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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
2
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pubmed:dateCreated |
2007-2-9
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pubmed:abstractText |
Increased production of very low-density lipoprotein (VLDL) is a critical feature of the metabolic syndrome. Here we report that a selective increase in brain glucose lowered circulating triglycerides (TG) through the inhibition of TG-VLDL secretion by the liver. We found that the effect of glucose required its conversion to lactate, leading to activation of ATP-sensitive potassium channels and to decreased hepatic activity of stearoyl-CoA desaturase-1 (SCD1). SCD1 catalyzed the synthesis of oleyl-CoA from stearoyl-CoA. Curtailing the liver activity of SCD1 was sufficient to lower the hepatic levels of oleyl-CoA and to recapitulate the effects of central glucose administration on VLDL secretion. Notably, portal infusion of oleic acid restored hepatic oleyl-CoA to control levels and negated the effects of both central glucose and SCD1 deficiency on TG-VLDL secretion. These central effects of glucose (but not those of lactate) were rapidly lost in diet-induced obesity. These findings indicate that a defect in brain glucose sensing could play a critical role in the etiology of the metabolic syndrome.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
1078-8956
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
13
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
171-80
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:17273170-Animals,
pubmed-meshheading:17273170-Blotting, Western,
pubmed-meshheading:17273170-Brain,
pubmed-meshheading:17273170-DNA Primers,
pubmed-meshheading:17273170-Dose-Response Relationship, Drug,
pubmed-meshheading:17273170-Glucose,
pubmed-meshheading:17273170-Insulin,
pubmed-meshheading:17273170-Insulin Resistance,
pubmed-meshheading:17273170-Lipoproteins, VLDL,
pubmed-meshheading:17273170-Liver,
pubmed-meshheading:17273170-Male,
pubmed-meshheading:17273170-Metabolic Syndrome X,
pubmed-meshheading:17273170-Obesity,
pubmed-meshheading:17273170-Oxamic Acid,
pubmed-meshheading:17273170-Rats,
pubmed-meshheading:17273170-Rats, Sprague-Dawley,
pubmed-meshheading:17273170-Sodium Lactate,
pubmed-meshheading:17273170-Somatostatin,
pubmed-meshheading:17273170-Stearoyl-CoA Desaturase,
pubmed-meshheading:17273170-Triglycerides
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pubmed:year |
2007
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pubmed:articleTitle |
Brain glucose metabolism controls the hepatic secretion of triglyceride-rich lipoproteins.
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pubmed:affiliation |
Department of Medicine, Diabetes Research Center, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, New York 10461, USA.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, N.I.H., Extramural
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