Library

X
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
    The effect of acute and chronic insulin administration on insulin-like growth factor-I expression in the pituitary-intact and hypophysectomised rat (1989)
    Springer
    Diabetologia 32 (1989), S. 348-353 
    Details
    ISSN: 1432-0428
    Keywords: Growth hormone ; insulin ; insulin-like growth factor-I ; diabetes ; growth ; somatomedin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Although growth hormone is known to be the main regulator of insulin-like growth factor-I, insulin has also been shown to play a role in regulating serum insulin-like growth factor I levels in diabetic animals. While this effect is thought to be due to correction of metabolic perturbations, some studies have suggest that insulin may have a direct effect on growth and/or insulin-like growth factor-I levels. We have examined the effects of acute and chronic insulin administration to non-diabetic, pituitary-intact and hypophysectomised rats. Rats were injected intraperitoneally with insulin as an acute bolus (10 U) or a chronic subcutanious infusion (low dose; 2.4 U/day, high dose; 12 U/day) over 5 days. Insulin-like growth factor-I mRNA was quantitated by Northern and slot blots of RNA from various tissues. A small (less than 2-fold) but significant increase (p〈0.05) was seen in hepatic insulin-like growth factor-I mRNA abundance in pituitary-intact rats following acute insulin injection and chronic low dose insulin infusion. An increase in insulin-like growth factor-I mRNA levels was also seen in other tissues including diaphragm, lung, kidney and heart. A significant increase (p〈0.05) in serum insulin-like growth factor-I levels was also observed 6 h after insulin injection. In contrast, in pituitary-intact rats which received high dose insulin infusion and were hypoglycaemic at the time of death, tissue levels of insulin-like growth factor-I mRNA were reduced compared to saline-treated control groups. Similarly in the hypophysectomised rats neither acute nor chronic insulin administration had any consistent effect on insulin-like growth factor-I mRNA abundance in any of the tissues examined. This data suggests that insulin has no direct effect in regulating insulin-like growth factor-I gene expression. The small effects demonstrable in pituitary-intact rats may result from a synergistic action of insulin with growth hormone or other pituitary factors.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00277257
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Effects of insulin-like growth factors (IGF) on pancreatic islet function in IGF binding protein-1 transgenic mice (1996)
    Springer
    Diabetologia 39 (1996), S. 1249-1254 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Insulin-like growth factors ; islets ; transgenic mice ; binding proteins.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We have previously reported fasting hyperglycaemia, hyperinsulinaemia, and glucose intolerance in transgenic (Tg) mice which overexpress rat insulin-like growth factor binding protein-1 (IGFBP-1). An increase in pancreatic islet size and number was also observed in this model. Islets from Tg mice had relatively more beta cells and less alpha cells than islets from wild-type (Wt) mice. These observations prompted us to investigate the effects of glucose and insulin-like growth factor-I (IGF-I) on insulin and glucagon release by isolated islets from Tg and Wt mice. Under basal glucose conditions, islets from Tg mice released significantly more insulin and less glucagon than islets from Wt mice. This difference was significant even when corrected for the increased size and cellularity of islets from Tg mice. A dose-dependent increase in insulin release was observed with increased glucose concentrations in both Wt and Tg mice. At all but the highest glucose concentration, islets from Tg mice released significantly greater amounts of insulin than islets from Wt mice. Addition of IGF-I to islet incubations resulted in a dose-dependent increase in insulin release. However, the effect of IGF-I on islets from Tg mice was reduced compared to islets from Wt mice. From these data we conclude that IGF-I stimulates rather than inhibits insulin secretion in isolated murine islets. Furthermore, an intrinsic defect in pancreatic islet insulin release is not responsible for the glucose intolerance in Tg mice. Rather, the data suggest that the hyperglycaemia or local effects of IGFBP-1 over-expression results in a state of enhanced insulin secretion which persists under short-term in vitro culture conditions. [Diabetologia (1996) 39: 1249–1254]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050566
