bluuebunny/crossref_metadata_2025_split huggingface dataset:
Plasma somatolactin concentrations in salmonid fish are elevated by stress
Authors: Rand-Weaver M. , Pottinger T. G. , Sumpter J. P. 
Published: December 2008

ABSTRACT
The preliminary finding that plasma levels of somatolactin (SL) were markedly elevated following stress caused by confinement in chinook salmon (Oncorhynchus tshawytscha) prompted a more detailed study of SL dynamics during stress. SL levels have been determined in the plasma of rainbow trout (Oncorhynchus mykiss) during exposure to acute (0–30 min) and short (0–24 h) periods of stress resulting from handling and confinement. The results show that SL levels increase rapidly within minutes following the onset of stress, reach a peak between 1 and 2 h, decline over the next 3 h, and then show an additional increase again by 24 h. During acute stress caused by confinement, the increase in plasma SL levels occurred within 2 min, thus showing a more rapid response than cortisol. This suggests that the response is mediated directly by the hypothalamus and is not a result of a feedback mechanism. The results also demonstrate that SL secretion in response to stress is at least partially under genetic control. In the short-term stress experiment, progeny of fish selected as high responders or low responders to stress, based on the magnitude of the plasma cortisol levels induced by stress, were used, and these fish showed similarly accentuated or attenuated release of SL following stress. These results clearly demonstrate that non-specific environmental stress causes rapid activation of SL-secreting cells in the pars intermedia, suggesting that this hormone has an important role in the adaptive response of fish to stress.
Journal of Endocrinology (1993) 138, 509–515
Regulation of 11β-hydroxysteroid dehydrogenase by sex steroids in vivo: further evidence for the existence of a second dehydrogenase in rat kidney
Authors: Low S. C. , Assaad S. N. , Rajan V. , Chapman K. E. , Edwards C. R. W. , Seckl J. R. 
Published: December 2008

ABSTRACT
11β-Hydroxysteroid dehydrogenase (11β-OHSD) catalyses the reversible conversion of corticosterone to inactive 11-dehydrocorticosterone, thus regulating glucocorticoid access to mineralocorticoid and perhaps glucocorticoid receptors in vivo. 11β-OHSD has been purified from rat liver and an encoding cDNA isolated from a liver library. However, several lines of indirect evidence suggest the existence of at least two isoforms of 11β-OHSD, one found predominantly in glucocorticoid receptor-rich tissues and the other restricted to aldosterone-selective mineralocorticoid target tissues and placenta. Here we have examined the effects of chronic (10 day) manipulations of sex-steroid levels on 11β-OHSD enzyme activity and mRNA expression in liver, kidney and hippocampus and present further evidence for the existence of a second 11β-OHSD isoform in kidney.
Gonadectomized male and female rats were given testosterone, oestradiol or blank silicone elastomer capsules, controls were sham-operated. In male liver, gonadectomy+ oestradiol treatment led to a dramatic decrease in both 11β-OHSD activity (69 ± 8% decrease) and mRNA expression (97 ± 1% decrease). Gonadectomy and testosterone replacement had no effect on male liver 11β-OHSD. However, in female liver, where 11β-OHSD activity is approximately 50% of that in male liver, gonadectomy resulted in a marked increase in 11β-OHSD activity (120 ± 37% rise), which was reversed by oestradiol replacement but not testosterone treatment.
In male kidney, gonadectomy+oestradiol treatment resulted in a marked increase in 11β-OHSD activity (103 ± 4% rise). By contrast, 11β-OHSD mRNA expression was almost completely repressed (99 ± 0·1% decrease) by oestradiol treatment. This effect of oestradiol was reflected in a loss of 11β-OHSD mRNA in all regions of the kidney showing high expression by in-situ hybridization. In female kidney, oestradiol replacement also led to an increase in 11β-OHSD activity (70 ± 15% rise) while mRNA expression fell by 95 ± 3%. None of the treatments had any effect on enzyme activity or mRNA expression in the hippocampus, although transcription starts from the same promoter as liver.
We conclude that (i) sex steroids regulate 11β-OHSD enzyme activity and mRNA expression in a tissue-specific manner and (ii) the concurrence of increased enzyme activity with near absent 11β-OHSD mRNA expression in the kidney following oestradiol treatment suggests that an additional gene product is responsible, at least in part, for the high renal activity observed.
Journal of Endocrinology (1993) 139, 27–35
Regulation of serum insulin-like growth factor-I (IGF-I), hepatic growth hormone binding and IGF-I gene expression in the rat during pregnancy and lactation
Authors: Travers M. T. , Madon R. J. , Flint D. J. 
Published: December 2008

