Biomedical subjects

A Lopez-Calderon

Publications and source records attributed to A Lopez-Calderon.

6 recordsLinked to original sources

PubMed2001

The decrease in hepatic IGF-I gene expression in arthritic rats is not associated with modifications in hepatic GH receptor mRNA.

OBJECTIVE: Adjuvant-induced arthritis induces a catabolic response, and a decrease in circulating IGF-I. Hypermetabolism and GH insensitivity have been described in acute inflammation. The aim of this study was to analyze whether impaired IGF-I secretion in arthritic rats can be attributed to hepatic GH resistance. DESIGN AND METHODS: Male Wistar rats were injected with complete Freund's adjuvant, and 14 days afterwards arthritic and control rats were injected daily with recombinant human GH (rhGH) (3 IU/kg) or saline for 8 days. GH receptor (GHR) gene expression in the liver and the effect of rhGH on hepatic IGF-I synthesis in arthritic rats were examined. RESULTS: There was a significant decrease in hepatic concentrations of IGF-I (P < 0.01) as well as in the IGF-I gene expression in arthritic but not in pair-fed rats. In contrast, arthritis did not modify GHR mRNA levels in the liver. The 8 day administration of rhGH resulted in an increase in body weight gain in arthritic but not in control rats. There was an increase in hepatic IGF-I synthesis and in GHR mRNA levels after rhGH treatment, both in control and in arthritic rats. Two endotoxin lipopolysaccharide (LPS) (1 mg/kg) injections decreased hepatic concentrations of IGF-I and IGF-I mRNA (P < 0.01). Contrary to the results obtained in arthritic rats, mRNA expression of GHR in the liver was lower in LPS- than in saline-treated rats (P < 0.01). CONCLUSION: These data suggest that the decrease in IGF-I synthesis induced by chronic arthritis is not secondary to GH resistance.

Animals↗

PubMed1987

Gonadotropin inhibition during chronic stress: role of the adrenal gland.

The effect of adrenalectomy, metyrapone and dexamethasone treatments on gonadotropin response to chronic stress were studied. Adult male rats were submitted to chronic restraint (6 h daily over 4 days). At the end of the last stress period animals were decapitated and trunk blood was collected. Chronic restraint evoked a decrease in plasma LH and to a lesser degree in plasma FSH in the intact rat. Adrenalectomy did not prevent the LH reduction induced by stress and magnified the inhibitory effect of restraint on FSH secretion. Administration of the corticosterone synthesis blocker metyrapone increased the inhibitory effect of restraint on plasma LH and to a lesser degree on plasma FSH. Dexamethasone treatment did not significantly modify plasma gonadotropin levels in adrenalectomized unstressed rats, but this treatment totally blocked plasma LH and FSH reduction after chronic restraint. These results indicate that plasma LH and FSH reduction during chronic restraint is not due to the increase in glucocorticoid secretion, but seems to be mediated by the increase of the hypothalamic-pituitary components of the adrenal axis.

Adrenal Glands↗

PubMed1986

Response of anterior pituitary hormones to chronic stress. The specificity of adaptation.

The effect of chronic noise stress on the response of anterior pituitary hormones to the same or to another stressor (forced swimming) was studied in adult male Wistar rats. Both acute stressors increased corticosterone, prolactin, LH and TSH secretion and inhibited GH secretion. Previous chronic exposure to noise reduced corticosterone response to the same stimulus without modifying corticosterone response to a novel acute stress. Neither prolactin nor TSH responses to acute noise were reduced by previous chronic exposure to noise. Since chronic noise increased basal levels of LH and decreased those of GH, the response of these hormones to acute stress was expressed as percent changes of their respective basal values. It was found that chronically stressed rats showed diminished LH response to noise but not to forced swimming. GH showed the same pattern without reaching statistical significance. These data indicate that the response of some anterior pituitary hormones can adapt after repeated exposure to the same stressor. When adaptation occurred, this was specific for the stressor which the animals were repeatedly exposed to. The pituitary-adrenal axis appears to be the most reliable index of adaptation to chronic stress among all the anterior pituitary endocrine axes.

Acute Disease↗

PubMed1985

Possible role of prolactin in the inhibitory effect of testosterone on the hypothalamic-pituitary-testicular axis in the rat.

To study the role of testosterone on the regulation of the hypothalamic-pituitary-testicular axis, young intact male Wistar rats were given acute (24 h) or chronic (5 days) subcutaneous treatments of 500 micrograms testosterone propionate (TP) or vehicle alone. Plasma LH, prolactin and testosterone levels were measured both basally and after administration of LH-releasing hormone (LHRH) or human chorionic gonadotrophin (hCG) by means of specific radioimmunoassay systems using materials supplied by the NIADDK. After acute treatment with TP there was an increase in basal plasma testosterone concentrations and no modification in the hCG response when compared with vehicle-treated animals. No difference could be detected in basal plasma testosterone levels after the chronic treatment, but a significant reduction in the hCG response was observed. Both acute and chronic treatments with TP resulted in a significant decrease of basal plasma LH levels. A reduced LH response to LHRH in acutely treated rats and no response in the chronically treated rats was detected. Plasma prolactin levels showed an increase after both acute and chronic treatments. To evaluate the possible role of the increased plasma prolactin levels on the above modifications during TP treatment, another group of animals was treated with TP and bromocriptine (dopamine agonist) simultaneously to avoid the increase in plasma prolactin levels. In this situation, neither basal plasma LH levels nor the response to LHRH were altered when compared to vehicle-treated rats; a normal testosterone response to hCG stimulation was observed in spite of the high basal plasma testosterone levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1981

Possible role of prolactin in the inhibitory effect of estradiol on the hypothalamic-pituitary-testicular axis in the rat.

Acute estradiol benzoate (EB) administration to intact adult male rats reduced basal and hCG-stimulated plasma testosterone (T) levels and decreased basal and LHRH-stimulated LH levels. Long term EB administration had similar effects on T levels. Basal LH levels were more markedly depressed than during short term administration, but the response to LHRH stimulation was increased. PRL levels were significantly elevated during both short and long term EB treatment. Hyperprolactinemia induced by grafting two pituitaries of littermate donors under the kidney capsule of a male adult intact rat was associated with reduced basal and LHRH-stimulated LH levels and reduced T responses to hCG. The administration of bromocriptine to EB-treated rats prevented the increase in serum PRL in response to estrogen and restored normal LH responses to LHRH and T responses to hCG. This suggests that PRL may play an intermediary role in the inhibitory effect of estrogens on pituitary-testicular function.

Animals↗

PubMedDate not supplied

Pituitary-gonadal function in adult male rats subjected to chronic water restriction.

The effect of water restriction on the pituitary-gonadal axis has been studied in adult male rats. Water restriction did not modify FSH, LH and testosterone levels. However, both LH and testosterone responses to acute noise stress were impaired by water restriction. It was unlikely that the inhibition of the pituitary-gonadal response to stress was due to an alteration of the circadian pattern of LH since no evidence for such a daily rhythm was found in either of the two experimental groups. The effects of water restriction on the pituitary-gonadal axis appear to be at least partially a consequence of the resulting reduction in food intake, so that the pituitary-gonadal response to stress would be a more sensitive index of abnormalities induced by protein-calorie deficit than basal concentrations of LH, FSH, or T.

Animals↗