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Biomedical subjects

Z Harel

Publications and source records attributed to Z Harel.

At least 37 records · Page 2Linked to original sources
PubMed1993

Dietary protein restriction impairs both spontaneous and growth hormone-releasing factor-stimulated growth hormone release in the rat.

Restriction of dietary protein stunts growth in the rat, but the mechanism is not well understood. In the present study, we examined the effects of dietary protein restriction on spontaneous and GH-releasing factor (GRF)-stimulated GH release and assessed the possible involvement of endogenous somatostatin (SRIF). Spontaneous 6-h plasma GH profiles were obtained from free-moving adult male rats fed either a 23% (normal) or 4% (low) isocaloric protein diet. Control rats exhibited the typical pulsatile pattern of GH release. In contrast, rats fed the low protein diet showed a significant reduction in GH peak amplitude (85.0 +/- 10.4 vs. 171.3 +/- 20.5 ng/ml; P < 0.01) and mean 6-h plasma GH level (18.1 +/- 2.0 vs. 40.9 +/- 6.0 ng/ml; P < 0.01) as early as 4 days after diet onset and a more than 3-fold suppression of GH pulse amplitude by 7 days. Although protein-restricted animals exhibited the typical cyclic responsiveness to 1 microgram rGRF-(1-29)NH2 i.v., the magnitude of the GH response to GRF challenge was attenuated 3- to 4-fold in these rats compared to that in normal diet-fed controls. Passive immunization of protein-restricted rats with SRIF antiserum resulted in a significant augmentation of both GH pulse amplitude (115.3 +/- 16.7 vs. 36.0 +/- 2.8 ng/ml; P < 0.01) and mean 6-h plasma GH level (34.4 +/- 5.0 vs. 10.0 +/- 1.6 ng/ml; P < 0.01) compared to those in protein-deprived rats administered normal sheep serum. Pituitary size (7.8 +/- 0.2 vs. 12.1 +/- 0.4 mg; P < 0.001) and pituitary GH content (320.5 +/- 18.9 vs. 526.6 +/- 26.8 micrograms; P < 0.001) were markedly reduced after 3-week maintenance on the 4% protein diet. In a separate study, rats fed 70% of the control diet (calorically equivalent to that consumed by rats fed 4% protein) showed no significant alteration in pulsatile GH release, thus excluding caloric restriction as a cause of the GH suppression. These results demonstrate that lack of dietary protein 1) blunts spontaneous pulsatile GH release, 2) attenuates GH responsiveness to GRF challenge, and 3) reduces pituitary GH content and size. Our findings suggest that the low protein-induced suppression of GH release is mediated at least in part by increased SRIF secretion. Such impairments in the GH neuroendocrine axis probably contribute to the growth retardation observed in this model.

Animals↗
PubMed1992

Centrally administered insulin-like growth factor II fails to alter pulsatile growth hormone secretion or food intake.

Insulin-like growth factor II (IGF-II) peptide, mRNA, and receptors are widely distributed in the central nervous system, yet the physiological role of IGF-II in brain remains largely unknown. In the present study, we examined the in vivo effects of central administration of recombinant human IGF-II on pulsatile GH secretion and food intake. The IGF-II preparation used was shown to stimulate 3H-thymidine incorporation in MG-63 human osteosarcoma cells in vitro. Free-moving adult male rats bearing chronic intracerebroventricular (icv) and intracardiac venous cannulae were icv administered 10 microliters of either IGF-II (in doses of 300 ng and 1 microgram) or the vehicle solution, and blood samples were obtained every 15 min for 6 h. Vehicle-injected control animals exhibited the typical pulsatile pattern of GH secretion with most peak GH values greater than 100 ng/ml and trough levels less than 1.2 ng/ml. Central administration of IGF-II, at both doses, failed to alter the spontaneous 6-hour GH secretory profile; there were no significant differences in either GH peak amplitude, GH trough level, GH interpeak interval, or mean 6-hour plasma GH level, compared to vehicle-injected controls. There was also no effect of icv administered IGF-II on mean plasma glucose or insulin levels. Compared to vehicle-injected control rats, the icv injection of IGF-II (at doses of 300 ng and 1 microgram) did not significantly alter 24-h food intake or body weight gain in normal feeding rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Synergistic interaction between insulin-like growth factors-I and -II in central regulation of pulsatile growth hormone secretion.

