bluuebunny/crossref_metadata_2025_split huggingface dataset:
Ontogeny of anti-Mullerian hormone, 3β-hydroxysteroid dehydrogenase and androgen receptor expression during ovine fetal gonadal development
Authors: Sweeney T , Saunders P T K , Millar M R , Brooks A N 
Published: December 2004

Abstract
Anti-Mullerian hormone (AMH) and androgenic steroids are key factors regulating the masculinisation of the internal and external genitalia during fetal development. AMH is produced in Sertoli cells and causes regression of the Mullerian ducts in the male. 3β-Hydroxysteroid dehydrogenase (3β-HSD) is one of the key steroidogenic enzymes regulating testosterone production in Leydig cells. The objective of this experiment was to elucidate the development of the ovine fetal testes by identifying the spatio-temporal expression of AMH, 3β-HSD and androgen receptor expression within them. Fetuses from days 30 and 40 of gestation were fixed intact, while the gonads were dissected from the fetuses on days 70, 100 and 130 of gestation. Tissue was fixed in Bouin's fixative for 6 h, processed into paraffin wax and sections immunostained using rabbit anti-human AMH, 3β-HSD or androgen receptor antibodies.
While seminiferous cords were absent on day 30 of gestation, pre-cord organisation was apparent and the gonad could be clearly distinguished from surrounding tissue by the presence of AMH and 3β-HSD immunopositive cells. Androgen receptor expression was not apparent at this stage. By day 40 of gestation the testis was organised into distinct seminiferous cords and intense immunostaining for AMH and 3β-HSD was present in Sertoli cells within the cords and Leydig cells in the interstitium respectively. Androgen receptor immunopositive cells were present in the interstitium but cells destined to develop into rete testis were immunonegative. By day 70 of gestation, the rete testis was organised in the centre of the testis and was strongly androgen receptor immunopositive. AMH and 3β-HSD expression was present in Sertoli and Leydig cells respectively. The expression of AMH, 3β-HSD and androgen receptor in the 100 and 130 day gestation fetuses was similar to that identified in the 70 day fetuses. In conclusion, Sertoli and Leydig precursor cells are present in the gonad prior to seminiferous cord formation and contain AMH and 3β-HSD at all stages of gestation examined. While androgen receptor immunoexpression was present in nuclei of interstitial cells from day 40 of gestation and in the rete testis from day 70 of gestation, Sertoli cells were immunonegative for androgen receptor at all of the stages examined.
Journal of Endocrinology (1997) 153, 27–32
Evidence that systemic relaxin promotes moderate water consumption during late pregnancy in rats
Authors: Omi E C , Zhao S , Shanks R D , Sherwood O D 
Published: December 2004

Abstract
The protein hormone relaxin is secreted by the ovaries throughout the second half of the 23 day pregnancy in the rat. We recently reported that neutralization of endogenous relaxin with monoclonal antibodies for rat relaxin decreases water consumption during the daily light period during the second half of pregnancy in rats. The apparent effects of relaxin on water consumption, however, were extremely modest. One explanation for the failure to observe a greater relaxin-dependent effect on water consumption is failure of the monoclonal antibody for rat relaxin to neutralize all circulating relaxin. A second explanation is that circulating relaxin has only slight effects on water consumption. This investigation was conducted with an experimental model in which circulating relaxin was removed in order to re-examine the effects of relaxin on water consumption during the daily light period in late pregnancy in rats.
On day 9 (D9) of pregnancy, before the presence of relaxin (R) in the circulation, primiparous pregnant rats were ovariectomized (O) or sham ovariectomized (C). Throughout the remainder of pregnancy, rats were treated with combinations of either progesterone (P) and estrogen (E, group OPE) or progesterone, estrogen and porcine relaxin (group OPER) in doses that restore physiological parameters to values similar to those that occur during the second half of pregnancy in intact rats. Progesterone and estrogen were administered by Silastic tubing implants and porcine relaxin was administered via miniature osmotic pump. Sham-ovariectomized animals received either the hormone vehicles (group SC) or no implants (group IC). Water consumption was measured daily from D4 to D20 at both 0700 and 2100 h which was when the lights went on and off respectively.
Water consumption increased as pregnancy continued from D10 to D20 during the daily 10 h dark periods (P<0·01), but not during the 14 h light periods for all four groups. Daily water consumed by rats in group OPE was significantly lower (P<0·05) than that consumed by shamovariectomized rats from D17 to D20 and lower than that consumed by rats in group OPER on D20. During the dark period there was no difference in water consumption among groups. During the light period, however, group OPE consumed significantly less water (P<0·05) than group C from D18 to D22. Moreover, there was a consistent tendency (P<0·13) for the water consumption to be greater in rats in group OPER than in those in the relaxin-deficient group OPE during the daily light period from D11 to D20 of pregnancy.
We conclude that the increase in water consumption that occurs during the daily dark periods during the second half of pregnancy is not attributable to circulating relaxin. Circulating relaxin promotes only modest increases in water consumption during the daily light periods during late pregnancy in the rat.
Journal of Endocrinology (1997) 153, 33–40
Roles of GTP and phospholipase C in the potentiation of Ca2+-induced insulin secretion by glucose in rat pancreatic islets
Authors: Vadakekalam J , Rabaglia M E , Metz S A 
Published: December 2004

