Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
33
pubmed:dateCreated
2005-8-15
pubmed:abstractText
Type 2 diabetics have an increased risk of developing atherosclerosis, suggesting the mechanisms that cause this disease are enhanced by insulin resistance. In this study we examined the effects of gene knock-out (KO) of lipocalin-type prostaglandin D(2) synthase (L-PGDS), a protein found at elevated levels in type 2 diabetics, on diet-induced glucose tolerance and atherosclerosis. Our results show that L-PGDS KO mice become glucose-in-tolerant and insulin-resistant at an accelerated rate when compared with the C57BL/6 control strain. Adipocytes were significantly larger in the L-PGDS KO mice compared with controls on the same diets. Cell culture data revealed significant differences between insulin-stimulated mitogen-activated protein kinase phosphatase-2, protein-tyrosine phosphatase-1D, and phosphorylated focal adhesion kinase expression levels in L-PGDS KO vascular smooth muscle cells and controls. In addition, only the L-PGDS KO mice developed nephropathy and an aortic thickening reminiscent to the early stages of atherosclerosis when fed a "diabetogenic" high fat diet. We conclude that L-PGDS plays an important role regulating insulin sensitivity and atherosclerosis in type 2 diabetes and may represent a novel model of insulin resistance, atherosclerosis, and diabetic nephropathy.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Adiponectin, http://linkedlifedata.com/resource/pubmed/chemical/Blood Glucose, http://linkedlifedata.com/resource/pubmed/chemical/Focal Adhesion Kinase 1, http://linkedlifedata.com/resource/pubmed/chemical/Focal Adhesion Protein-Tyrosine..., http://linkedlifedata.com/resource/pubmed/chemical/Insulin, http://linkedlifedata.com/resource/pubmed/chemical/Intercellular Signaling Peptides..., http://linkedlifedata.com/resource/pubmed/chemical/Intramolecular Oxidoreductases, http://linkedlifedata.com/resource/pubmed/chemical/Lipocalins, http://linkedlifedata.com/resource/pubmed/chemical/Protein Phosphatase 2, http://linkedlifedata.com/resource/pubmed/chemical/Protein Tyrosine Phosphatases, http://linkedlifedata.com/resource/pubmed/chemical/Protein-Tyrosine Kinases, http://linkedlifedata.com/resource/pubmed/chemical/Ptk2 protein, mouse, http://linkedlifedata.com/resource/pubmed/chemical/prostaglandin R2 D-isomerase
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
19
pubmed:volume
280
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
29946-55
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:15970590-Adipocytes, pubmed-meshheading:15970590-Adiponectin, pubmed-meshheading:15970590-Animals, pubmed-meshheading:15970590-Arteriosclerosis, pubmed-meshheading:15970590-Blood Glucose, pubmed-meshheading:15970590-Diabetic Nephropathies, pubmed-meshheading:15970590-Focal Adhesion Kinase 1, pubmed-meshheading:15970590-Focal Adhesion Protein-Tyrosine Kinases, pubmed-meshheading:15970590-Glucose Intolerance, pubmed-meshheading:15970590-Insulin, pubmed-meshheading:15970590-Insulin Resistance, pubmed-meshheading:15970590-Intercellular Signaling Peptides and Proteins, pubmed-meshheading:15970590-Intramolecular Oxidoreductases, pubmed-meshheading:15970590-Lipocalins, pubmed-meshheading:15970590-Male, pubmed-meshheading:15970590-Mice, pubmed-meshheading:15970590-Mice, Inbred C57BL, pubmed-meshheading:15970590-Mice, Knockout, pubmed-meshheading:15970590-Protein Phosphatase 2, pubmed-meshheading:15970590-Protein Tyrosine Phosphatases, pubmed-meshheading:15970590-Protein-Tyrosine Kinases
pubmed:year
2005
pubmed:articleTitle
Accelerated glucose intolerance, nephropathy, and atherosclerosis in prostaglandin D2 synthase knock-out mice.
pubmed:affiliation
Vascular Biology Laboratory, Winthrop-University Hospital, Mineola, New York 11501, USA. lragolia@winthrop.org
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural