Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2004-1-23
pubmed:abstractText
High-fructose feeding causes diet-induced alterations of lipid metabolism and decreased insulin sensitivity with alterations of hepatic pyruvate dehydrogenase and hepatic very low-density lipoprotein secretion. Inflammatory cytokines also induce dramatic changes in lipid metabolism, particularly in serum triglycerides via increased hepatic secretion and/or delayed clearance of very low-density lipoprotein. The aim of this study was to determine whether the mechanism of lipid dysregulation in the high-fructose diet is induced by stress response pathways. Animals were fed a high-fructose diet for 14 d to establish hypertriglyceridemia and then were treated with lipoxygenase inhibitors for 4 d concurrent with the diet. At the end of drug treatment, the animals were divided into two groups and treated with lipopolysaccharide or a vehicle. Serum samples were taken pretreatment and posttreatment, and liver tissue was harvested at the end of study. Serum samples were tested for metabolic parameters, and the tissue samples were tested for metabolic and stress pathway responses. Our results show that fructose-fed rats have changes in the c-Jun N-terminal kinase pathway with correspondingly elevated activator protein-1 activity, consistent with an inflammatory response. Treatment with lipoxygenase inhibitors reversed the hypertriglyceridemia and also reduced activator protein-1 activation, suggesting that the basis for lipid dysregulation in this model is due to activation of inflammatory pathways in the liver.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0013-7227
pubmed:author
pubmed:issnType
Print
pubmed:volume
145
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
548-55
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:14576175-Acute-Phase Reaction, pubmed-meshheading:14576175-Animals, pubmed-meshheading:14576175-Corticosterone, pubmed-meshheading:14576175-Dietary Carbohydrates, pubmed-meshheading:14576175-Fructose, pubmed-meshheading:14576175-Hypercholesterolemia, pubmed-meshheading:14576175-Hypertriglyceridemia, pubmed-meshheading:14576175-JNK Mitogen-Activated Protein Kinases, pubmed-meshheading:14576175-Lipid Metabolism, pubmed-meshheading:14576175-Lipid Peroxidation, pubmed-meshheading:14576175-Lipopolysaccharides, pubmed-meshheading:14576175-Lipoproteins, VLDL, pubmed-meshheading:14576175-Lipoxygenase Inhibitors, pubmed-meshheading:14576175-Liver, pubmed-meshheading:14576175-Male, pubmed-meshheading:14576175-Mitogen-Activated Protein Kinases, pubmed-meshheading:14576175-Pyruvate Dehydrogenase Complex, pubmed-meshheading:14576175-Rats, pubmed-meshheading:14576175-Rats, Sprague-Dawley, pubmed-meshheading:14576175-Thiobarbituric Acid Reactive Substances
pubmed:year
2004
pubmed:articleTitle
High dietary fructose induces a hepatic stress response resulting in cholesterol and lipid dysregulation.
pubmed:affiliation
Insmed Incorporated, 4851 Lake Brook Drive, Glen Allen, VA 23058, USA. gkelley@insmed.com
pubmed:publicationType
Journal Article