Abstract
Glucose can augment insulin secretion independently of K+ channel closure, provided cytoplasmic free Ca2+ concentration is elevated. A role for phospholipase C (PLC) in this phenomenon has been both claimed and refuted. Recently, we have shown a role for GTP in the secretory effect of glucose as well as in glucose-induced PLC activation, using islets pre-treated with GTP synthesis inhibitors such as mycophenolic acid (MPA). Therefore, in the current studies, we examined first, whether glucose augments Ca2+-induced PLC activation and second, whether GTP is required for this effect, when K+(ATP) channels are kept open using diazoxide. Isolated rat islets pre-labeled with [3H]myo-inositol were studied with or without first priming with glucose. There was a 98% greater augmentation of insulin secretion by 16·7 mm glucose (in the presence of diazoxide and 40 mm K+) in primed islets; however, the ability of high glucose to augment PLC activity bore no relationship to the secretory response. MPA markedly inhibited PLC in both conditions; however, insulin secretion was only inhibited (by 46%) in primed islets. None of these differences were attributable to alterations in labeling of phosphoinositides or levels of GTP or ATP. These data indicate that an adequate level of GTP is critical for glucose's potentiation of Ca2+-induced insulin secretion in primed islets but that PLC activation can clearly be dissociated from insulin secretion and therefore cannot be the major cause of glucose's augmentation of Ca2+-induced insulin secretion.
Journal of Endocrinology (1997) 153, 61–71
Extrapancreatic islets of Langerhans: ontogenesis and alterations in diabetic condition
Authors: Bendayan M , Park I-S 
Published: December 2004

Abstract
The existence of extrapancreatic islets in the duodenal mucosa of the adult rat has been established by morphological studies and the development of these islets has been followed from the early embryonic stage to neonatal and adult life. Like the pancreatic islets, glucagon cells were the first to appear at day 12 of gestation. However, in contrast to the pancreatic islets, insulin was not detected in the extrapancreatic islets until birth. At this stage, the different endocrine cells assume their classical topography, insulin cells being surrounded by non-insulin endocrine cells. In addition, the behaviour of these extrapancreatic islets in diabetic conditions was evaluated on streptozotocin-induced diabetic rats as well as on spontaneous BB Wistar diabetic rats. In both conditions, the extrapancreatic islets were found in the duodenal mucosa but were mainly composed of glucagon cells, the insulin cells having disappeared. These results demonstrate that the extrapancreatic islets are a common normal feature of the rat duodenal mucosa. They appear during fetal development, are present in different strains of rats and behave similarly to the pancreatic islets under spontaneous or chemically induced diabetic conditions. Although their exact role remains to be established, they probably react to local hyperglycaemic environment due to intestinal absorption.
Journal of Endocrinology (1997) 153, 73–80
Release of Type II phospholipase A2 immunoreactivity and phospholipase A2 enzymatic activity from human placenta
Authors: Farrugia W , Rice G E , Wong M H , Scott K F , Brennecke S P 
Published: December 2004

