Linked Life Data

18924245

Source:http://linkedlifedata.com/resource/pubmed/id/18924245

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2008-11-4
pubmed:abstractText
There is controversy regarding whether fructose in liquid beverages constitutes another dietary ingredient of high caloric density or introduces qualitative changes in energy metabolism that further facilitate the appearance of metabolic diseases. Central to this issue is the elucidation of the molecular mechanism responsible for the metabolic alterations induced by fructose ingestion. Fructose administration (10% wt/vol) in the drinking water of Sprague-Dawley male rats for 14 days induced hyperleptinemia and hepatic leptin resistance. This was caused by impairment of the leptin-signal transduction mediated by both janus-activated kinase-2 and the mitogen-activated protein kinase pathway. The subsequent increase in activity in the liver of the unphosphorylated and active form of the forkhead box O1 nuclear factor, which transrepresses peroxisome proliferator-activated receptor alpha activity, and a lack of activation of the adenosine monophosphate-activated protein kinase, led to hypertriglyceridemia and hepatic steatosis. These alterations are attributable to two key events: (1) an increase in the amount of suppressor of cytokine signaling-3 protein, which blocks the phosphorylation and activation of janus-activated kinase-2 and Tyr(985) on the long form of the leptin receptor; and (2) a common deficit of phosphorylation in serine/threonine residues of key proteins in leptin-signal transduction pathways. The latter is probably produced by the early activation of protein phosphatase 2A, and further sustained by the accumulation in liver tissue of ceramide, an activator of protein phosphatase 2A, due to incomplete oxidation of fatty acids. CONCLUSION: Our data indicate that fructose ingestion as a liquid solution induces qualitative changes in liver metabolism that lead to metabolic diseases.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
1527-3350
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
48
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1506-16
pubmed:meshHeading
pubmed-meshheading:18924245-Adenine Phosphoribosyltransferase, pubmed-meshheading:18924245-Adiponectin, pubmed-meshheading:18924245-Animals, pubmed-meshheading:18924245-Carcinoma, Hepatocellular, pubmed-meshheading:18924245-Cell Line, Tumor, pubmed-meshheading:18924245-Enzyme Activation, pubmed-meshheading:18924245-Fructose, pubmed-meshheading:18924245-Glucose, pubmed-meshheading:18924245-Leptin, pubmed-meshheading:18924245-Liver, pubmed-meshheading:18924245-Liver Neoplasms, pubmed-meshheading:18924245-Male, pubmed-meshheading:18924245-Phosphoproteins, pubmed-meshheading:18924245-Phosphoserine, pubmed-meshheading:18924245-Phosphothreonine, pubmed-meshheading:18924245-Polymerase Chain Reaction, pubmed-meshheading:18924245-Rats, pubmed-meshheading:18924245-Rats, Sprague-Dawley, pubmed-meshheading:18924245-Signal Transduction, pubmed-meshheading:18924245-Suppressor of Cytokine Signaling Proteins
pubmed:year
2008
pubmed:articleTitle
Suppressor of cytokine signaling-3 (SOCS-3) and a deficit of serine/threonine (Ser/Thr) phosphoproteins involved in leptin transduction mediate the effect of fructose on rat liver lipid metabolism.
pubmed:affiliation
Department of Pharmacology and Therapeutic Chemistry, School of Pharmacy, University of Barcelona, Barcelona, Spain.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't