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| http://purl.uniprot.org/citations/15554902 | http://www.w3.org/2000/01/rdf-schema#comment | "The liver plays an important role in insulin-regulated glucose homoeostasis. To study the function of the PDK1 (3-phosphoinositide-dependent protein kinase-1) signalling pathway in mediating insulin's actions in the liver, we employed CRE recombinase/loxP technology to generate L(liver)-PDK1-/-mice, which lack expression of PDK1 in hepatocytes and in which insulin failed to induce activation of PKB in liver. The L-PDK1-/-mice were not insulin-intolerant, possessed normal levels of blood glucose and insulin under normal feeding conditions, but were markedly glucose-intolerant when injected with glucose. The L-PDK1-/-mice also possessed 10-fold lower levels of hepatic glycogen compared with control littermates, and were unable to normalize their blood glucose levels within 2 h after injection of insulin. The glucose intolerance of the L-PDK1-/-mice may be due to an inability of glucose to suppress hepatic glucose output through the gluconeogenic pathway, since the mRNA encoding hepatic PEPCK (phosphoenolpyruvate carboxykinase), G6Pase (glucose-6-phosphatase) and SREBP1 (sterol-regulatory-element-binding protein 1), which regulate gluconeogenesis, are no longer controlled by feeding. Furthermore, three other insulin-controlled genes, namely IGFBP1 (insulin-like-growth-factor-binding protein-1), IRS2 (insulin receptor substrate 2) and glucokinase, were regulated abnormally by feeding in the liver of PDK1-deficient mice. Finally, the L-PDK1-/-mice died between 4-16 weeks of age due to liver failure. These results establish that the PDK1 signalling pathway plays an important role in regulating glucose homoeostasis and controlling expression of insulin-regulated genes. They suggest that a deficiency of the PDK1 pathway in the liver could contribute to development of diabetes, as well as to liver failure."xsd:string |
| http://purl.uniprot.org/citations/15554902 | http://purl.org/dc/terms/identifier | "doi:10.1042/bj20041782"xsd:string |
| http://purl.uniprot.org/citations/15554902 | http://purl.uniprot.org/core/author | "Alessi D.R."xsd:string |
| http://purl.uniprot.org/citations/15554902 | http://purl.uniprot.org/core/author | "Mora A."xsd:string |
| http://purl.uniprot.org/citations/15554902 | http://purl.uniprot.org/core/author | "Sutherland C."xsd:string |
| http://purl.uniprot.org/citations/15554902 | http://purl.uniprot.org/core/author | "Tronche F."xsd:string |
| http://purl.uniprot.org/citations/15554902 | http://purl.uniprot.org/core/author | "Lipina C."xsd:string |
| http://purl.uniprot.org/citations/15554902 | http://purl.uniprot.org/core/date | "2005"xsd:gYear |
| http://purl.uniprot.org/citations/15554902 | http://purl.uniprot.org/core/name | "Biochem J"xsd:string |
| http://purl.uniprot.org/citations/15554902 | http://purl.uniprot.org/core/pages | "639-648"xsd:string |
| http://purl.uniprot.org/citations/15554902 | http://purl.uniprot.org/core/title | "Deficiency of PDK1 in liver results in glucose intolerance, impairment of insulin-regulated gene expression and liver failure."xsd:string |
| http://purl.uniprot.org/citations/15554902 | http://purl.uniprot.org/core/volume | "385"xsd:string |
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