Abstract
The aim of this study was to determine whether Type II phospholipase A2 (PLA2) is released from late pregnant human placental tissue. Placental explants were incubated in vitro and the release of immunoreactive (ir) Type II PLA2 and PLA2 enzymatic activity into the medium was determined. Both irType II PLA2 and PLA2 enzymatic activity accumulated in the incubation medium in a time-dependent manner (P<0·0001). This release was not associated with a loss of cell membrane integrity, as indicated by measurement of the intracellular enzyme, lactate dehydrogenase, in the incubation medium. The concentration of irType II PLA2 and PLA2 enzyme activity present in incubation medium were significantly correlated (P<0·01). Consistent with the hypothesis that Type II PLA2 may be stored in secretory granules within human placental tissue, incubation in the presence of a membrane depolarising concentration of KCl (60 mm) caused the release of irType II PLA2 2·0-fold (P<0·001). PLA2 enzyme activity released into the incubation medium displays biochemical characteristics consistent with those previously reported for secretory PLA2 isozymes, that is, a requirement for millimolar concentrations of calcium for optimal enzyme activity, inhibited by reducing agents, such as dithiothreitol and insensitive to heat inactivation. The data obtained in this study establish that irType II PLA2 is released from term placenta, when incubated in vitro. The release of this extracellularly-active PLA2 isozyme may contribute to gestational and labour-associated increases in glycerophospholipid metabolism and prostaglandin formation.
Journal of Endocrinology (1997) 153, 151–157
Induction of 24-hydroxylase cytochrome P450 mRNA by 1,25-dihydroxyvitamin D and phorbol esters in normal rat kidney (NRK-52E) cells
Authors: Armbrecht H J , Chen M L , Hodam T L , Boltz M A 
Published: December 2004

Abstract
The biologically active form of vitamin D, 1,25-dihydroxyvitamin D (1,25(OH)2D), acts on intestinal, renal, and bone cells to regulate skeletal and mineral metabolism. 1,25(OH)2D also induces 24-hydroxylase activity in these target cells. The 24-hydroxylase hydroxylates 1,25(OH)2D to 1,24,25-trihydroxyvitamin D and 25(OH)D to 24,25-dihydroxyvitamin D. The production of 1,24,25-trihydroxyvitamin D is thought to be the first step in the inactivation of 1,25(OH)2D by its target tissues. Previous studies have characterized the induction of the 24-hydroxylase by 1,25(OH)2D in clonal cell lines from intestine and bone. The purpose of these studies was to characterize the induction of the 24-hydroxylase by 1,25(OH)2D in the kidney, using the clonal rat renal cell line NRK-52E. 1,25(OH)2D (10−7 m) increased the mRNA levels for the cytochrome P450 component of the 24-hydroxylase (P450cc24) by sevenfold after 36 h in NRK-52E cells. 1,25(OH)2D increased P450cc24 mRNA levels in a dose-dependent manner with an EC50 of 10−8 m. In parallel experiments, 1,25(OH)2D significantly increased 24-hydroxylase enzyme activity after 48–72 h. The increase in P450cc24 mRNA induced by 1,25(OH)2D required on-going transcription and translation and was inhibited by H-7, a protein kinase C inhibitor. Tetradecanoyl phorbol acetate markedly increased the magnitude of the tissue responsiveness to 1,25(OH)2D by a protein kinase C-dependent pathway. These studies demonstrate that 1,25(OH)2D increases P450cc24 mRNA levels in NRK-52E cells by a mechanism requiring new protein synthesis and involving protein kinase C. This is in contrast to the action of 1,25(OH)2D in intestinal cells, which does not require new protein synthesis, and in osteoblastic cells, which does not involve protein kinase C.
Journal of Endocrinology (1997) 153, 199–205
Associations between insulin-like growth factor-I (IGF-I), IGF-binding protein-1, insulin and other metabolic measures after controlling for genetic influences: results from middle-aged and elderly monozygotic twins
Authors: Hong Y , Brismar K , Hall K , Pedersen N L , de Faire U 
Published: December 2004

