypoglycemia, each individual branched-chain amino acid and their sum were significantly negatively correlated with blood sugar values ranging between 11 and 92 mg/dl (P < 0.001). In infants with hyperinsulinism, branched-chain amino acid concentrations were significantly lower (P < 0.001) without correlation with blood sugar values ranging between 13 and 51 mg/dl, and plasma insulin concentrations (9 to 85 microU/ML). In all the children the sum of branched-chain amino acids was positively correlated with blood beta OH butyrate concentrations measured at the same time (r = 0.75, P < 0.001). The association of low blood sugar and low branched-chain amino acid concentrations during fasting seems characteristic of hyperinsulinism, and the measurement of branched-chain amino acids in these infants offers a physiologic indicator of the diagnosis of hyperinsulinism.

Amino Acids, Branched-Chain↗
PubMed1980

Serum somatomedin activity measured as sulphation factor in peripheral, hepatic and renal veins of mongrel dogs: basal levels.

Serum somatomedin (SM) activity measured as sulphation factor on chick embryo cartilage was determined in peripheral (PV), hepatic (HV) and renal (RV) veins or 36 mongrel dogs. Mean SM activity +/- SEM was 0.53 +/- 0.03 U/ml in peripheral and hepatic veins, and 0.61 +/- 0.04 U/ml in renal vein (P less than 0.005). When the gradient of SM activity in hepatic or renal vein to that in peripheral vein, [HV]-[PV] or [HV]-[PV], was plotted versus SM activity in peripheral blood [PV], a negative correlation was found in the case of hepatic but not of renal blood. These data indicate that the kidney may be a production site of SM activity, whereas the liver is differently implicated in the overall regulation of SM activity.

Animals↗
PubMed1980

A possible relationship between serum transferrin, growth hormone secretion and height velocity in children.

Since transferrin (Tf) in vitro has a growth-promoting activity and is associated with NSILA properties, the aim of this work was to study in vivo the relationships between Tf, somatomedin activity (SM), growth hormone (GH) secretion, and height velocity in children. An iv infusion of ornithine hydrochloride was given to 23 controls; the induced rise of GH was accompanied by a simultaneous fall of SM (r = -0.711, P less than 0.001) and was preceded by a fall of Tf (r = -0.610, P less than 0.01). In 17 obese children SM was within the normal range, when Tf levels were higher and arginine-induced GH peaks lower than in the controls, and a negative correlation was found between Tf basal levels and GH peaks (r = -0.608, P less than 0.01). In 9 children with confirmed hypopituitarism the Tf levels were significantly lower than in the controls. In 14 children with confirmed or suspected hypopituitarism a single im injection of hGH (6 mg) failed to induce Tf variations over 24 h. In 39 of these children the height velocity was significantly correlated with Tf basal levels (r = 0.701, P less than 0.001). These data suggest that transferrin is involved in growth regulation, and that GH secretion is related to transferrin levels by a feed-back mechanism.

Adolescent↗
PubMed1980

Serum somatomedin activity measured as sulphation factor in peripheral, hepatic and renal veins in normal mongrel dogs: Early effects of intravenous injection of growth hormone.

The aim of this work was to study the early effects of an intravenous growth hormone (GH) injection on serum somatomedin (SM) activity in samples from peripheral (PV), hepatic (HV) and renal (RV) veins in dogs: 5 dogs were given one bovine growth hormone (bGH) injection, 1 dog was given 5 different doses of human growth hormone (hGH) and 6 control dogs were given saline. In bGH-treated dogs, a significant increase of SM activity occurred in the three vessels without difference between vessels. An early paradoxical decrease of serum somatomedin activity appeared in the dogs given more than 1.15 IU/kg. In the dog given hGH, the response of SM activity was significantly related to the hGH dose in the PV and not in the other vessels. These data seem to indicate that other sites than the liver and the kidney are involved in the production of GH-induced serum somatomedin activity. Following GH injection as well as in basal status, the liver may be implicated in the regulation of serum somatomedin activity.

Animals↗
PubMed1980

[Transferrin, somatomedins and growth].

Plasma transferrin is significantly positively correlated to the growth velocity in normal children and children with various growth disorders. In hypopituitary dwarfs, both plasma transferrin and somatomedin are significantly lower than in controls. Acute variations of the plasma transferrin levels could be involved in the regulation of the GH secretion by a feedback mechanism. Yet, transferrin is neither a somatomedin or a somatomedin-binding protein, and the mechanisms relating growth to transferrin remain unknown.

Adolescent↗
PubMed1980

[Early effects of intramuscular growth hormone on plasma somatomedin activity (author's transl)].

The early effects of intramuscular injection of human growth hormone (hGH) on plasma sulfation activity (Sm) have been followed for 72 hours: 1) after one injection of 6 mg in control children and in pituitary dwarfs (isolated idiopathic GH deficiency, multiple idiopathic pituitary deficiencies, and post-surgical or post-radiotherapic hypopituitarism); 2) after 6 injections of 1 mg every 12 hours in idiopathic pituitary dwarfs. Following injection of 6 mg, Sm decreases during 2-4 hours in all groups studied, then rises and peaks at 24 hours. The early decrease of Sm could relate to a rise of Sm-binding protein, as suggested by data obtained in the dog after intravenous injection of bovine GH. Following 6 injections of 1 mg, the rise of Sm is slower but higher and more protracted than with one injection of 6 mg. This fact suggests that the clinical effects of fractionation of treatment with HGH require further study. The lack of correlation between the biological data obtained and the clinical effects of hGH treatment upon the growth of pituitary dwarfs shows that the short-term hGH test used does not allow to foresee the effects of treatment.

Adolescent↗