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Biomedical subjects

I Gil-Ad

Publications and source records attributed to I Gil-Ad.

60 records · Page 4Linked to original sources
PubMed1977

Light and electron microscopic studies of thyrotrophin releasing hormone-induced growth hormone and prolactin release in hypophysectomized rats bearing an ectopic pituitary gland.

A light microscopic and ultrastructural study of anterior pituitary glands transplanted under the kidney capsule of hypophysectomized rats was performed, in basal conditions and after stimulation with thyrotrophin releasing hormone, at various intervals (24 h-2 months) after transplantation. Confirming previous biochemical findings, the results suggest that with time, somatotrophs acquire sensitivity to thyrotrophin releasing hormone and respond with increased exocytosis at doses that were found ineffective in pituitary glands in situ. Thyrotrophin releasing hormone stimulation did not seem to influence the morphology of prolactin cells, which were already highly active under basal conditions at all time intervals.

Animals↗
PubMed1976

Stimulation of growth hormone release by thyrotropin-releasing hormone in the hypophysectomized rat bearing an ectopic pituitary.

Hypophysectomized female rats which received renal grafts of anterior pituitary (AP) or weight-matched intact controls were sampled under urethane anesthesia. Plasma growth hormone (GH) in sequential samples from each rat was measured by radioimmunoassay to determine the effect of exogenous thyrotropin-releasing hormone (TRH) on GH release from ectopic or intact AP. In a first experiment, following a baseline sample, a pre-treatment sample was taken from each rat 30 min after urethane injection, after which TRH (0.3 or 0.6 mug) or isotonic saline was injected iv, and samples were taken at 10 and 30 min post-treatment. Baseline GH levels in hypophysectomized-transplanted rats were in the range of 4.0 to 8.0 ng/ml, and were not modified significantly by urethane. TRH caused a significantly greater increase in growth hormone at 10 min than did saline. Plasma GH tended to be higher at 30 min post-treatment only in the 0.6 mug TRH-treated group. In further experiments the above described protocol was followed except that four doses of TRH were used (0.15, 0.3, 0.6, and 1.2 mug) and post-TRH blood samples were taken at 5 and 10 min. TRH caused a clear-cut increase in plasma GH both at 5 and 10 min, although no dose-effect relationship was present. In intact controls, baseline GH levels were in the range 40.0 to 80.0 ng/ml and were drastically reduced by urethane. In these animals, only the 1.2 mug TRH dose induced a GH rise at 5 and 10 min. In similar experiments, iv administration of vasopressin (100, 200, or 400 mU) induced a rise in plasma GH when given to the hypohysectomized-transplanted rats, but was ineffective in intact controls; the administration of prostaglandin E2 (5.0 and 50.0 mug) increased plasma GH in both experimental conditions. The results indicate that TRH in the hypophysectomized-transplanted rat acts directly on the AP tissue to increase GH release and that the ectopic pituitary is more susceptible than the in situ pituitary to some GH-releasing stimuli.

Animals↗
PubMed1975

Hyporesponsiveness to glucoprivation during postnatal period in the rat.

2-Deoxy-D-glucose (2-DG), a glucose analogue, blocks glycolysis and induces intracellular glucoprivation. In the adult rat intraperitoneal administration of 2-DG or its injection into the lateral ventricle (IVT) of the brain induces hyperglycemia which is divorced from a rise in plasma insulin (IRI). In the present study, responsiveness to 2-DG-induced glucoprivation, after central or intraperitoneal injection of the drug, was studied in rats of 7, 14, 21, and 28 days of age and compared to that of the adult rat (50 days old). In 7-, 14-, 21-, and 28-day-old rats, the overall blood glucose (BG) response to IVT-injected 2-DG was equivalent to 4, 3.3, 17, and 33%, respectively, of the BG response present in the adult rat. Following intraperitoneal injection of 2-DG , the BG response evoked in the same age groups corresponded to 27, 31, 41, and 93%, respectively, of the adult response. Base-line plasma IRI levels were significantly lower in pups than in adults and increased progressively with age, but no difference was present in IRI levels between 2-DG-treated and control pups whether the 2-DG was given via the laterl ventricle or intraperitoneally. These results demonstrate the presence in the infant rat of clear-cut hyporesponsiveness to 2-DG-induced glucoprivation. The different response pattern between experiments involving central and peripheral 2-DG administration supports the existence of separate peripheral glucoreceptors for 2-DG and their earlier ontogenic activation. Since the infant mammal glucose is of minor relevance as an energy substrate, an interrelationship appears to be present between requirements for fuel(s) and homeostatic response to fuel deprivation.

Age Factors↗