bluuebunny/crossref_metadata_2025_split huggingface dataset:
Comparison of the effects of parathyroid hormone (PTH) and recombinant PTH-related protein on bicarbonate excretion by the isolated perfused rat kidney
Authors: Ellis A. G. , Adam W. R. , Martin T. J. 
Published: December 2008

ABSTRACT
The isolated perfused rat kidney was used to study the effects of amino-terminal fragments of human parathyroid hormone, hPTH(1–34), bovine parathyroid hormone, bPTH(1–84) and of PTH-related proteins, PTHrP(1–34), PTHrP(1–84), PTHrP(1–108) and PTHrP(1–141) on urinary bicarbonate excretion. PTHrP(1–34) (7 nmol/l), bPTH(1–84) (5·5 nmol/l) and hPTH(1–34) (7 nmol/l) had similar effects in increasing bicarbonate excretion with respect to the control. At lower concentrations (0·7 nmol/l) all PTHrP components, but not hPTH(1–34) or bPTH(1–84) increased bicarbonate excretion significantly. Infusions of PTHrP(1–108) and PTHrP(1–141) at 0·7 nmol/l, while associated with a rise in urinary bicarbonate concentration and excretion during the early stages of perfusion, produced a sharp decline in bicarbonate concentration and excretion in the latter part of perfusion. The different peptides produced no significant differences in glomerular filtration rate, fractional excretion of sodium or urine volume. The absence of substantial differences between the effects of hPTH(1–34) and PTHrP(1–34) are as noted in previous studies. The differences between PTHrP(1–108)/PTHrP(1–141) and PTHrP(1–34) demonstrated here are consistent with (1) the clinical manifestations of acidosis in hyperparathyroidism and alkalosis in humoral hypercalcaemia of malignancy, and (2) an independent action of a component of PTHrP beyond amino acids 1–34.
Journal of Endocrinology (1990) 126, 403–408
MOLECULAR EVIDENCE FOR THE PRESENCE OF GROWTH HORMONE RECEPTORS IN THE BOVINE MAMMARY GLAND
Authors: Glimm D.R. , Baracos V.E. , Kennelly J.J. 
Published: December 2008

ABSTRACT
GH receptor messenger RNA (mRNA) was identified and characterized in mammary tissue from normal and GH-treated lactating cows using Northern and in-situ hybridization analyses. One major GH receptor transcript of 4.4 kilobases and a less abundant transcript of 9.2 kilobases were detected in mammary tissue from both normal and GH-treated cows. In-situ hybridization analysis revealed that the GH receptor gene is primarily expressed in the alveolar epithelial cells of mammary tissue. These results are evidence that the lactating mammary gland may synthesize GH receptors. On the basis of these observations it seems likely that the lactating bovine mammary gland is a GH target tissue. This finding challenges the widely accepted view that GH does not directly regulate mammary growth or function.
Influence of pregnancy on G-protein coupling to adenylate cyclase activation in guinea-pig myometrium
Authors: Arkinstall S. J. , Jones C. T. 
Published: December 2008