ABSTRACT
An apparent GH resistance occurs in pregnancy, since GH concentrations in serum are reported to be normal or elevated, whereas serum IGF-I falls to very low levels. To determine whether this GH resistance is manifest at the level of the hepatic GH receptor or in the ability of GH to initiate IGF-I gene expression, we have determined hepatic IGF-I mRNA expression, circulating IGF-I and hepatic GH binding during various stages of pregnancy and lactation in the rat. The concentration of IGF-I in serum fell from 37 ± 5 nmol/l (means ± s.e.m.) in virgin rats to 17 ± 1 nmol/l in rats in late pregnancy, recovered in early lactation (31 ± 3 nmol/l) but was again significantly lower than in virgin animals by mid-lactation (22 ± 3 nmol/l).
Hepatic GH binding did not vary significantly during pregnancy but showed a small significant decrease in early lactation when expressed per mg membrane protein. When expressed as GH binding per liver, however, there were no significant changes in GH binding at any stage. Liver weight increased significantly between virgin and early pregnant animals (7·1 ± 0·2 g compared with 9·2 ± 0·5 g respectively, P<0·01) and continued to increase up to late lactation (14·3 ± 0·4 g).
Similarly, although the amount of IGF-I gene expression/unit RNA declined in late pregnant when compared with virgin animals (6·0 ± 0·6 versus 3·4 ± 0·4 arbitrary optical density units respectively, P<0·05), when the increase in liver weight and RNA content during pregnancy was taken into account there was actually a steady increase in IGF-I gene expression per total liver throughout both pregnancy and lactation, the difference becoming significant by mid-lactation (P<0·05). Thus, when the changes in liver weight which take place during pregnancy and lactation are taken into account we conclude that any hepatic resistance to GH in late pregnancy and lactation must be a post-receptor event which is mitigated in large part by increase in liver size, cell number and RNA content.
Journal of Endocrinology (1993) 139, 89–95
Suppressed expression of the cytochrome P45017α protein in the testicular feminized (Tfm) mouse testes
Authors: Le Goascogne C. , Sananès N. , Gouézou M. , Baulieu E. E. , Robel P. 
Published: December 2008

ABSTRACT
The testes of testicular feminized (Tfm) mice synthesize and secrete abnormally low amounts of testosterone, as a consequence of selectively decreased cytochrome P45017α activity. To investigate the mechanism of this deficiency, three steroidogenic enzymes were immunolabelled in the testes of normal and Tfm adult (2·5–6 month old) mice. Cholesterol side-chain cleavage cytochrome P450 (P450scc) and Δ5-3β-hydroxysteroid dehydrogenase (3β-HSD) were detected in the Leydig cells of both normal and Tfm mice whereas, in contrast to normal mice, only a small proportion of Leydig cells were immunostained for cytochrome P450-17α-hydroxylase,C17→20 lyase (P45017α) in the testes of Tfm mice. The numbers of cells differed from male to male and interestingly were markedly higher in the right testis. Explants of testes from Tfm mice were kept in organ culture at 32 °C for 45 h, with or without dibutyryl cyclic AMP (100 or 500 μmol/l). All Leydig cells remained positive for P450scc and 3β-HSD, and P45017α became detectable in the majority of Leydig cells in both left and right testes, showing that the lack of expression of P45017α protein in Tfm mouse testes in vivo is not structural but is a regulatory phenomenon.
Journal of Endocrinology (1993) 139, 127–130
Investigation of mechanisms mediating the increase in plasma concentrations of thyroid hormones after a meal in young growing pigs
Authors: Dauncey M. J. , Morovat A. 
Published: December 2008

