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http://purl.uniprot.org/citations/17762172 | http://www.w3.org/2000/01/rdf-schema#comment | "Glycosuria is one of the well-documented characteristics in ClC-5 knockout (KO) mice and patients with Dent's disease. However, the underlying pathophysiology of its occurrence is unknown. In this study, we have compared ClC-5 KO mice with age and gender matched wild-type (WT) control mice to investigate if the underlying cause of manifested glycosuria is an impairment of glucose homeostasis and/or an alteration in expression levels of proximal tubule (PT) glucose transporters. We observed that, the blood glucose concentration (n=12, p<0.01) and the fractional excretion of glucose and insulin (n=6, p<0.05) were higher in KO mice. In contrast, the fasting blood glucose levels (n=7) were not significantly different in the two groups. Plasma glucose increased to a greater extent in KO mice (n=7, p<0.05) when challenged by an intraperitoneal injection of glucose. However, no peripheral tissue insulin resistance was observed following an intraperitoneal injection of insulin (n=9) in the KO mice. ELISA analysis demonstrated low plasma insulin concentrations after a 12 hour fasting period and also following glucose injection in KO mice. The total insulin released during a 2 hour period following glucose challenge was significantly lower in KO mice (n=6, p<0.05). By western blot, we observed a significant decrease in GLUT2 protein expression levels in isolated PT ((n=10, p<0.01)) of KO mice. This decrease in protein levels was corroborated by a significant decrease in GLUT2 mRNA levels estimated semi quantitatively by RT-PCR in isolated PT (n=10, p<0.01). No significant changes in mRNA expression levels of SGLT2, SGLT1 and GLUT1, as analyzed by RT-PCR, could be detected in the isolated PT (n=10). Also, we have shown by western blot analysis that expression of megalin is lower in the renal cortex of KO mice when compared to WT mice (n=3, p<0.05). Our results suggest that low plasma insulin concentration together with renal function changes observed in KO mice significantly contribute towards the glucose intolerance and documented glycosuria observed in this animal."xsd:string |
http://purl.uniprot.org/citations/17762172 | http://purl.org/dc/terms/identifier | "doi:10.1159/000107529"xsd:string |
http://purl.uniprot.org/citations/17762172 | http://purl.uniprot.org/core/author | "Guggino W.B."xsd:string |
http://purl.uniprot.org/citations/17762172 | http://purl.uniprot.org/core/author | "Tukaye D.N."xsd:string |
http://purl.uniprot.org/citations/17762172 | http://purl.uniprot.org/core/author | "Guggino S.E."xsd:string |
http://purl.uniprot.org/citations/17762172 | http://purl.uniprot.org/core/author | "Morales M.M."xsd:string |
http://purl.uniprot.org/citations/17762172 | http://purl.uniprot.org/core/author | "Souza-Menezes J."xsd:string |
http://purl.uniprot.org/citations/17762172 | http://purl.uniprot.org/core/date | "2007"xsd:gYear |
http://purl.uniprot.org/citations/17762172 | http://purl.uniprot.org/core/name | "Cell Physiol Biochem"xsd:string |
http://purl.uniprot.org/citations/17762172 | http://purl.uniprot.org/core/pages | "455-464"xsd:string |
http://purl.uniprot.org/citations/17762172 | http://purl.uniprot.org/core/title | "Absence of ClC5 in knockout mice leads to glycosuria, impaired renal glucose handling and low proximal tubule GLUT2 protein expression."xsd:string |
http://purl.uniprot.org/citations/17762172 | http://purl.uniprot.org/core/volume | "20"xsd:string |
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