ABSTRACT
The regulatory factors controlling uterine activity during pregnancy remain unclear in many species. Since myometrial relaxants raise intracellular cyclic AMP, modulation of signalling pathways coupling cell-surface receptors to adenylate cyclase activation could be an important site for control. To assess the functional activity of the stimulatory GTP-binding protein Gs we have measured adenylate cyclase activation by GTP, its non-hydrolysable analogue guanosine 5′-(β-γ-imido)triphosphate (Gpp(NH)p), fluoride, forskolin and manganese in a 50 000 g membrane fraction prepared from the myometrium of non-pregnant, mid-pregnant (30–32 days) and late-pregnant (62–66 days) guinea-pigs (full term 67±2 days). While forskolin- and manganese-dependent enzyme activation was unaltered by pregnancy, maximal stimulation by Gpp(NH)p and fluoride was enhanced by up to 200%. Recovery of adenylate cyclase activity in the 50 000 g fraction was essentially constant at 20–24% of the total activity throughout pregnancy, and thus cannot explain the increases observed. Since guanine nucleotides and fluoride stimulate adenylate cyclase through activating Gs, and forskolin and manganese act at the level of the catalytic unit, these data are consistent with a pregnancy-related increase in Gs functional coupling while adenylate cyclase activity is unaltered. These observations suggest a physiological regulation of myometrial Gs activity during pregnancy which could facilitate hormonal stimulation of adenylate cyclase and contribute to uterine quiescence by increasing uterine sensitivity to relaxants.
Journal of Endocrinology (1990) 127, 15–21
Reversal of long-term LH deprivation on testosterone secretion and Leydig cell volume, number and proliferation in adult rats
Authors: Keeney D. S. , Sprando R. L. , Robaire B. , Zirkin B. R. , Ewing L. L. 
Published: December 2008

ABSTRACT
The purpose of this study was to determine whether Leydig cell volume and function could recover fully from long-term LH deprivation upon restoration of endogenous LH secretion, and whether the restoration of LH would elicit a mitogenic response, i.e. stimulate Leydig cell proliferation or affect Leydig cell number per testis. LH secretion was inhibited by treating adult rats with testosterone and oestradiol-filled (TO) silicone elastomer implants (16 weeks), and was restored by removing the implants. Changes in serum concentrations of LH and FSH, LH-stimulated testosterone secretion by testes perfused in vitro, Leydig cell volume and number per testis, average Leydig cell volume and Leydig cell [3H]thymidine incorporation were measured at weekly intervals following implant removal.
The TO implants inhibited (P < 0·01) LH secretion, but serum concentrations of FSH were not significantly different (P > 0·10) from control values. After implant removal, serum LH returned to control values within 1 week, whereas serum FSH increased twofold (P < 0·01) and returned to control values at 4 weeks. LH-stimulated in-vitro testosterone secretion was inhibited by more than 99% in TO-implanted rats, but increased (P < 0·01) to 80% of control values by 8 weeks after implant removal. The total volume of Leydig cells per testis and the volume of an average Leydig cell were 14 and 19% of control values respectively, after 16 weeks of TO implantation (P < 0·01), but returned to 83 and 86% of controls (P > 0·10) respectively, by 6 weeks after implant removal.
Leydig cell proliferation ([3H]thymidine labelling index) was low (< 0·1%) in both control and TO-implanted rats, increased (P < 0·01) fivefold from 1 to 4 weeks after implant removal and then declined to control values at 6 weeks. The increase in Leydig cell [3H]thymidine incorporation was mimicked by treating TO-implanted rats with exogenous LH, but not FSH.
Leydig cells were identified in both the interstitium and the lamina propria of the seminiferous epithelium. The proportion of Leydig cell nuclei in the lamina propria was 30-fold greater (P < 0·01) at 1 and 3 weeks after implant removal (3%) compared with that for control and TO-implanted rats (0·1%). Total Leydig cell number per testis was marginally but not significantly (P = 0·06) decreased in rats treated with TO implants for 16 weeks when compared with controls (18·4±2·2 vs 25·4±1·2 × 106). Three weeks after implant removal, the numbers of Leydig cells per testis were identical (26·8±2·8 × 106) to those in control animals. These results not only demonstrate dramatic morphogenic effects of LH on mature rat Leydig cells, but also suggest that endogenous LH might be mitogenic at least to a subpopulation of Leydig cells.
Journal of Endocrinology (1990) 127,47–58
Effects of crude and highly purified bovine inhibin (Mr 32 000 form) on gonadotrophin production by ovine pituitary cells in vitro: inhibin enhances gonadotrophin-releasing hormone-induced release of LH
Authors: Muttukrishna S. , Knight P. G. 
Published: December 2008