Insulin-like growth factor (IGF)-I and -II peptides, receptors, mRNAs, and binding proteins are widely distributed in the central nervous system (CNS), yet their physiological role in the brain remains largely unknown. While earlier in vivo studies in the rat suggested that IGF-I may participate in feedback regulation of GH secretion at a CNS level, the preparations used were only partially pure. The recent availability of purified recombinant IGF-I and -II peptides prompted us to reexamine the involvement of the IGFs in vivo in central regulation of pulsatile GH secretion. Five groups of free-moving adult male rats bearing chronic intracerebroventricular (icv) and intracardiac venous cannulae were icv administered IGF-I (in doses of 0.5, 2, 3, and 10 micrograms) or the acid-saline vehicle; an additional group received 1 microgram of the potent IGF-I analog, long R3 IGF-I. Spontaneous 6-h plasma GH secretory profiles were obtained from all groups. Vehicle-injected control animals exhibited the typical pulsatile pattern of GH secretion, with most peak GH values above 150 ng/ml and trough levels below 1.2 ng/ml. Central administration of IGF-I alone or long R3 IGF-I at all doses tested failed to alter the pulsatile pattern of GH release; there were no significant differences in GH peak amplitude, GH trough level, GH interpeak interval, or mean 6-h plasma GH level compared to those in vehicle-injected controls. In a second study, designed to determine the effects of central administration of IGF-I and IGF-II, in combination, icv injection of 1 microgram IGF-I and 1 microgram IGF-II resulted in a marked suppression in the amplitude of spontaneous GH secretory bursts approximately 3 h after injection; both GH pulse amplitude (43.5 +/- 5.6 vs. 130.6 +/- 14.6 ng/ml; P less than 0.001) and mean plasma GH level (16.3 +/- 1.9 vs. 35.2 +/- 1.8 ng/ml; P less than 0.001) were severely reduced 3-6 h after injection compared to those in vehicle-injected controls. These results demonstrate that IGF-I alone does not play a physiologically important role in feedback regulation of GH secretion at the level of the CNS. Our findings suggest a synergistic interaction between IGF-I and -II in the brain for central control of pulsatile GH secretion.

Animals↗
PubMed1990

Alterations of human growth hormone binding by rat liver membranes during hypo- and hyperthyroidism.

Hypothyroid rats treated with human GH (hGH) were partially refractory to the latter's effects. The present study was undertaken to investigate the role of hypo- and hyperthyroidism on the GH receptor. Seven-week-old rats were rendered either hypothyroid, by methimazole, or hyperthyroid, by a daily overdose of T4, during weeks 7-14 of life. Livers were homogenized and overlaid on sucrose discontinuous density gradient. Removal of endogenous ligand from the receptor was performed by exposing the membranes to MgCl2. hGH was used with excess ovine PRL to characterize somatogenic specific binding. Lactogenic specific binding was calculated by subtracting somatogenic specific binding from the total specific binding. Creatine kinase was also measured in homogenized livers. Liver membranes of the hypothyroid rats showed a significant decline in somatogenic and lactogenic binding of hGH. This was true for both the free unoccupied binding sites and total binding after dissociation of the endogenous ligand. Replacement of T4 for 2 weeks restored hGH binding to control values. Hyperthyroid rats had high somatogenic and lactogenic hGH binding. Creatine kinase activity decreased significantly in liver homogenates of hypothyroid rats, was restored by T4 replacement, and increased significantly in hyperthyroid rats. Thus, lactogenic and somatogenic receptors are directly related to the thyroid status in vivo.

Animals↗
PubMed1989

Effect of thyroid hormone and growth hormone on recovery from hypothyroidism of epiphyseal growth plate cartilage and its adjacent bone.

