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Biomedical subjects

R Collu

Publications and source records attributed to R Collu.

53 records · Page 3Linked to original sources
PubMed1977

Thyrotropin-releasing hormone in rat brain: nyctohemeral variations.

The concentration of thyrotropin-releasing hormone (TRH) was measured by specific radioimmunoassay in three different brain regions of rats sacrificed every 4 h over a 24 h period. TRH concentration reached a zenith at 1200 h both in the hypothalamus and the amygdala but did not vary in the forebrain. These results indicate that a nyctohemaral variation of TRH levels exists in hypothalamic and extrahypothalamic brain areas.

Amygdala↗
PubMed1977

Increase in plasma growth hormone levels following thyrotropin-releasing hormone injection in children with primary hypothyroidism.

Thyrotropin-releasing hormone (TRH) induced a significant increase in plasma growth hormone (GH) levels in 4 of 8 children with primary hypothyroidism, while a slight decrease was observed in 8 control children. Base-line plasma prolactin (PRL) levels and peak responses to TRH were higher in hypothyroid children than in controls. These data may indicate the existence of dysfunction of central nervous system mechanisms of control of GH and PRL secretion in subjects with primary hypothyroidism.

Adolescent↗
PubMed1976

Effects of thyrotropin-releasing hormone on prolactin, growth hormone and corticosterone secretions in adult male rats treated with pentobarbital or morphine.

Thyrotropin-releasing hormone (TRH) injected either IP (10 mg/kg) or intraventricularly (10 mug/rat) antagonized the pentobarbital-induced secretion of prolactin (PRL). This effect was not blocked by propranolol. In thyroidectomized animals the effect was not apparent; tri-iodothyronine (T3) injection was however ineffective. The injections of luteinizing hormone-releasing hormone (LH-RH) and of melanocyte stimulating hormone release-inhibiting factor (MIF) were also ineffective. Of six TRH analogues, only those containing histidine antagonized pentobarbital-induced PRL release, but none modified plasma levels of growth hormone (GH) or corticosterone (B). Brain levels of serotonin (5-HT) and 5-hydroxyindoleacetic acid (5-HIAA) were not modified by TRH. Morphine-induced secretion of PRL and GH was also significantly antagonized by TRH. Since pentobarbital and morphine-induced hormonal changes are probably exerted through a central nervous system depressant action, these data indicate that TRH can influence brain activity through an extrapituitary mechanism.

Animals↗
PubMed1976

Glucose and insulin metabolism in Friedreich's ataxia.

Our prospective survey of 50 ataxic patients confirms the previous finding of frequent clinical or chemical diabetes in Friedreich's ataxia. Eighteen percent of our typical cases have clinical diabetes and 40% at least an abnormal glucose tolerance curve. However, this finding does not appear to be specific to that form of ataxia. Furthermore, we have shown that most patients with ataxia have normal or low fasting insulin levels, but a hyperinsulinic response to a glucose load.

Blood Glucose↗
PubMed1976

Pituitary response to auditory stress: effect of treatment with alpha-methyl-p-tyrosine. Usefulness of a factorial mixed design for statistical analysis.

Eight adult male rats were chronically cannulated in the jugular vein and placed individually in a sound-attenuated cubicle. Four of the animals were also implanted with a permanent cannula in the right lateral ventricle of the brain. Each animal was submitted twice to auditory stress at a 24-h interval. Before each stress, the rats were pretreated with either saline or alpha-methyl-p-tyrosine (alpha-MT), the order of administration of the drug and its vehicle being alternated in the eight rats. The injections were made either intravenously or intraventricularly. Auditory stress significantly depressed plasma growth hormone (GH) levels irrespective of the type of pretreatment. Mean plasma GH levels were significantly lower after alpha-MT pretreatment. alpha-MT pretreated animals had higher mean plasma corticosterone (B) levels which remained unchanged during stress. Plasma follicle stimulating hormone (FSH) levels were not modified by stress nor by alpha-MT pretreatment. The intraventricular administration of alpha-MT at a dose (20 mg/kg) which is ineffective by a systemic route produced the same effects on GH and B levels as the intravenous injection (250 mg/kg). These data seem to indicate that auditory stress exerts its inhibitory effect on GH secretion through a noncatecholaminergic pathway. They show, on the other hand, the existence of a central catecholaminergic tonus, stimulatory for GH and inhibitory for B. Statistical analysis was based on a factorial mixed design for repeated measurements after logarithmic transformation of the data. The purpose, advantages and limits of this procedure are presented and discussed.

Acoustic Stimulation↗
PubMed1976

Effect of rat stalk median eminence extracts on rat GH secretion in vivo.

Estradiol (0.2 mug), injected subcutaneously for 10 days to adult male rats, increased plasma growth hormone (GH) levels as compared with oil-treated controls. In estradiol-pretreated (10 days), urethane-anesthetized rats, the first as well as the second of two successive intracarotid injections, at 1-hour intervals, of one rat stalk median eminence equivalent evoked a significant rise in plasma radioimmunoassayable GH. Under the same conditions, cerebral cortex extracts (1 equivalent) induced a slight elevation whereas vasopressin (30 mU) or serotonin (200 ng) were ineffective. These results indicate that estrogen-primed, urethane-anesthetized rats can be used to demonstrate GH-releasing activity in rat SME extracts.

