Library

feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neuroendocrinology 7 (1995), S. 0 
    ISSN: 1365-2826
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Although previous studies have demonstrated that acute hypoglycemia inhibits growth hormone (GH) secretion due to stimulation (hypothalamic somatostatin (SS) neurones in the rat, the effect of hypoglycemia on GH secretion has not yet been elucidated in the mouse In this study, the effects of insulin-induced hypoglycemia on mouse GH secretion, hypothalamic c-fos expression, GH-releasing hormon (GRH) and SS mRNA levels were investigated in conscious male mice. Seven days after implantation of chronic atrial catheters, bloo samples were taken every 20 min from 1200–1600 h under unrestrained conditions. Insulin was administered iv every 20 min fro1 1200-1240 h to induce moderate hypoglycemia (MH) and severe hypoglycemia (SH), respectively. Expression of hypothalamic c-fos protei was examined 30 min and 60 min after induction of hypoglycemia by immunohistochemistry. Hypothalamic GRH and SS mRNA level were examined 1 h and 3 h after induction of hypoglycemia by Northern blot analysis. The lowest mean plasma glucose levels after insuli injections were 49.1 ± 4.1 mg/dl and 34.2 ± 5.6 mg/dl in conscious mice, respectively. However, pulsatile GH secretion was no significantly altered in either group. Although both MH and SH markedly stimulated c-fos expression in specific hypothalamic nuclc including the paraventricular nucleus, they did not induce c-fos protein in the periventricular nucleus. Neither MH nor SH altere hypothalamic GRH or SS mRNA levels. These results suggest that hypoglycemia does not activate SS neurons which inhibit GH secretio in the mouse.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neuroendocrinology 7 (1995), S. 0 
    ISSN: 1365-2826
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The mechanisms involved in 2-deoxy-D-glucose (2-DG)-induced growth hormone (GH) suppression in the rat were examined. Conscious male rats were given 2-DG by intracerebroventricular (icv) injection and the pulsatile GH secretion was monitored for 6 h. The single icv injection of 2-DG (8 mg/rat) eliminated pulsatile GH secretion in conscious rats. Pretreatment with somatostatin (SS) antiserum completely restored the suppressed GH secretion in the 2-DG treated rats. Hypothalamic GH-releasing hormone (GRH) and SS mRNA levels were not altered by single and multiple icv injections of 2-DG. These findings suggest that 2-DG-induced GH suppression is primarily due to hypersecretion of SS without a significant change at the transcription level in the rat.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 3
    ISSN: 1365-2826
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The episodic pattern of growth hormone (GH) secretion of the male rat was simulated in rats exhibiting impaired GH-releasing factor (GRF) and Somatostatin (SRIF) secretion, by administering various combinations of human GRF-(1–44)NH2 (hGRF) and SRIF. Electrical lesions of the arcuate nucleus resulted in a marked decrease in the amplitude of GH secretory bursts, while the administration of cysteamine (200 mg/kg) did not change the GH secretory profile in rats with arcuate nucleus lesions. Immunohistochemical examinations revealed a marked decrease of GRF and SRIF immunoreactivity in the median eminence of the cysteamine-treated rats with arcuate nucleus lesions. The intravenous injection of 5 μg of hGRF every 3 h caused equivalent surges of GH in the cysteamine-treated rats with arcuate nucleus lesions. The additional infusion of 4 μg/h of SRIF during the trough periods of GH secretion did not affect the amplitude of the GH surges. Hourly injection of 5 μg of hGRF caused transient desensitization to hGRF. Interestingly, the additional infusion of 4 μg/h of SRIF every 3 h enhanced the amplitude of the GH bursts induced by the fourth and the seventh hGRF injections. However, the more frequent injection of 5 μg of hGRF every 30 min caused constant desensitization to hGRF with time, and the additional infusion of 4 μg/h of SRIF every 3 h did not change the attenuated responses to hGRF. These results indicated that the simultaneous administration of hourly GRF and continuous SRIF with brief pauses was most effective for producing high GH peaks. This simulation model suggests that SRIF may play an important role not only in the production of GH troughs, but also in the maintenance of GH surges with distinct peaks in the male rat.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
  • 4
    ISSN: 1437-7780
    Keywords: HGF ; cancer chemotherapy ; pneumonia ; silicosis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In this study, we report plasma hepatocyte growth factor (HGF) levels during cancer chemotherapy and the relationship between plasma HGF and pneumonia onset in 19 patients with primary lung cancer. These measurements are compared with patients plasma HGF levels prior to cancer chemotherapy, as well as with plasma HGF levels in 23 control patients with silicosis. Plasma HGF, as well as peripheral white blood cells and C-reactive protein, were measured every three days during cancer chemotherapy. In the eight patients who did not develop pneumonia, plasma HGF remained within normal limits. In the 11 patients who did develop pneumonia, however, HGF exceeded normal limits three days after the onset of infection. Further-more, the maximum HGF concentration was significantly higher in the 11 patients with pneumonia (0.62±0.12 ng/mL) than in the eight without complications (0.24±0.02,P〈0.01), in the entire lung cancer group prior to chemotherapy (0.17±0.01,P〈0.01), or in the 23 control patients with silicosis (0.22±0.01,P〈0.01). This suggests that HGF may play a role in repairing lung damage due to pneumonia.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...