Hypothyroidism was induced in young female Sprague-Dawley rats by the addition of methimazole (0.67 mg/ml) to drinking water for a period of 7 weeks (7-14 weeks of age). The responses of the articular cartilage, epiphyseal growth plate cartilage, epiphyseal trabecular bone, and metaphyseal trabecular bone in the proximal tibia were assessed by structural parameters. In addition, replacement therapies were introduced for the last 2 weeks of the experimental period. These included 0.7 U/kg BW human GH (hGH), 15 micrograms/kg BW L-T4 (T4), and a combination of hGH and T4 at the same doses. In the hypothyroid rats, the width of epiphyseal growth plate cartilage decreased by 27%, that of articular cartilage by 35%, epiphyseal trabecular bone volume by 30%, and metaphyseal trabecular bone volume by 66% relative to those in age-matched control tissues. T4 treatment led to a full restoration of the epiphyseal trabecular bone and surpassed by 40% the control value. The magnitude of the articular cartilage and the epiphyseal trabecular bone volume returned to control values, while that of metaphyseal trabecular bone was 68% of control values. Treatment with hGH did not improve the epiphyseal growth plate cartilage or articular cartilage. It did restore epiphyseal trabecular bone to almost normal values, but metaphyseal trabecular bone improved to only a small though significant level (45% of control value). The combination of T4 and hGH resulted in an additional enlargement in the width of the epiphyseal growth plate cartilage and an increase in metaphyseal trabecular bone volume compared to those in the T4 group. Qualitative examinations indicated that it was only in the T4 and T4 plus hGH groups that the lowest chondrocytes in the epiphyseal growth plate cartilage resumed their normal hypertrophied size. These results suggest that the change in the hypothyroid state do not rely solely on the lack of pituitary GH synthesis and secretion, as replacement by exogenous GH did not restore normal epiphyseal growth plate cartilage morphology or its remodeling into metaphyseal trabecular bone. Treatment with T4 (which restored endogenous pituitary GH to 30% of control levels) results in full recovery of the epiphyseal growth plate cartilage morphology along with its associated metaphyseal trabecular bone. In addition, it can also be concluded that the decrease in epiphyseal trabecular bone volume observed in the hypothyroid animals was due solely to the GH-deficient state that accompanied hypothyroidism.

Animals↗
PubMed1984

Social resources and mental health: an empirical refinement.

A factor analysis of the social resources measures included in the Older Americans Resources and Services instrument (Blazer, 1978) yielded four factors. These factors were labeled attachments, social interaction, social support, and adequacy of social resources. Of these, attachments and social interaction measures were found to have a very limited degree of association with mental health measures (self- and interviewer-rated mental health and the Minnesota Multiphasic Personality Inventory). The overall rating of social resources and the perceived adequacy of social resources, however, had a higher degree of association with the mental health measures.

Aged↗
PubMed1983

Racial differences in social integration and life satisfaction among aged public housing residents.

The effects of social activity, social resources, health, and functional status on the life satisfaction of black and white aged were examined, based on interviews with 330 residents of age-integrated and age-segregated public housing estates in Cleveland, Ohio. The results of multivariate analysis call into question previous conclusions that age-segregation is conducive to greater life satisfaction. However, the findings do lend support to previous research indicating that social integration has a greater degree of importance in determining the life satisfaction of black than of white aged.

Aged↗
PubMed1983

Social support networks of the elderly: racial differences and health care implications.

Interest in social support networks has increased in recent years. A configuration of family, friendships, neighbors, neighborhood groups, comprise the social support network of individuals and families. Other entities referred to in social network of individuals and families. Other entities referred to in social support literature include self-help and mutual help organizations. Interest in descriptive studies of social support networks includes both structural and interactional factors. In analyses of structural factors in social support networks, the focus is most frequently on size (number of persons), density (proportion of linkages) and centrality (extent of accessibility).

Black or African American↗
PubMed1980

Dinosterol in model membranes: fluorescence polarization studies.

The interaction between the phospholipids of Crypthecodinium cohnii, a heterotropic marine dinoflagellate, and its major sterol dinosterol is less soluble in model membranes and as effective in increasing the microviscosity. These results indicate that the unique side chain of dinosterol does not play a special role in terms of complementary interaction with the phospholipids of this organism.

Animals↗