ISSN:0028-3835    

DOI:10.1159/000125678

出版商:S. Karger AG    

年代:1990

数据来源: Karger

ISSN:0028-3835    

DOI:10.1159/000125679

出版商:S. Karger AG    

年代:1990

数据来源: Karger

摘要:

The effects of hepatic vagotomy upon the circadian rhythm of lipogenesis and body fat store levels were tested in seasonally obese Syrian hamsters. Lipogenesis was studied 8 weeks after surgery by measuring the incorporation of label into epididymal and retroperitoneal fat pad lipid in animals killed 30 min after intraperitoneal [3H]-glucose injection and 2 h after bovine insulin injections. A marked circadian variation in insulin-stimulated lipogenesis was present in sham-operated controls. The peak of lipogenic activity occurred at light onset and was 3-fold greater than during the middle of the photophase. The peak in the circadian variation of plasma insulin coincided with the peak of lipogenic responsiveness to insulin in these animals. Hepatic vagotomy completely abolished the circadian variation in insulin-stimulated lipogenesis and reduced the magnitude of the daily lipogenic peak at light onset by 65%, but only slightly altered the phase of the circadian variation in plasma insulin by 4 h. Hepatic vagotomy did not influence plasma glucose levels, which did not vary as a function of time of day in either group. Body fat stores were severely reduced (40%) by hepatic vagotomy when examined 8 weeks after surgery. The present study demonstrates important roles for interactions of the circadian rhythms of insulin and tissue lipogenic responses to insulin in the regulation of body fat stores. Furthermore, this study demonstrates that hepatic vagal activity regulates the daily interval of lipogenic responsiveness to insulin and thereby directly influences body fat stores in the Syrian hamster.

ISSN:0028-3835    

DOI:10.1159/000125531

出版商:S. Karger AG    

年代:1990

数据来源: Karger

摘要:

The precursor protein of gonadotropin-releasing hormone (GnRH) contains a 56-amino acid peptide, known as GnRH-associated peptide (GAP), and GnRH. Both of these peptides are localized in the same neurons and coprocessed under varieties of physiological conditions. In the present study, we evaluated whether these two peptides are cosecreted into the pituitary portal blood in female rats under the conditions in which the secretion of hypothalamic GnRH and pituitary luteinizing hormone (LH) are known to be altered. The immunoreactivities of GAP-like peptide (IR-GAP-LI) and GnRH (IR-GnRH) in the portal plasma were 2- to 15-fold higher than those observed in peripheral plasma of female rats. In the pubertal females, the preovulatory LH surge which occurred in the afternoon of the day before vaginal opening (puberty) was found to coincide with surges of IR-GAP-LI and IR-GnRH in the pituitary portal plasma. The surges of IR-GAP-LI and IR-GnRH in portal plasma corresponded with a fall in the preoptic and hypothalamic contents of these peptides. In the adult rats, the levels of IR-GAP-LI and IR-GnRH in portal plasma and LH in peripheral plasma were significantly higher during the afternoon of proestrus than those in the afternoon of diestrus. Ovariectomy increased the portal plasma levels of IR-GAP-LI and GnRH and peripheral plasma levels of LH as compared to the level of these hormones in diestrous females. These results indicate that both GnRH and GAP-LI are cosecreted into pituitary portal blood and that changes in the endocrine environment similarly affect both GnRH and GAP secretion.

ISSN:0028-3835    

DOI:10.1159/000125532

出版商:S. Karger AG    

年代:1990

数据来源: Karger

ISSN:0028-3835    

DOI:10.1159/000317584

出版商:S. Karger AG    

年代:1990

数据来源: Karger

摘要:

To evaluate a possible physiological role of endogenous substance P (SP) in the control of prolactin (PRL) release, conscious adult male rats were given injections of a specific antiserum against SP (anti-SP) into the third ventricle (3 µl) or intravenously (0.5 ml). Third-ventricular injection of anti-SP induced a significant increase in plasma PRL levels when compared to values in control animals injected with normal rabbit serum (p < 0.02). Plasma PRL concentrations were significantly elevated within 2 h after injection of antiserum and remained elevated for the 4-hour duration of the experiment. In contrast, injections of large doses of anti-SP intravenously had no effect on plasma PRL levels. In order to confirm the effect of SP itself, synthetic SP was injected intravenously and intraventricularly. Opposite effects of SP on PRL release were observed after intravenous and intraventricular injections of low or high doses of the peptide. A lower dose of SP (10 ng, 7.42 pmol) injected into the third ventricle suppressed the release of PRL (p < 0.01), whereas higher doses (1 µg, 0.74 nmol, or 5 µg, 3.71 nmol) had a stimulatory effect on PRL release (p < 0.01). Similarly, a low dose of SP (0.1 µg, 0.07 nmol) injected intravenously lowered plasma PRL (p < 0.05). Large doses of intravenous SP (50 µg, 37.1 nmol) dramatically stimulated PRL release (p < 0.001). To evaluate a possible direct action of SP on PRL release from the anterior pituitary, the peptide was incubated with dispersed anterior pituitary cells for 1 h. The release of PRL from incubated anterior pituitary cells was not affected at any dose of synthetic SP tested (10–9–10–6M. These data indicate that in the male rat endogenous SP is a physiologically significant inhibitor of basal release of PRL, via a hypothalamic action, although higher, presumably pharmacological doses of SP stimulate the release of this hormone also via hypothala