ABSTRACT
Primary cultures of ovine pituitary cells (from adult ewes) were used to investigate the actions of steroid-free bovine follicular fluid (bFF) and highly-purified Mr 32 000 bovine inhibin on basal and gonadotrophin-releasing hormone (GnRH)-induced release of FSH and LH. Residual cellular contents of each hormone were also determined allowing total gonadotrophin content/well to be calculated.
As in rats, both crude and highly purified inhibin preparations promoted a dose (P < 0·001)- and time (P < 0·001)-dependent suppression of basal and GnRH-induced release of FSH as well as an inhibition of FSH synthesis, reflected by a fall in total FSH content/well. However, while neither inhibin preparation affected basal release of LH or total LH content/well, GnRH-induced LH release was significantly (P< 0·001) increased by the presence of either bFF (+ 75%) or highly-purified inhibin (+ 64%) in a dose- and time-dependent manner. This unexpected action of bFF on GnRH-induced LH release was abolished in the presence of 5 μl specific anti-inhibin serum, confirming that the response was indeed mediated by inhibin. Furthermore, neither oestradiol-17β (1 pmol/l–10 nmol/l) nor monomeric α-subunit of bovine inhibin (2·5–40 ng/ml) significantly affected basal or GnRH-induced release of LH.
These in-vitro findings for the ewe lend support to a number of recent in-vivo observations and indicate that, in addition to its well-documented suppressive effect on the synthesis and secretion of FSH, inhibin may actually facilitate LH release in this species, in marked contrast to its action in the rat.
Journal of Endocrinology (1990) 127, 149–159
Importance of the concentration of ATP in rat pancreatic β cells in the mechanism of streptozotocin-induced cytotoxicity
Authors: Nukatsuka M. , Yoshimura Y. , Nishida M. , Kawada J. 
Published: December 2008

ABSTRACT
The effects of streptozotocin (STZ) and N-methyl-N′-nitro-N-nitrosoguanidine (MNNG) on monolayer cultures of rat pancreatic β cells were compared. The intracellular NAD concentration was markedly decreased by both 2 mmol STZ/l and 13·6 μmol MNNG/l, but insulin secretion was decreased significantly only by STZ. The intracellular ATP level decreased rapidly and in a time-dependent manner with STZ, but decreased less on treatment with MNNG: 80% decrease with STZ but only 35% decrease with MNNG in 12 h in the cells exposed to the chemicals for 1 h and then washed thoroughly. STZ decreased oxygen consumption of rat liver mitochondria in a time- and dose-dependent manner and enhanced the generation of hydroxyl radicals (DMPO-adducts). This enhancement was doubled on the addition of succinate as a substrate. Mitochondrial ATP production was also decreased significantly by STZ, but not by MNNG. Thus the marked depletion of intracellular ATP in β cells by STZ seems to be due mainly to a direct effect on mitochondrial production. From these results, we suggest that the cytotoxic effect of STZ in pancreatic β cells is due to a reduction in the intracellular level of ATP, rather than of NAD.
Journal of Endocrinology (1990) 127, 161–165
Analysis of the ratio of biological to immunological LH secreted during the oestrogen-induced LH surge in the ewe
Authors: Clarke I. J. , Foulds L. M. , Hayward S. , Cummins J. T. , Robertson D. M. 
Published: December 2008

ABSTRACT
Plasma concentrations of in-vitro biological and immunological LH were measured throughout the LH surge in cyclic ewes and in ovariectomized ewes treated i.m. with oestradiol benzoate. Both activities increased in parallel during the LH surge in both groups, although the ratio of biological to immunological activities (B/I ratio) was highest at the peak of the LH surge. The two activities were highly correlated (r = 0·86–0·92), with similar slopes from their regression analysis for the cyclic and ovariectomized groups (1·15 and 1·16 respectively). However, the intercepts of the regression lines did not pass through the origin, but intersected the y (radio-immunoassay) axis, suggesting that these serum samples contained immunoactivity not associated with LH bioactivity. In conclusion, an increase in the LH B/I ratio was observed during the LH surge in oestrogen-treated ovariectomized ewes and in cyclic ewes. This increase was not attributable to a change in the relationship between these two LH activities during the LH surge, but rather to the detection of bioinactive immunoactive material in plasma of unknown composition.
Journal of Endocrinology (1990) 127, 217–222
Ovarian secretion rates and peripheral concentrations of inhibin in normal and androstenedione-immune ewes with an autotransplanted ovary
Authors: Campbell B. K. , Baird D. T. , McNeilly A. S. , Scaramuzzi R. J. 
Published: December 2008

