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Biomedical subjects

R Collu

Publications and source records attributed to R Collu.

At least 37 records · Page 2Linked to original sources
PubMed1978

Effects of clofibrate on plasma tryptophan, growth hormone, and prolactin and on brain tryptophan and serotonin in prepubertal rats.

The effects of clofibrate administration (200 mg/kg, po) on somatic growth, plasma levels of lipids, tryptophan, growth hormone (GH), and prolactin (PRL), as well as on brain concentrations of tryptophan and 5-hydroxytryptamine (5-HT) were studied in prepubertal male rats. The drug did not significantly alter ponderal growth, but an appreciable reduction of tail length was observed in rats treated for 30 days. Triglyceride concentrations in plasma showed a 43% diminution after 30 days of treatment, whereas free fatty acid (FFA) levels were not modified. Clofibrate administration for 7, 15, or 30 days caused a fall in total tryptophan and a significant increase of the free fraction in plasma with no change in brain tryptophan levels. Brain 5-HT was generally unaffected but a marked elevation of this parameter was noted in rats treated for 15 days. Plasma GH and PRL concentrations remained unaltered. It may be concluded from these findings that the slight reduction of somatic growth, the diminution of triglycerides, and the increase of free tryptophan in plasma, induced by chronic clofibrate treatment, are not associated with variations in brain tryptophan and 5-HT levels or with modifications of plasma GH and PRL titers.

Animals↗
PubMed1978

Pattern of adenohypophyseal hormone changes induced by various stressors in female and male rats.

Plasma modifications of adenohypophyseal hormones were investigated in groups of female and male rats stressed for 15, 30 min, 1, 2, 4 or 6 h, either by cold (4 degrees C), forced muscular exercise (FME), or immobilization. GH levels in both female and male rats were consistently decreased by the 3 stressing agents. Immobilization in the female and the 3 stressors in the male elicited an early secretory response of prolactin (Prl), while only in immobilized female rats plasma LH levels showed an early, short-lived increment. A more prolonged exposure to stress had an inhibitory influence on plasma Prl and LH levels in both sexes. FSH concentrations were not modified in females, but were decreased in male rats submitted to either one of the 3 stressors. In both male and female rats plasma TSH levels rose during cold exposure, while they were decreased by FME and by immobilization. Our data indicate that the character of the hormonal secretory response during stress is nonspecific. Indeed, to the exception of the specific stimulation of TSH release by cold, stress-induced hormonal changes are not related to the nature but rather to the intensity and duration of the stressing agent.

Animals↗
PubMed1978

Pattern of adenohypophyseal hormone changes in male rats following chronic stress.

To delineate the pattern of adenohypophyseal hormone secretion following chronic stress, adult male rats were exposed daily to 6 h of cold, forced exercise or immobilization for 3, 6, 10, 15, 28 or 42 consecutive days. Groups of these animals were sacrificed at the end of the last stress sessions, and plasma growth hormone (GH), luteinizing hormone (LH), prolactin (Prl) and follicle-stimulating hormone (FSH) levels were measured by radioimmunoassay (RIA). Irresspective of the different stimuli used, long-term stress induced a morphologic and hormonal response characterized by decreased ponderal growth, adrenal enlargement, thymus involution and significant diminutions in GH, Prl and LH levels with no modifications in FSH titers. The magnitude and duration of these changes varied with the severity of the stressors.

Adrenal Glands↗
PubMed1978

Reevaluation of levodopa-propranolol as a test of growth hormone reserve in children.

The growth hormone (GH) reserve of 15 short children was evaluated with the levodopa-propranolol test (DPT) and the sequential arginine-insulin test (AIT). Four patients failed to respond to both tests and were classified as hyposomatotropic. In the other 11 children, the mean GH peak response to the DPT was significantly higher than that to the AIT, mainly because five subjects who had a normal response to the DPT failed to respond to the AIT. These children had a generally poor yearly growth increment prior to testing associated in three with an obvious emotional problem, and were found at follow-up to have resumed a normal growth pattern. These data confirm the effectiveness of the DPT as a test of GH reserve. Although hypoglycemia can occur occasionally during test, this procedure is safer and easier to perform than the widely used AIT. Finally, the DPT seems to detect a category of children who have a temporary growth failure and nonresponse to the usual GH tests but who are not hyposomatotropic and consequently do not require human GH.

Adolescent↗
PubMed1978

Antagonism by taurine of morphine induced growth hormone secretion.

The intraperitoneal (IP) or intraventricular (IVT) administration of small amounts of taurine did not modify pentobarbital-induced sleep or pituitary hormone release. However, the drastic increment in plasma GH values induced by morphine administration was completely blocked by the IVT injection of the amino acid. Whether taurine plays a physiological role in the control of GH secretion is highly speculative.

Animals↗
PubMed1977

Antagonism of pentobarbital-induced hormonal changes by TRH in rats.

In adult male rats, injection of TRH into a lateral ventricle of the brain 5 min prior to pentobarbital (PB) administration caused a significant dose-related inhibition of prolactin (PRL) release, in doses ranging from 500 to 5 ng. Among 8 TRH analogues devoid of thyrotropin-releasing activity, 6 were found to significantly suppress PB-induced PRL secretion at an intraventricular dose level of 10 microgram, and the 3 most effective in this respect were also able to counteract growth hormone (GH) release elicited by PB. The derivative [1,3'-DCM2]TRH was still potent enough to block PB-induced PRL secretion at an intraventricular dosage of 50 ng. The peptide ACTH 4--10 was ineffective, whereas another ACTH derivative H-Met(O2)-Glu-His-Phe-D-Lys-Phe-OH (Org 2766) reduced PRL release. TRH did not affect the increase of plasma PRL induced by acute stress. alpha-Methyl-p-tyrosine (alpha-MT) failed to influence the inhibiting effect of TRH on GH secretion but significantly reduced that on PRL release. p-Chlorophenylalanine (PCPA) completely blocked the antagonistic effect of TRH on all PB-induced hormonal changes, suggesting that serotoninergic mechanisms may be involved in the extra-pituitary effect of TRH.

Adrenocorticotropic Hormone↗
PubMed1977

Effects of chronic stress on pituitary hormone release induced by combined hemi-extirpation of the thyroid, adrenal and ovary in rats.

Morphologic and hormonal changes, induced by combined ablation of a thyroid lobe, one adrenal and one ovary, were studied over a 15-day period in rats, some of whom were subjected to 8 h of daily immobilization. The compensatory hypertrophy (CH) of the contralateral glands in non-stressed animals was associated with a significant increase in the plasma levels of LH (from the 1st to the 10th day), prolactin (PRL, from the 3rd to the 6th day), FSH (on the 3rd day) and corticosterone (from the 6th to the 15th day), whereas GH titers were not altered. Immobilization for 1, 3, 6, 10 or 15 days inhibited the b.w. gain, induced involution of the thymus, enhanced compensatory enlargement of the adrenal, and blocked the CH of the ovary and, to a lesser degree, of the thyroid. This chronic stressor produced a marked rise in plasma corticosterone, antagonized the surge of PRL, FSH and LH, and decreased the plasma levels of GH. On the basis of these morphological and hormonal variations, it appears that severe chronic stress in hemi-thyroidectomized-adrenalectomized-ovariectomized animals further increases the ACTH response but antagonizes the increased secretion of the other pituitary hormones.

Adrenal Glands↗
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↗