ISSN:0028-3835    

DOI:10.1159/000125533

出版商:S. Karger AG    

年代:1990

数据来源: Karger

摘要:

The effects of neuropeptide Y (NPY) on release of growth hormone (GH) and gonadotropin (GTH) from the goldfish pituitary in vitro were investigated. Exposure of perifused pituitary fragments, taken from female goldfish at late stages of gonadal recrudescence, to 5-min pulses of human NPY resulted in a rapid dose-dependent stimulation of GH and GTH release, with half-maximal effective dosages of 0.51 ± 0.24 and 2.37 ± 1.05 nM for GH and GTH, respectively. Repeated treatments with pulses of NPY (10 nM for GH, 5 nM for GTH) at 55-min intervals did not significantly alter the responsiveness of pituitary fragments to NPY; however, prior exposure of pituitary fragments to pulses of higher doses of NPY (50 nM GH, 10 nM for GTH) significantly reduced the subsequent hormone responses. When given at 85-min intervals repeated treatment with NPY did not blunt hormone responses to the second and third stimulations at these higher dosages. These results indicate that NPY acts at the pituitary level to stimulate GH and GTH secretion in female goldfish. The GTH response and, to a lesser extent, the GH response become desensitized to further stimulation by NPY in dose- and time-dependent manners. NPY should be considered as one element in the multifactorial systems regulating the GH and GTH secretion in goldfis

ISSN:0028-3835    

DOI:10.1159/000125534

出版商:S. Karger AG    

年代:1990

数据来源: Karger

摘要:

The effect of naloxone, an opiate receptor antagonist, on the secretory pattern of luteinizing hormone (LH) was evaluated in 4-, 16- and 32-week ovariectomized (OVX) rats. Freely moving rats bearing cardiac cannulae were bled every 6 min for 3 h. During the first 90 min of bleeding, an equal volume of saline was injected after withdrawal of each blood sample, while during the second 90 min the replacement was done with saline containing naloxone at a dose of 0.5 (lower dose) or 1.0 (higher dose) mg/kg/h; statistical comparison was done between both treatment periods. In 4-week OVX rats, a significant increase in the mean LH level was observed through the 90-min period of lower-dose naloxone treatment, without significant changes in the pulse frequency and amplitude. In 4-week OVX rats treated with the higher dose and in 16-week OVX rats treated with either the lower or the higher dose, a significant elevation in mean LH levels was observed only during the first 30 min of treatment, which was probably related to the first, large LH peak in the naloxone treatment period. However, together with pulses appearing later in the treatment period, no significant changes were found in the LH pulsatility except for a decrease in frequency in 4-week OVX rats. In 32-week OVX rats, even the lower-dose naloxone did not induce an elevation in mean LH levels. The results demonstrate that naloxone can increase the LH secretion in the absence of ovarian hormones, and further that the effect on LH changes depending upon the dose of naloxone and the time after ovariectomy.

ISSN:0028-3835    

DOI:10.1159/000125535

出版商:S. Karger AG    

年代:1990

数据来源: Karger

ISSN:0028-3835    

DOI:10.1159/000125681

出版商:S. Karger AG    

年代:1990

数据来源: Karger

摘要:

The coadministration of growth hormone (GH) secretagogues can provide insight into the neuroregulation of GH secretion. The GH response to L-dopa (125, 250 and 500 mg orally for body weights 30 kg, respectively), arginine (Arg; 0.5 g/kg infused intravenously over 30 min) and galanin (GAL; 15 µg/kg infused intravenously over 60 min) when administered alone or combined with Pyridostigmine (PD; 60 mg orally), a cholinergic agonist that likely acts via inhibition of endogenous somatostatin secretion, was studied in children with familial short stature. The GH-releasing effect of PD was also evaluated. In 8 children, PD and L-dopa when administered alone induced an equivalent GH rise (area under the response curve, mean ± SEM: 241.4 ± 31.1 vs. 202.9 ± 38.6 µg/l/h) while their coadministration had an additive effect (435.4 ± 41.4 µg/l/h; p < 0.02 vs. PD and L-dopa alone). On the contrary, in other 8 children, PD and Arg induced similar GH increases either when administered alone (394.2 ± 68.5 vs. 405.8 ± 103.9 µg/l/h) or in combination (535.8 ± 97.3 µg/l/h). GH increases almost superimposable were also observed when PD and GAL were administered alone (405.2 ± 72.3 vs. 412.6 ± 94.1 µg/l/h) or in combination (537.9 ± 139.0 µg/l/h) in other 7 children. These data show that the enhancement of the cholinergic activity by PD increases the L-dopa-induced GH release but fails to modify both Arg- and GAL-induced GH release in short children. They may be taken to indicate that a common mechanism, i.e. suppression of endogenous somatostatin secretion, underlies the GH-releasing effect of PD, Arg and GAL, while an extra-somatostatinergic mechanism mediates the

ISSN:0028-3835    

DOI:10.1159/000125536

出版商:S. Karger AG    

年代:1990

数据来源: Karger