ABSTRACT
These studies investigated a number of possible mechanisms which could mediate the increase in plasma concentrations of thyroid hormones after a meal in young growing pigs. It has been established that in animals fed one meal a day, an immediate rise in plasma 3,5,3′-tri-iodothyronine (T3) and a slightly delayed increase in thyroxine (T4) levels are followed by a more sustained peak in both hormones several hours later. The increase in thyroid hormones involves both total and free T3 and T4, and there is no change in plasma albumin, the high-capacity thyroid hormone-binding protein in the pig. It has also been shown that the immediate rise in plasma T3 is not mediated either by an increase in plasma glucose concentration or by neural mechanisms associated with distension of the gastrointestinal tract. However, the finding that plasma T3 increases rapidly after feeding in thyroidectomized animals maintained on a replacement dose of T4 alone, indicates the source of T3 to be non-thyroidal.
It is concluded that the rise in plasma thyroid hormones after a meal depends on the energy content of the food but not directly on the circulating glucose levels. The immediate increases in plasma T3 and T4 are probably due largely to a redistribution of the hormonal pools, and peripheral 5′-monodeiodination of T4 may also contribute significantly to the post-prandial rise in T3. The potential significance of these findings in relation to both the metabolic and growth-promoting effects of thyroid hormones is discussed.
Journal of Endocrinology (1993) 139, 131–141
Ovarian and hepatic insulin-like growth factor-I gene expression and associated metabolic responses in prepubertal gilts subjected to feed restriction and refeeding
Authors: Charlton S. T. , Cosgrove J. R. , Glimm D. R. , Foxcroft G. R. 
Published: December 2008

ABSTRACT
The effects of feed restriction and refeeding on ovarian and hepatic insulin-like growth factor-I (IGF-I) gene expression, systemic and ovarian IGF-I concentrations and on associated metabolic changes were measured in prepubertal gilts. Eleven pairs of littermate gilts (70·7 ± 4·7 kg) were placed on a maintenance level of feeding for 7 days (days 1–7). On day 8, littermates were either fed at a maintenance level of energy or fed to appetite for a further 6 days. Blood samples were taken on day 13 (07.00–16.00 h) to determine plasma insulin and IGF-I, and on day 14 (02.00–06.00 h) to determine plasma GH levels. Following slaughter on day 14, one ovary from each animal was retained to measure follicular fluid IGF-I and oestradiol concentrations. The remaining ovary and a sample of liver were retained for IGF-I mRNA analysis using a ribonuclease protection assay. Six days of refeeding significantly increased plasma IGF-I (P<0·005) and basal insulin (P<0·05) but there was no effect on plasma GH. Ovarian follicular volume and diameter were significantly larger after refeeding (P<0·05), with no effect on follicular fluid oestradiol concentrations. Mean follicular fluid IGF-I concentrations were unaffected by treatment. However, the relationships between individual follicular IGF-I concentrations, absolute follicular fluid IGF-I contents and follicle volume were affected by feeding level (P<0·05). Regression analysis of the same data also revealed that at this stage of maturity, small follicles had greater follicular fluid concentrations of IGF-I than larger follicles. Refeeding increased the amount of IGF-I mRNA in hepatic but not ovarian tissue. We conclude that there is differential regulation of the IGF-I gene in porcine hepatic and ovarian tissues, and that ovarian factors other than, or as well as, IGF-I are involved in the regulation of ovarian responses to refeeding.
Journal of Endocrinology (1993) 139, 143–152
The influence of the maternal thyroid hormone environment during pregnancy on the ontogenesis of brain and placental ornithine decarboxylase activity in the rat
Authors: Pickard M. R. , Sinha A. K. , Ogilvie L. , Ekins R. P. 
Published: December 2008

ABSTRACT
The influence of maternal hypothyroxinaemia on early brain and placental development was examined in a partially thyroidectomized (parathyroid-spared; TX) rat dam model. Ornithine decarboxylase (ODC) specific activity, along with more general indices of cell growth, were determined in prenatal whole brain (at 15, 19 and 22 days of gestation), postnatal brain regions (at 5, 10 and 14 days) and placenta.
Maternal hypothyroxinaemia resulted in reductions in fetal body weight, brain weight, brain DNA content and brain total protein content at 15 days of gestation; the latter effect persisting until 19 days of gestation. Further changes in brain cell growth were observed near term, when an increase in the DNA concentration was accompanied by a decrease in the total protein: DNA ratio. Growth of the postnatal brain regions appeared normal, with the exception of an isolated increase in the protein content of the cerebellum at postnatal day 5. Determination of the specific activity of brain ODC revealed a complex pattern of change in the progeny of TX dams, super-imposed upon the normal ontogenetic decline. In the fetal brain, activity was initially deficient at 15 days of gestation but was increased at 22 days of gestation relative to controls. The compromise extended into the postnatal period; ODC specific activity being transiently reduced in the brainstem, the subcortex and the cerebral cortex. Placental development was less consistently affected; wet weight, gross indices of cell growth (DNA content, DNA concentration, total protein: DNA ratio) and ODC specific activity were all normal in the TX dam. However, cytosolic and total protein concentrations were reduced at 15 and 19 days of gestation respectively.
These results demonstrate abnormal fetal brain cell development as a consequence of maternal hypothyroxinaemia. The damage extended into the neonatal period, well after the onset of fetal thyroid hormone synthesis. Although the reduced supply of maternal thyroxine to the fetal brain may play a major role in this dysgenesis, factors such as the impairment of placental function must be taken into consideration.
Journal of Endocrinology (1993) 139, 205–212
Adrenal progesterone facilitates the negative feedback of oestrogen on LH release in ovariectomized rats
Authors: Salicioni A. M. , Carón R. W. , Deis R. P. 
Published: December 2008