ABSTRACT
Active immunization of sheep against androstenedione results in an increase in ovulation rate that is associated with increased plasma levels of LH and progesterone, but not FSH. Although immunized ewes have more activated follicles the secretion rate of oestradiol is not increased. An experiment was conducted to examine the effect of androstenedione immunity on the ovarian secretion and peripheral plasma concentrations of inhibin.
Merino ewes in which the left ovary had been autotransplanted to a site in the neck were divided into control (n = 5) and androstenedione-immune (n = 6) groups. Ovarian and jugular venous blood was collected every 10 min at two stages of the follicular phase, 21–27 h and 38–42 h after a luteolytic dose of an analogue of prostaglandin F2α (PG), and every 15 min for 6 h on day 10 of the subsequent luteal phase. The ewes were monitored regularly for luteal function by measurement of the concentration of progesterone and preovulatory LH surges. The concentration of inhibin in jugular and ovarian venous plasma was determined by radioimmunoassay and ovarian secretion rates and peripheral concentrations are expressed as pg of 1–26 peptide fragment of the α chain.
The ovarian secretion rate of inhibin tended to be greater in androstenedione-immune ewes at all stages of the oestrous cycle measured, with this difference being statistically significant (P <0·05) during the luteal phase (100±40 and 260±80 (s.e.m.) pg/min for control and immune groups respectively). The pattern of ovarian inhibin secretion exhibited pulsatile-like fluctuations which were not associated with LH pulses. Peripheral concentrations of inhibin were generally higher in immunized than in control ewes with this difference being significant (P < 0·01) from day 4 to 14 of the luteal phase (59±5 and 110±7 ng/1 for control and immune respectively). The ovarian secretion rate of immunoactive inhibin was greater (P <0·01) during the follicular phase than during the luteal phase in both groups of ewes, and peripheral concentrations of inhibin increased (P < 0·001) following injection of PG in ewes from both treatment groups.
We concluded that androstenedione immunity results in an increase in ovarian inhibin secretion, an effect that can probably be attributed to the greater number of large oestrogenic follicles present in the ovaries of these ewes. Furthermore, this increase in the concentration of inhibin may override any decrease in the negative feedback effects of ovarian steroid produced by immunization and, hence, explain the paradoxical findings of normal concentrations of FSH and raised concentrations of LH in ewes which are immunized against androstenedione.
Journal of Endocrinology (1990) 127, 285–296
Ontogeny of gonadotrophin receptors and gonadotrophin-stimulated cyclic AMP production in the neonatal rat ovary
Authors: Sokka T. , Huhtaniemi I. 
Published: December 2008