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Connexin43 in rat pituitary: localization at pituicyte and stellate cell gap junctions and within gonadotrophs (1993)
    Springer
    Histochemistry and cell biology 100 (1993), S. 53-64 
    Details
    ISSN: 1432-119X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Immunohistochemical methods were employed to investigate the cellular and ultrastructural localization of the gap junction protein connexin43 (Cx43) in rat pituitary. Western blots of pituitary homogenates probed with anti-Cx43 antibodies showed the presence of Cx43 in both anterior and posterior pituitary lobes. By light microscopy (LM), Cx43-immunoreactive (Cx43-IR) puncta were found in all areas of the posterior lobe, but at greater concentrations in peripheral regions of this structure. By electron microscopy (EM), immunogold labelling for Cx43 was seen at gap junctions between thin cytoplasmic processes of pituicytes. No immunoreactivity was detected in the intermediate lobe. The anterior lobe contained puncta similar to but more sparsely scattered than those in the posterior lobe, and by EM analysis these were demonstrated to correspond to labelled gap junctions between stellate cells. In addition, anti-Cx43 antibodies produced intracellular labelling in a small percentage of endocrine cells, which were distributed throughout the anterior lobe and determined by double immunostaining methods to be cells containing luteinizing hormone. By EM, labelling within these cells was associated with predominantly large secretory granules and other loosely organized organelles. The results indicate that gap junctions in the pituitary are composed of Cx43 and that this or a related protein may have a novel intracellular function within gonadotrophs.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00268878
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Phosphorylated Forms of Connexin43 Predominate in Rat Brain: Demonstration by Rapid Inactivation of Brain Metabolism (1994)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 62 (1994), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The gap junction protein connexin43 (Cx43) has been reported to exist as several phosphorylated forms migrating at ˜43 kDa on sodium dodecyl sulfate-polyacrylamide gel electrophoresis as well as an unphosphorylated 41-kDa form. In brain, Cx43 is expressed predominantly in astrocytes and is also expressed in several other cell types. Whereas the phosphorylated forms of Cx43 predominate in heart, several studies have indicated that high levels of the unphosphorylated form of Cx43 are present in brain. Various experiments in this report indicate that the 41-kDa molecular form in brain is a postmortem dephosphorylation product of phosphorylated Cx43. In rats killed by cranial high-energy microwave irradiation leading to rapid inactivation of brain metabolism, Cx43 in cerebral cortex was present almost exclusively as the 43-kDa phosphorylated form. Rapid dissection of brain followed by heat treatment or inclusion of phosphatase inhibitors during tissue homogenization also largely prevented the conversion of the 43-to the 41-kDa form. The 41-kDa species was generated after alkaline phosphatase digestion of the 43-kDa material obtained by immunoprecipitation from microwave-irradiated brain. Immunolabeling patterns and relative regional levels of Cx43 as seen by immunohistochemical and western blot detection were the same whether or not metabolism to the 41-kDa species was prevented. In developing rat brain, Cx43 levels in frontal cortex and brainstem increased with age, but the degree of dephosphorylation of the 43-to the 41-kDa form was greater at earlier ages in the brainstem. It appears that brain contains a phosphatase that may be involved in modulating the phosphorylation state of Cx43 and thus may regulate intercellular communication via astrocytic gap junctions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1994.62062394.x
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 5
    Electronic Resource
    Electronic Resource
    Expression and regulation of insulin-like growth factor binding protein-1 in the rat uterus throughout estrous cycle (1993)
    Springer
    Molecular and cellular biochemistry 124 (1993), S. 43-49 
    Details
    ISSN: 1573-4919
    Keywords: IGF-1 ; IGFBP ; uterus ; mRNA expression
