Source:http://linkedlifedata.com/resource/pubmed/id/11246886
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
3
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pubmed:dateCreated |
2001-3-14
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pubmed:abstractText |
Apolipoprotein A-II (apoA-II) is the second most abundant protein in HDLs. Genetic studies in humans have provided evidence of linkage of the apoA-II gene locus to plasma free fatty acid (FFA) levels and to type 2 diabetes, and transgenic mice overexpressing mouse apoA-II have elevated levels of both FFA and triglycerides. We now show that apoA-II promotes insulin resistance and has diverse effects on fat homeostasis. ApoA-II transgenic mice have increased adipose mass and higher plasma leptin levels than C57BL/6J control mice. Fasting glucose levels were similar between apoA-II transgenic and control mice, but plasma insulin levels were elevated approximately twofold in the apoA-II transgenic mice. Compared with control mice, apoA-II transgenic mice exhibited a delay in plasma clearance of a glucose bolus. Adipose tissue isolated from fasted apoA-II transgenic mice exhibited a 50% decrease in triglyceride hydrolysis compared with adipose tissue from control mice. This is consistent with a normal response of adipose tissue to the increased insulin levels in the apoA-II transgenic mice and may partially explain the increased fat deposition. Skeletal muscle isolated from fasted apoA-II transgenic mice exhibited reduced uptake of 2-deoxyglucose compared with muscles isolated from control mice. Our observations indicate that a primary disturbance in lipoprotein metabolism can result in several traits associated with insulin resistance, consistent with the hypothesis that insulin resistance and type 2 diabetes can, under certain circumstances, be related primarily to altered lipid metabolism rather than glucose metabolism.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Apolipoprotein A-II,
http://linkedlifedata.com/resource/pubmed/chemical/Blood Glucose,
http://linkedlifedata.com/resource/pubmed/chemical/Deoxyglucose,
http://linkedlifedata.com/resource/pubmed/chemical/Lipoproteins, HDL,
http://linkedlifedata.com/resource/pubmed/chemical/Triglycerides
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0012-1797
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
50
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
643-51
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:11246886-Adipose Tissue,
pubmed-meshheading:11246886-Animals,
pubmed-meshheading:11246886-Apolipoprotein A-II,
pubmed-meshheading:11246886-Blood Glucose,
pubmed-meshheading:11246886-Deoxyglucose,
pubmed-meshheading:11246886-Fasting,
pubmed-meshheading:11246886-Hydrolysis,
pubmed-meshheading:11246886-Insulin Resistance,
pubmed-meshheading:11246886-Lipoproteins, HDL,
pubmed-meshheading:11246886-Mice,
pubmed-meshheading:11246886-Mice, Inbred C57BL,
pubmed-meshheading:11246886-Mice, Transgenic,
pubmed-meshheading:11246886-Muscle, Skeletal,
pubmed-meshheading:11246886-Reference Values,
pubmed-meshheading:11246886-Triglycerides
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pubmed:year |
2001
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pubmed:articleTitle |
Studies with apolipoprotein A-II transgenic mice indicate a role for HDLs in adiposity and insulin resistance.
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pubmed:affiliation |
Department of Medicine, University of California, Los Angeles 90095, USA. lcastellani@mednet.ucla.edu
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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