Abstract
It has previously been shown that the serum levels of insulin-like growth factor-I (IGF-I), IGF-binding protein-1 (IGFBP-1), and insulin are influenced by genetic effects to various degrees. From a clinical and preventive point of view, however, it is important to identify potentially modifiable non-genetic factors influencing the levels of these measures. Because monozygotic twin pairs share the same genetic background, differences in phenotypic levels within monozygotic twin pairs are believed to be due to non-genetic influences. Accordingly, the associations between intrapair differences in one phenotype and intrapair differences in another phenotype are also due to non-genetic influences. The present sample of 97 pairs of monozygotic twins from the population-based Swedish Adoption/Twin Study of Aging (SATSA) provided the opportunity to assess non-genetic influences on the levels of IGF-I, IGFBP-1, and insulin. Several metabolic measures were found to account for the variation of IGF-I, IGFBP-1, and insulin after controlling for the genetic influences. IGFBP-1 and glucose were significant predictors for the levels of IGF-I. IGFBP-1 and glucose together explained about one quarter of the non-genetic variation of IGF-I. However, when IGFBP-1 was dropped from the regression model, insulin was the only independent predictor of IGF-I, and explained about 19% of the non-genetic variation for IGF-I. For IGFBP-1, insulin and IGF-I were the significant non-genetic predictors. Insulin and IGF-I explained about 28 and 8% respectively of the non-genetic variation for IGFBP-1, while for insulin, IGF-I, triglycerides, body height, glucose, and body mass index (BMI) explained approximately 20, 12, 6, 5 and 5% respectively of the non-genetic variation.
Journal of Endocrinology (1997) 153, 251–257
Localization of angiotensin II receptor subtypes AT1 and AT2 in the pancreas of rodents
Authors: Leung P S , Chan H C , Fu L X M , Wong P Y D 
Published: December 2004

Abstract
Previous studies have demonstrated the existence of several key components of the renin–angiotensin system in the pancreas. In the present study, the localization of angiotensin II receptor subtypes, type I (AT1) and type II (AT2), in the mouse and the rat pancreas was studied by immunocytochemistry using specific antipeptide antibodies against the second extracellular loops of AT1 and AT2 receptors in conjunction with confocal laser scanning microscopy. In the mouse, immunoreactivity for AT1 and AT2 was observed predominantly in the endothelia of the blood vessels and the epithelia of the pancreatic ductal system. Similar distribution of immunoreactivity for AT1 and AT2 was also observed. However, the intensity of immunoreactivity for AT1 and AT2 was stronger in the rat than that found in the mouse pancreas. Much weaker immunostaining for both AT1 and AT2, as compared with that found in ductal regions, was also found in the acini of the rodent pancreas. Together with the previous findings, the present results suggest that AT1 and/or AT2 receptors may play a role in regulating pancreatic functions in the rodent.
Journal of Endocrinology (1997) 153, 269–274
Trehalose inhibits the release of adipokinetic hormones from the corpus cardiacum in the African migratory locust, Locusta migratoria, at the level of the adipokinetic cells
Authors: Passier P C C M , Vullings H G B , Diederen J H B , Van der Horst D J 
Published: December 2004

Abstract
The effect of trehalose at various concentrations on the release of adipokinetic hormones (AKHs) from the adipokinetic cells in the glandular part of the corpus cardiacum of Locusta migratoria was studied in vitro. Pools of five corpora cardiaca or pools of five glandular parts of corpora cardiaca were incubated in a medium containing different concentrations of trehalose in the absence or presence of AKH-release-inducing agents. It was demonstrated that trehalose inhibits spontaneous release of AKH I in a dose-dependent manner. At a concentration of 80 mm, which is the concentration found in the hemolymph at rest, trehalose significantly decreased the release of AKH I induced by 100 μm locustatachykinin I, 10 μm 3-isobutyl-1-methylxanthine (IBMX) or high potassium concentrations. The specificity of the effect of trehalose was studied by incubating pools of corpora cardiaca with the non-hydrolyzable disaccharide sucrose or with glucose, the degradation product of trehalose, both in the presence and absence of 10 μm IBMX. Sucrose had no effect at all on the release of AKH I, whereas glucose strongly inhibited its release. The results point to the inhibitory effect of trehalose on the release of AKH I being exerted, at least partly, at the level of the adipokinetic cells, possibly after its conversion into glucose. The data presented in this study support the hypothesis that in vivo the relatively high concentration of trehalose (80 mm) at rest strongly inhibits the release of AKHs. At the onset of flight, the demand for energy substrates exceeds the amount of trehalose that can be mobilized from the fat body and consequently the trehalose concentration in the hemolymph decreases. This relieves the inhibitory effect of trehalose on the release of AKHs, which in turn mobilize lipids from the fat body.
Journal of Endocrinology (1997) 153, 299–305
Differential effect of carbamazepine and valproate monotherapy on plasma levels of oestrone sulphate and dehydroepiandrosterone sulphate in male epileptic patients
Authors: Geisler J , Engelsen B A , Berntsen H , Geisler S , Lønning P E 
Published: December 2004