ABSTRACT
There is evidence that the adrenals play a role in the regulation of the synthesis and release of gonadotrophins in various vertebrates. The aim of this study was to determine the part played by adrenal steroids, with special reference to progesterone, on the concentration of LH in ovariectomized (OVX) and oestrogen-primed rats. OVX rats received a single s.c. injection of vehicle or oestradiol benzoate (OB, 20 μg/rat). This day was designated as day 0. Three or four days later (day 3–day 4), the rats were treated with mifepristone (10 mg/kg) or with two doses of progesterone antiserum and blood samples were obtained at 13.00 and 18.00 h. OB treatment of OVX rats reduced serum LH at 13.00 h and 18.00 h on day 3 but only at 13.00 h on day 4. The administration of mifepristone at 08.00 h to OVX and oestrogen-treated rats induced a significant increase in serum LH at 18.00 h on days 3 and 4, without modifying the values at 13.00 h. When mifepristone was given at 13.00 h a much larger increase in serum LH was obtained at 18.00 h. In OVX and oestrogen-treated rats, adrenalectomy on day 2 (08.00–09.00 h) induced an increase in serum LH at 18.00 h similar to that observed in the OVX and oestrogen-primed rats after mifepristone treatment. In order to determine the specificity of the effect of mifepristone, a group of OVX and oestrogentreated rats was injected with progesterone antiserum at 08.00 and 13.00 h on day 3. Serum LH concentrations at 13.00 and 18.00 h on day 3 were similar to values obtained in OVX rats treated with oestrogen and mifepristone. Serum progesterone was measured at 08.00 and 13.00 h in OVX and OVX and oestrogenprimed rats. At both times, values were similar in OVX rats but oestrogen treatment significantly increased serum progesterone levels. The important role of adrenal progesterone on the regulation of LH secretion in OVX and oestrogen-primed rats is evident from these results. Blocking progesterone action at the receptor level, we showed that OB significantly increased LH values at 18.00 h. On the basis of these studies it is tempting to speculate on the possibility of an inhibitory or stimulatory effect of oestrogen on serum LH concentration in OVX rats, according to the presence or absence of adrenal progesterone action.
Journal of Endocrinology (1993) 139, 253–258
Effects of insulin-like growth factor-I and its analogues on bovine hydrogen peroxide release by neutrophils and blastogenesis by mononuclear cells
Authors: Zhao X. , McBride B. W. , Trouten-Radford L. M. , Burton J. H. 
Published: December 2008

ABSTRACT
The biological potencies of recombinant human insulin-like growth factor-I (IGF-I) and two of its analogues were examined for hydrogen peroxide release by neutrophils and blastogenesis by mononuclear cells. The binding affinities of these peptides for bovine serum IGF-binding proteins (IGFBPs) and IGF-I receptors on bovine neutrophils and mononuclear cells were also investigated. Relative to control treatment containing no IGF-I, preincubation of neutrophils with 12·5 μg/l of IGF-I, des(1–3)IGF-I (an analogue of human IGF-I lacking the N-terminal tripeptide Gly-Pro-Glu) and long R3 IGF-I (an analogue of human IGF-I with arginine replacing glutamate at position 3 of human IGF-I and the N-terminal extension Met-Phe-Pro-Ala-Met-ProLeu-Ser-Ser-Leu-Phe-Val-Asn) increased the release of H2O2 by 65%, 64% and 32% respectively. However, the difference in stimulating the release of H2O2 between long R3 IGF-I and other two (IGF-I and des(1–3)IGF-I) was reduced at a dosage of 100 μg/l. In the absence or presence of 2·5% fetal calf serum (FCS), 100 μg/l of IGF-I, des(1–3)IGF-I but not long R3 IGF-I significantly stimulated thymidine incorporation into mononuclear cells. In addition, des(1–3)IGF-I was more potent than IGF-I in stimulating thymidine incorporation into mononuclear cells in the presence of 2·5% FCS. IGF-I displaced 125I-labelled IGF-I binding to serum IGFBPs with half-maximal inhibitory concentrations of approximately 1·5 nmol/1, while des(1–3)IGF-I and long R3 IGF-I only inhibited binding by 20% and 6% respectively, even at a concentration of 35 nmol/l. Similar affinities for IGF-I receptors on neutrophils and mononuclear cells were shown for IGF-I and des(1–3)IGF-I. Conversely, much lower affinities for these receptors were demonstrated for long R3 IGF-I. These results suggest that the biological activities of IGF-I and its analogues in cells of the bovine immune system depend on their binding characteristics both to receptors and to binding proteins.
Journal of Endocrinology (1993) 139, 259–265
11β-Hydroxylase gene expression in the rat adrenal cortex
Authors: Ho M. M. , Vinson G. P. 
Published: December 2008