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract In previous studies, we have demonstrated that IGF-1 and IGF-1 receptor are expressed in rat uterus and that the expression is up-regulated by estrogen. The present study examines the expression and regulation of IGFBP-1 and IGFBP-3 in rat uterus throughout the estrous cycle. The stage of the estrous cycle in 16 mature female rats was determined by microscopic examination of daily prepared vaginal smears. Rat uteri were then used for RNA extraction. The results of the Northern blot analysis demonstrate that uterine cells express both IGFBP-1 and IGFBP-3 mRNA throughout the estrous cycle. When autoradiograms were quantitated by a densitometry, a significant reduction in expression of IGFBP-1 mRNA was found in uteri at stages of proestrous and estrous relative to that in diestrus. Although the level of IGFBP-3 mRNA varied in uteri throughout estrous cycle but this variation was not statistically significant. The lowest expression of IGFBP-1 (8.5% relative to diestrus, p〈0.05, n=4) and IGFBP-3 (71% relative to diestrus) was found in the uteri prepared from rats at the stage of proestrus, while the highest expression of IGFBP-1 and IGFBP-3 was observed in the uteri obtained from rats at the stage of diestrus and metestrus, respectively. Using anti-rabbit IGFBP-1 antibody raised against an oligo-synthetic IGFBP-1 peptide, immunohistochemical staining demonstrates the presence of IGFBP-1 in the luminal and stromal glandular epithelial cells. In summary, rat uterine cells express IGFBP-1 and IGFBP-3 mRNA and expression is regulated throughout the estrous cycle. A marked reduction in IGFBP-1 and IGFBP-3 during the proestrous stage of the estrous cycle may facilitate the biovailability of elevated IGF-1 to interact with IGF-1 receptor through a paracrine and/or autocrine mechanism.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01096380
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 6
    Electronic Resource
    Electronic Resource
    Impaired estrogen-induced uterine insulin-like growth factor-I gene expression in the streptozotocin diabetic rat (1988)
    Springer
    Diabetologia 31 (1988), S. 842-847 
    Details
    ISSN: 1432-0428
    Keywords: Estrogen ; somatomedins ; streptozotocin ; diabetes ; uterine growth
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Circulating somatomedin-C/insulin-like growth factor-I levels are low in the diabetic rat and unresponsive to exogenous growth hormone. However, the nature of this defect in growth hormone action remains unclear and there is little data on insulin-like growth factor-I gene expression in response to other stimuli and in non-hepatic tissues where insulin-like growth factor-I may have important paracrine and/or autocrine actions. We have previously shown that 17-beta estradiol stimulates uterine insulin-like growth factor-I expression in the ovariectomised rat. In this report uterine and hepatic insulin-like growth factor-I gene expression have been examined in the streptozotocin-diabetic rat. Serum insulin-like growth factor-I concentrations were significantly reduced in diabetic rats compared to normal rats (0.72±0.08 vs 1.23±0.05U/ml, p〈0.0005) and hepatic insulin-like growth factor-I mRNA abundance was similarly reduced in diabetic rats to 49±5% of that seen in non-diabetic intact rats (p〈0.005). In contrast, uterine insulin-like growth factor-I mRNA abundance was not significantly reduced in diabetic rats compared to control rats (76±12%, p = NS). Although both diabetic and non-diabetic rats demonstrated a significant increase in uterine wet weight following a single injection of 17-beta estradiol the increase in uterine insulinlike growth factor-I expression was significantly less marked in diabetic rats. Acute administration of insulin together with estradiol had no significant effect on serum insulin-like growth factor-I concentrations or hepatic insulin-like growth factor-I mRNA abundance; however, the uterine insulin-like growth factor-I response was significantly (p〈0.01) augmented. The observations reported here demonstrate that hepatic insulin-like growth factor-I gene expression is markedly reduced in the diabetic rat and that the estradiol-induced uterine insulin-like growth factor-I response is significantly diminished, consistent with the hypothesis that there is a defect in insulin-like growth factor-I gene activation in the diabetic rat.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00277488
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 7
    Electronic Resource
    Electronic Resource
    Overexpression of insulin-like growth factor binding protein-1 in transgenic mice (2000)
    Springer
    Pediatric nephrology 14 (2000), S. 567-571 
    Details
    ISSN: 1432-198X
    Keywords: Key words Hyperglycemia ; Glucose intolerance ; Diabetes ; Metabolic effects ; Insulin-like growth factors ; Growth
