|
rdf:type |
|
|
lifeskim:mentions |
|
|
pubmed:issue |
9
|
|
pubmed:dateCreated |
2002-9-20
|
|
pubmed:abstractText |
Insulin receptor null mutant mice develop severe diabetes, ketoacidosis and liver steatosis and die within 1 week after birth. Since the liver plays an essential role in the control of glucose homeostasis, we examined in this work whether the metabolic disorders of insulin receptor-deficient mice could be improved upon restoration of hepatic glucose metabolism by transgenic constitutive overexpression of glucokinase selectively in the liver.
|
|
pubmed:language |
eng
|
|
pubmed:journal |
|
|
pubmed:citationSubset |
IM
|
|
pubmed:chemical |
|
|
pubmed:status |
MEDLINE
|
|
pubmed:month |
Sep
|
|
pubmed:issn |
0012-186X
|
|
pubmed:author |
|
|
pubmed:issnType |
Print
|
|
pubmed:volume |
45
|
|
pubmed:owner |
NLM
|
|
pubmed:authorsComplete |
Y
|
|
pubmed:pagination |
1292-7
|
|
pubmed:dateRevised |
2009-11-19
|
|
pubmed:meshHeading |
pubmed-meshheading:12242462-Animals,
pubmed-meshheading:12242462-Base Sequence,
pubmed-meshheading:12242462-Blood Glucose,
pubmed-meshheading:12242462-Cloning, Molecular,
pubmed-meshheading:12242462-Crosses, Genetic,
pubmed-meshheading:12242462-DNA, Complementary,
pubmed-meshheading:12242462-Diabetic Ketoacidosis,
pubmed-meshheading:12242462-Glucokinase,
pubmed-meshheading:12242462-Glucose Tolerance Test,
pubmed-meshheading:12242462-Glycosuria,
pubmed-meshheading:12242462-Homozygote,
pubmed-meshheading:12242462-Humans,
pubmed-meshheading:12242462-Liver,
pubmed-meshheading:12242462-Mice,
pubmed-meshheading:12242462-Mice, Knockout,
pubmed-meshheading:12242462-Mice, Transgenic,
pubmed-meshheading:12242462-Organ Specificity,
pubmed-meshheading:12242462-Phenylalanine Hydroxylase,
pubmed-meshheading:12242462-Promoter Regions, Genetic,
pubmed-meshheading:12242462-Rats,
pubmed-meshheading:12242462-Receptor, Insulin,
pubmed-meshheading:12242462-Reverse Transcriptase Polymerase Chain Reaction
|
|
pubmed:year |
2002
|
|
pubmed:articleTitle |
Improved metabolic disorders of insulin receptor-deficient mice by transgenic overexpression of glucokinase in the liver.
|
|
pubmed:affiliation |
Department of Genetics, Development and Molecular Pathology, Cochin Institute, INSERM, CNRS, University of René Decartes, Paris, France.
|
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|