ABSTRACT
It is now known that in the rat there are two distinct species of cytochrome P45011β/18, namely aldosterone synthase and 11β-hydroxylase. Whereas aldosterone synthase is located exclusively in the zona glomerulosa, the zonal distribution and site of production of 11 β-hydroxylase is not entirely clear. In the present study we examined the zonal expression of 11β-hydroxylase mRNA in adrenals from control rats and animals subjected to ACTH treatment and dietary sodium restriction using a non-isotopic in-situ hybridization technique. The results were compared with those obtained using an inner zone specific antigenic (IZAg) marker to give unequivocal identification of the adrenocortical cell types.
11 β-Hydroxylase mRNA was clearly shown to be expressed in the inner zones of the control rat adrenal cortex, and none was detected in the zona glomerulosa and medulla. The message was more abundant in the outer zona fasciculata. A similar pattern of distribution of 11β-hydroxylase mRNA was observed in adrenals from rats subjected to dietary sodium restriction, although the width of the negatively staining layer of zona glomerulosa was significantly increased. In rats treated with 100 μg ACTH for 1 day, the number of cells expressing 11β-hydroxylase mRNA was increased, especially in the zona reticularis. With continued ACTH treatment, 11β-hydroxylase mRNA was found in the region of the zona glomerulosa, and after 3 and 5 days of ACTH treatment cells expressing 11β-hydroxylase mRNA extended to the connective tissue capsule. At this time there was a significant reduction in the total expression of the message compared with the controls.
These results suggest that the presence of 11β-hydroxylase in the zona glomerulosa cells is not essential for the late pathway for aldosterone biosynthesis from deoxycorticosterone. Like IZAg, the distribution of 11β-hydroxylase mRNA after prolonged ACTH treatment provides further evidence to support the hypothesis that ACTH increases the conversion of zona glomerulosa to zona fasciculata-like cells.
Journal of Endocrinology (1993) 139, 301–306
Fragments of chromogranin A are present in the urine of patients with carcinoid tumours: development of a specific radioimmunoassay for chromogranin A and its fragments
Authors: Stridsberg M. , Hellman U. , Wilander E. , Lundqvist G. , Hellsing K. , Öberg K. 
Published: December 2008

ABSTRACT
Chromogranin A is a well-known protein constituent in granules of neuroendocrine cells. It is also known that plasma levels of chromogranin A increase considerably in patients with neuroendocrine tumours and thus chromogranin A is used as a marker for these tumours. In the present study, we have shown that fragments of chromogranin A are excreted into the urine in some patients with carcinoid tumours. The chromogranin A molecule appeared in the urine N-terminally cleaved at amino acid positions 116 and 210, which are previously reported cleavage sites of the molecule. The fragments identified were mainly of about 35 kDa in size. The unprocessed chromogranin A molecule was not excreted in the urine. Five out of 40 patients excreting the fragments had slight tubular dysfunction in the kidneys. We also showed that these renally excreted split products of chromogranin A were immunogenic and could be used for production of antibodies against chromogranin A. These antibodies were used both for immunocytochemistry and for the development of a specific and sensitive radioimmunoassay for chromogranin A and its fragments. Measurements of plasma chromogranin A by radioimmunoassay appeared to be a better marker for tumour growth than were measurements of chromogranin A in the urine.
Journal of Endocrinology (1993) 139, 329–337