Animals↗
PubMed1976

Plasma adrenal and gonadal sex steroids in human pubertal development.

Plasma free dehydroepiandrosterone (DHA), androstenedione (delta), testosterone (T), dihydrotestosterone (DHT), estrone (E1), and estradiol (E2) were measured by radioimmunoassay in 55 boys and 54 girls 3.5 to 16.3 years of age. Plasma DHA increased significantly between 6 and 8 years of age in girls and between 8 and 10 years of age in boys. A further significant increase was noted between 10 and 12 years of age in both sexes. Delta rose significantly between 8 and 10 years of age in girls and between 10 and 12 years in boys. In contrast, no significant increase in T, DHT, or E1, was noted prior to 12 years of age in both sexes. However, E2 showed a significant increase between 10 and 12 years of age in girls. This early rise in the course of pubertal development of the two sex steroids predominantly of adrenal origin, DHA and delta, and its occurence 1 to 2 years earlier in girls than in boys, as does puberty itself, suggest a possible role for these steroids in the mechanisms involved in triggering the hypothalamic-pituitary-gonadal axis at puberty.

Adolescent↗
PubMed1975

Endocrine effects of chronic administration of psychoactive drugs to prepubertal male rats. II. LSD.

The endocrine effects of chronic D-lysergic acid diethylamide (LSD) administration to prepubertal animals were studied by injecting intraperitoneally three times a week for a month either 100 mug or 500 mug of the psychoactive drug per kilogram or the vehicle to groups of Sprague-Dawley male rats starting at 21 days of age. Animals injected with either dosage of LSD had smaller body weights than controls and tail length was significantly reduced in the high dosage group, plasma levels of growth hormone (GH) were decreased in the high dosage group, and pituitary levels in the low dosage group. Plasma levels and pituitary concentrations of luteinizing hormone and follicle stimulating hormone were not significantly modified by the drug. The low dosage of LSD decreased the brain levels of noradrenaline and increased those of dopamine, while the high dosage decreased those of 5-hydroxyindoleacetic acid. These data suggest that LSD, when administered chronically to developing animals, can inhibit body growth probably by altering the secretion of GH through modifications of its neuroendocrine control.

Animals↗
PubMed1975

Endocrine effects of pimozide, a specific dopaminergic blocker.

Pimozide, a specific blocker of dopaminergic receptors, was administered orally to 10 adult male volumteers for 4 days. Half of the subjects received 4 mg/day and the other half 2 mg/day. Blood samples were obtained the day before, the 4th day of Pimozide, and 4 days after the last dose of the drug for the determination of LH, FSH, GH, PRL, TSH, cortisol and testosterone levels. Twenty-four h urinary collections were obtained for the determination of LH and FSH levels. Plasma LH levels decreased and plasma PRL levels increased in the combined groups during Pimozide. Plasma TSH levels decreased during treatment in the 4 mg group only. Urinary LH and plasma testosterone levels decreased in the post-treatment period in the combined groups. These data support the concept of a dopaminergic control of the secretion of several hormones in the human.

Adult↗
PubMed1975

[Chronic hyperammonemia with orotic aciduria: evidence of pyrimidine pathway stimulation (author's transl)].

We have investigated a 3 year old girl with mental and physical retardation, chronic hyperammonemia and orotic aciduria. Plsma glutamine, alanine and proline concentrations were high. Alanine was present in her urine. She excreted only half the urea of control subjects on a similar protein intake. Raising protein intake induced NH4 intoxication with convulsion. Orotic aciduria was present (max: 693 mg/day) and was related to NH4 levels. Red blood cell orotate phosphoribosyl transferase and orotidine decarboxylase activieé were normal, eliminating congenital orotic aciduria, with induction of activity seen on repeated assay during protein load (form 1.37 to 7.5 nmole/109 RBC/hr). Blood ammonia rose with ornithine load, while ornithine levels were twice that of controls. Citrulline was normally metabolized. Although lacking liver assay, we have provided evidence of partial ornithine carbamyl transferase deficiency. The importance of orotic aciduria for ammonia detoxication in partial OCT deficiency is shown, and its possible effect on liver lipoprotein synthesis discussed. Our investigation also confirmed that OCT activity is not present in normal leukocytes rendering them useless for OCT deficiency diagnosis.

Alanine↗
PubMedDate not supplied

Influence of compensatory overload on glucocorticoid receptors in rat skeletal muscle.

The present study was undertaken to evaluate the state of glucocorticoid cytosol receptor binding in muscle hypertrophied by compensatory overload in normal, testosterone-treated, and castrated male rats. Compensatory hypertrophy in plantaris muscles was induced by myomectomy of the gastrocnemius and the soleus of 100 male Sprague-Dawley rats. The controlateral sham-operated limb was used as control. The rats were divided in 3 groups: control injected with peanut oil, castrated injected with peanut oil, and castrated injected with testosterone propionate (1 mg/rat). Five days later the animals were sacrificed and the muscles obtained for glucocorticoid receptor binding studies using [3H]dexamethasone as ligand. Receptor concentrations (Bmax) were significantly increased in hypertrophied muscle and the increase was not affected either by castration or by androgen treatment. These results tend to suggest that gonadal steroids do not participate in hypertrophy-induced proliferation of glucocorticoid receptors.

Androgens↗