Abstract
Steroid sulphates such as oestrone sulphate (OE1S) and dehydroepiandrosterone sulphate (DHEAS) have been suggested to be of biological importance in different disease states such as breast cancer and atherosclerosis. Previous studies have shown that drugs such as aminoglutethimide and rifampicin that induce P450-dependent mixed-function oxygenases selectively suppress plasma OE1S levels. The aim of this study was to evaluate the influence of treatment with carbamazepine, an antiepileptic drug known to stimulate mixed-function oxygenases, on plasma levels of OE1S and DHEAS. We measured plasma OE1S and DHEAS together with other plasma oestrogens and androgens in male epileptic patients before and during carbamazepine monotherapy. Patients treated with valproate monotherapy acted as a control group. Treatment with carbamazepine decreased plasma OE1S levels from a mean value of 810·8 to 411·6 pmol/l (mean suppression to 50·7% of pretreatment levels, P<0·001). Similarly, the ratio of OE1S to OE1 fell to 59·9% of pretreatment levels (P<0·001). DHEAS decreased from a mean level of 4·9 μmol/l before treatment to 3·0 μmol/l during carbamazepine therapy (mean reduction to 62·7% of pretreatment levels (P<0·001)), while the ratio of DHEAS to DHEA fell to 63·0% of pretreatment values (P<0·01). No significant change in plasma levels of the other oestrogens or androgens measured was observed. Treatment with valproate caused a slight decrease in FSH levels (P<0·05), but no change in any of the other hormones measured was observed. Studies are warranted to evaluate the possible effects of long-term treatment with carbamazepine on the risk of developing endocrine-sensitive tumours and cardiovascular disease and also the possible effects of alterations in plasma DHEAS on epileptic activity.
Journal of Endocrinology (1997) 153, 307–312
Dietary essential fatty acid supplementation, urinary calcium excretion and reproductive performance in the diabetic pregnant rat
Authors: Garland H O , Forshaw A G , Sibley C P 
Published: December 2004

Abstract
Hypercalciuria may be a contributory factor to the disturbed calcium homoeostasis seen in diabetic pregnant rats and their offspring. In diabetes, essential fatty acid metabolism is impaired. We have therefore investigated whether feeding a diet supplemented with essential fatty acids will ameliorate the hypercalciuria of diabetic pregnancy and improve reproductive performance.
Female rats were fed a standard rat diet, a fat-free diet plus evening primrose oil or a fat-free diet plus sunflower oil. They were injected with streptozotocin or vehicle and mated. Urine samples were analysed for calcium before injection and during gestation.
Term-pregnant diabetic rats fed evening primrose oil showed a 73% reduction in urinary calcium output compared with similar rats fed standard diet (P<0·001). The corresponding reduction was 44% in diabetic rats fed sunflower oil (P<0·001). A depletion of essential fatty acids in diabetes may therefore be associated with hypercalciuria; dietary supplementation, particularly with evening primrose oil, appears to correct the problem.
Diabetic pregnant rats fed evening primrose oil showed a significantly greater live fetal mass (85 ± 2 vs 33 ± 12 g; P<0·05) compared with similar rats fed standard diet. Such findings may imply a normalization of placental transport by essential fatty acids. Rats fed evening primrose, but not sunflower oil, also showed a reduced incidence of diabetes after streptozotocin injection compared with rats fed standard diet (63 vs 86%). Rats fed on evening primrose oil that did become diabetic were less hyperglycaemic than those on the standard diet (29 ± 2 vs 37 ± 2 mmol/l), suggesting that the oil may have anti-diabetic properties.
Journal of Endocrinology (1997) 153, 357–363