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Overexpression of insulin-like growth factor-1 binding protein (IGFBP-1) in transgenic mice has provided insight into the physiological role of this binding protein in modulating the metabolic and growth-promoting effects of the IGFs. IGFBP-1 transgenic mice demonstrate both intrauterine and postnatal growth retardation. Organ weight was proportionately reduced relative to body weight in most organs, with the exception of the brain, which was disproportionately small in transgenic mice. There were no gross neurological manifestations of the reduction in brain size. Transgenic mice also demonstrated fasting hyperglycemia, impaired glucose tolerance, and modest insulin resistance in skeletal muscle and hepatic tissue. From these data, we can conclude that overexpression of IGFBP-1 results in inhibition of IGF action and in profound impairment of brain development, modest inhibition of fetal and postnatal growth, and inhibition of the metabolic effects of the IGFs. Increased expression of IGFBP-1 has been documented in a variety of situations, such as fetal nutritional deprivation and hypoxia, and has been considered to be a marker of metabolic disturbances that cause fetal growth retardation. The observations in IGFBP-1 transgenic mice suggest expression of IGFBP-1 may itself contribute to the growth retardation and impaired fetal brain development.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s004670000347
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 8
    Electronic Resource
    Electronic Resource
    Modeling the transport and fate of mercury in an urban lake (Onondaga Lake, NY) (1995)
    Springer
    Water, air & soil pollution 80 (1995), S. 489-498 
    Details
    ISSN: 1573-2932
    Source: Springer Online Journal Archives 1860-2000
    Topics: Energy, Environment Protection, Nuclear Power Engineering
    Notes: Abstract A mass balance model was developed to simulate mercury (Hg) cycling in Onondaga Lake, New York. MERC4, a U.S. Environmental Protection Agency model of the physical and biogeochemical transport and transformation of Hg, was modified by the addition of input from two supporting models (Fish Bioenergetics Model 2 and a lake eutrophication model) to model the transport of Hg into and out of plankton and fish. The model calculates the concentrations of total Hg, methylmercury, elemental Hg, and ionic Hg in both dissolved and particulate forms in the water column. The model was calibrated to an extensive data set of temporally and spatially variable Hg concentrations in Onondaga Lake in 1992. In addition to standard transport processes of advection and dispersion included in MERC4, the Onondaga Lake Mercury Model includes remineralization to simulate release of Hg from settling particulates before incorporation into sediment. The model provides an analytical framework for understanding and predicting the behavior of Hg in Onondaga Lake and has potential use in evaluating the relative impact of different source control and remedial alternatives.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01189699
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 9
    Electronic Resource
    Electronic Resource
    Total mercury and methylmercury mass balance in an alkaline, hypereutrophic urban lake (Onondaga Lake, NY) (1995)
    Springer
    Water, air & soil pollution 80 (1995), S. 509-517 
    Details
    ISSN: 1573-2932
    Source: Springer Online Journal Archives 1860-2000
    Topics: Energy, Environment Protection, Nuclear Power Engineering
    Notes: Abstract A total mercury (total Hg) and methylmercury (CH3Hg) mass balance was developed for Onondaga Lake, NY, based on sampling of tributaries, sediments, water column, and biota in 1992. Thein situ flux of total Hg and CH3Hg from sediments to the overlying water and the rate of net CH3Hg production in the water column were determined experimentally. Fluxes from atmospheric deposition, groundwater, and volatilization were estimated from limited field data and the literature. Ultraclean sampling and analytical techniques developed specifically for Hg were used. Results indicate that tributaries contribute the majority of total Hg entering the lake (13.6 kg in 1992). Other sources of total Hg included groundwater flux (0.02 kg), atmospheric deposition (0.44 kg), and flux from sediments (0.056 kg). Net sedimentation (11.1 kg), outflow (2.8 kg), and volatilization (0.016 kg) were sinks for total Hg. The two major sources of CH3Hg were tributaries (0.26 kg) and net CH3Hg production in the water column (0.60 kg). Flux from sediments accounted for only 0.017 kg CH3Hg. Net sedimentation (0.47 kg), outflow (0.24 kg), and net uptake, by fish (0.20 kg) were sinks for CH3Hg. Gross sedimentation of CH3Hg exceeded net sedimentation by 90%, suggesting that release of CH3Hg from settling particles is a significant process.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01189701
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...