ABSTRACT
The sequence of appearance of FSH and LH receptors, and response of cyclic AMP (cAMP) production to these hormones and cholera toxin, were studied in the fetal and neonatal rat ovary. Specific binding of radio-labelled human (h)FSH and chorionic gonadotrophin (CG) to ovarian homogenates was first detectable on day 7 of life. The content of FSH receptors per ovary increased tenfold between days 7 and 16, and that of LH receptors 27-fold. A significant response of cAMP production in vitro to FSH appeared on day 4 of life, but no significant effect of hCG on cAMP was achieved until day 7. In contrast, cholera toxin had a marked effect on cAMP production by day 17 of fetal life. Although both FSH and LH receptors were detectable in the neonatal rat ovary by day 7, the present findings indicate that the FSH responsiveness of the ovary appears earlier than that of LH. The post-receptor machinery of cAMP production is already functional in the fetal ovary as shown by the experiments with cholera toxin. The appearance of the receptor may therefore be the last link in the ontogeny of the gonadotrophin signal transduction system in the ovary. To study the hormone dependence of the appearance of gonadotrophin responsiveness, neonatal female rats were treated on days 1–6 or 1–9 of life with a potent gonadotrophin-releasing hormone antagonist, and killed on the following day. In both treatment groups, the pituitary LH and FSH contents were suppressed. The body weights remained unaltered, but ovarian weights decreased significantly during both periods of treatment (days 1–6,26·1%, P < 0·05; days 1–9,54·0%, P <0·001). No difference in basal or FSH-stimulated cAMP production was achieved by antagonist treatment for the first 6 days of life. The basal and hCG-stimulated rates of cAMP production per ovary were reduced in animals treated for 9 days (P <0·01), but the FSH-stimulated cAMP production remained unaffected. Hence, whereas the responsiveness to FSH seems to develop in the absence of normal gonadotrophin secretion, a causal relationship between normal gonadotrophin levels and the appearance of LH/hCG responsiveness is apparent in the neonatal rat ovary.
Journal of Endocrinology (1990) 127, 297–303
Cytoplasmic pH in the action of insulin-like growth factor-I in cultured porcine thyroid cells
Authors: Takasu N. , Komiya I. , Nagasawa Y. , Asawa T. , Shimizu Y. , Yamada T. 
Published: December 2008

ABSTRACT
The effects of insulin-like growth factor-I (IGF-I) on cytoplasmic pH (pHi) and [3H]thymidine incorporation were studied in primary cultures of porcine thyroid cells. IGF-I alkalinized thyroid cells and stimulated thymidine incorporation in a dose-dependent manner; the effects of IGF-I on alkalinization (the maximal rates of change of cytoplasmic pHi/min ((dpHi/dt)max)) and thymidine incorporation were observed at 2 ng/ml and were maximal at 100 ng/ml, with half-maximal stimulation at approximately 10 ng/ml. The results indicate that Na+/H+ exchange or cell alkalinization may function as a transmembrane signal transducer in the action of IGF-I on thyroid cell proliferation. Several mitogens and comitogens which activate sodium hydrogen exchange, including epidermal growth factor, platelet-derived growth factor and nerve growth factor, have been listed. Activation with IGF-I has not, however, been presented before. Thus the present study constitutes the first demonstration of IGF-I-stimulated activation of Na+/H+ exchange or cell alkalinization.
Journal of Endocrinology (1990) 127, 305–309
Effect of gastrin-releasing peptide on the secretion of mouse islet hormones in vitro
Authors: Wilkes L. C. , Bailey C. J. , Thompson M. G. , Conlon J. M. , Buchanan K. D. 
Published: December 2008

ABSTRACT
Collagenase-isolated mouse islets were incubated with gastrin-releasing peptide (GRP). At 5·6 mmol glucose/1, 10 nmol GRP/l increased the release of insulin (by 50%) and glucagon (by twofold), decreased the release of pancreatic polypeptide (by 35%), but did not significantly affect the release of somatostatin. At 16·7 mmol glucose/l, 10 nmol GRP/l increased glucagon release (by fivefold) and decreased pancreatic polypeptide release (by 46%), without significantly altering insulin and somatostatin release. GRP (200 nmol/l) did not affect insulin release by perifused mouse islets at 2·8 mmol glucose/l, but increased both first and second phase insulin release after a square wave increase in the glucose concentration to 11·1 mmol/l. At 5·6 mmol glucose/l, GRP (100 pmol/1–100 nmol/l) increased (by 50–70%) insulin release by the RINm5F clonal cell line. GRP did not affect glucose oxidation or the cyclic adenosine monophosphate content of RINm5F cells. However, the intracellular free Ca2+ concentration of RINm5F cells was rapidly and transiently increased by GRP (maximum increase of 64% about 10 s after exposure to 1 μmol GRP/l). The rise of intracellular free Ca2+ was approximately halved in the absence of extracellular Ca2+. The results suggest that GRP may contribute to the normal regulation of the endocrine pancreas. The insulin-releasing effect of GRP is mediated via increased cytosolic free Ca2+, derived both from an increased net influx of extracellular Ca2+ and from mobilization of intracellular Ca2+ stores.
Journal of Endocrinology (1990) 127, 335–340
Characterization of insulin-like growth factor-binding proteins in rat serum, lymph, cerebrospinal and amniotic fluids, and in media conditioned by liver, bone and muscle cells
Authors: Gargosky S. E. , Walton P. E. , Wallace J. C. , Ballard F. J. 
Published: December 2008

