Linked Life Data

14681834

Source:http://linkedlifedata.com/resource/pubmed/id/14681834

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2003-12-18
pubmed:abstractText
The mechanism underlying hypertriglyceridemia-associated insulin resistance in humans remains poorly understood. It has been proposed that hypertriglyceridemia only produces insulin resistance when associated with an increased lipid delivery to muscle. Accordingly, hypertriglyceridemia secondary to a decreased clearance of triglyceride-rich particles should not cause insulin resistance. To verify this hypothesis, we assessed whole body and adipose tissue insulin sensitivity in 15 healthy male volunteers before and after a 5-day administration of isotretinoin (1 mg/kg/d), a vitamin A derivative that decreases the clearance of triglyceride-rich particles. Whole body insulin-mediated glucose disposal (6,6 (2)H(2)glucose), glucose oxidation (indirect calorimetry), lipolysis ((2)H(5) glycerol), and subcutaneous adipose lipolysis (microdialysis) were evaluated during a 3-step hyperinsulinemic euglycemic clamp. Isotretinoin increased plasma triglyceride from 0.97 +/- 0.15 to 1.30 +/- 0.22 mmol/L (P <.02), but did not change whole body insulin-mediated glucose disposal and lipolysis. These observations are consistent with an isotretinoin-induced inhibition of very-low-density lipoprotein (VLDL)-triglyceride clearance. The suppression of endogenous glucose production and the reduction in subcutaneous adipose glycerol concentrations by insulin remained equally unaffected after isotretinoin administration. We conclude that the impaired clearance of triglyceride-rich particles secondary to a 5-day isotretinoin administration does not impair insulin-mediated antilipolysis or glucose disposal. The data support the concept that hypertriglyceridemia-associated insulin resistance develops primarily when triglyceride production is increased.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0026-0495
pubmed:author
pubmed:issnType
Print
pubmed:volume
53
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4-10
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:14681834-Adipose Tissue, pubmed-meshheading:14681834-Adult, pubmed-meshheading:14681834-Blood Glucose, pubmed-meshheading:14681834-Calorimetry, Indirect, pubmed-meshheading:14681834-Deuterium, pubmed-meshheading:14681834-Epinephrine, pubmed-meshheading:14681834-Fasting, pubmed-meshheading:14681834-Glucose Clamp Technique, pubmed-meshheading:14681834-Glycerol, pubmed-meshheading:14681834-Humans, pubmed-meshheading:14681834-Hypertriglyceridemia, pubmed-meshheading:14681834-Insulin, pubmed-meshheading:14681834-Insulin Resistance, pubmed-meshheading:14681834-Isotretinoin, pubmed-meshheading:14681834-Kinetics, pubmed-meshheading:14681834-Lipolysis, pubmed-meshheading:14681834-Lipoproteins, VLDL, pubmed-meshheading:14681834-Male, pubmed-meshheading:14681834-Microdialysis, pubmed-meshheading:14681834-Oxidation-Reduction, pubmed-meshheading:14681834-Triglycerides
pubmed:year
2004
pubmed:articleTitle
Short-term administration of isotretinoin elevates plasma triglyceride concentrations without affecting insulin sensitivity in healthy humans.
pubmed:affiliation
Institute of Physiology, University of Lausanne School of Medicine, Switzerland.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't