2007
DOI: 10.1016/j.urology.2007.07.057
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Localization of Increased Insulin-Like Growth Factor Binding Protein-3 in Diabetic Rat Penis: Implications for Erectile Dysfunction

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Cited by 17 publications
(24 citation statements)
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“…3,24 Soh et al reported that in diabetic rats increased IGFBP-3 expression occurs before the decrease in smooth muscle density and intracavernous pressure. 9 Enhanced IGFBP-3 expression might limit the availability of IGF-I and, thus, result in the depletion of smooth muscle density and ED in diabetic patients. 25 The beneficial effect of PDE-5 inhibitors correlates with the amount of NO in the field.…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…3,24 Soh et al reported that in diabetic rats increased IGFBP-3 expression occurs before the decrease in smooth muscle density and intracavernous pressure. 9 Enhanced IGFBP-3 expression might limit the availability of IGF-I and, thus, result in the depletion of smooth muscle density and ED in diabetic patients. 25 The beneficial effect of PDE-5 inhibitors correlates with the amount of NO in the field.…”
Section: Discussionmentioning
confidence: 99%
“…8 Soh et al also reported that enhanced expression of IGFBP-3 during a hyperglycemic period might have a key role in the development of ED in diabetic rats. 9 About 60% of interindividual variability in circulating levels of IGFBP-3 are genetically determined. 10 The gene for IGFBP-3 (OMIM 146732) is located at 7p14-p12.…”
mentioning
confidence: 99%
“…7 Insulin-like growth factor-binding protein-3 (IGFBP-3) is a member of the insulin-like growth factor (IGF) family. A previous study has shown that ED was correlated with the increased expression of IGFBP-3 in patients with diabetes mellitus, 8 suggesting a potential role for IGFBP-3 in ED. In this study, we employed 2K-1C hypertensive rats as a model to investigate the expression of IGFBP-3 at both the mRNA and protein levels in this system.…”
Section: Introductionmentioning
confidence: 95%
“…Insulin-like growth factor binding protein, which regulates the availability of insulin-like growth factor (IGF-1), is increased in hyperglycemic rats. Treatment with IGF-1 results in improvement in rat intracavernosal pressure and expression of endothelial NOsynthase [49][50][51]. Further evidence for the role of insulin resistance on endothelial NO production comes from the observation in obese rats that metformin administration induces eNos expression in penile tissue, via activated protein kinase [52].…”
Section: Endothelial Dysfunctionmentioning
confidence: 99%