ABSTRACT
Insulin-like growth factor-binding proteins (IGFBPs) in rat serum, lymph, amniotic fluid and cerebrospinal fluid (CSF), and in rat cell-conditioned media were characterized using a combination of gel-permeation chromatography, Western immunoblots and Westernligand analysis. Adult serum and abdominal lymph contained a 200 kDa IGFBP (the putative type-II IGF receptor) and a 150 kDa IGFBP that contained subunits of 40–50 kDa aligning with porcine IGFBP-3 on Western-ligand blots. In addition, both fluids contained the smaller IGFBPs: a 30 kDa IGFBP which was immunoreactive with IGFBP-2 antiserum, a 28 kDa IGFBP which electrophoresed with human IGFBP-1, and a 24 kDa IGFBP. In contrast, fetal serum and amniotic fluid lacked the 150 kDa and the 28 kDa IGFBPs. CSF contained only a 30 kDa IGFBP, but this was not IGFBP-2. Several IGFBPs were detected in media conditioned by liver, bone and muscle cells. Liver-derived cells and some hepatoma cell lines produced similar patterns upon ligand blot analysis, i.e. IGFBPs of 30 kDa (which reacted with IGFBP-2 antiserum), 28 kDa and 24 kDa. A hepatoma cell line, HTC, and a smooth muscle cell line contained only an IGFBP of 26 kDa. Skeletal muscle-derived cells (L6 myoblasts) produced a 28 kDa, a 26 kDa and a 24 kDa IGFBP. Both calvarial osteoblasts and osteogenic sarcoma cells produced an IGFBP of 30 kDa that cross-reacted with IGFBP-2 antisera. In addition, osteogenic sarcoma cells produced a 28 kDa and a 24 kDa IGFBP. These results allow us partially to classify and to compare the IGFBPs in rat fluids and those produced by cultured cells.
Journal of Endocrinology (1990) 127, 391–400
Enhanced potency of truncated insulin-like growth factor-I (des(1–3)IGF-I) relative to IGF-I in lit/lit mice
Authors: Gillespie C. , Read L. C. , Bagley C. J. , Ballard F. J. 
Published: December 2008

ABSTRACT
The relative potencies of insulin-like growth factor (IGF-I) and the N-terminal truncated derivative, des(1–3)IGF-I, have been compared in lit/lit mice. Injection of 30 μg IGF-I, 30 μg des(1–3)IGF-I or 3 μg des(1–3)IGF-I daily for 3 weeks increased total length and nose-rump length of the animals substantially more than in controls or animals treated with 3 μg IGF-I daily.
Body weight changes were not statistically significant. The lower dose of des(1–3)IGF-I, but not that of IGF-I, led to increases in kidney and heart weights relative to controls, while the higher dose of either IGF-I or des(1–3)IGF-I also increased the weights of liver, lungs and stomach. These results indicate that the higher potency of des(1–3)IGF-I demonstrated in cultured cells also applies in vivo to at least one strain of GH-deficient animals.
Journal of Endocrinology (1990) 127, 401–405