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
    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
  • 2
    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
  • 3
    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
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...