Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2001-8-27
pubmed:abstractText
Insulin resistance and its dreaded consequence, type 2 diabetes, are major causes of atherosclerosis. Adiponectin is an adipose-specific plasma protein that possesses anti-atherogenic properties, such as the suppression of adhesion molecule expression in vascular endothelial cells and cytokine production from macrophages. Plasma adiponectin concentrations are decreased in obese and type 2 diabetic subjects with insulin resistance. A regimen that normalizes or increases the plasma adiponectin might prevent atherosclerosis in patients with insulin resistance. In this study, we demonstrate the inducing effects of thiazolidinediones (TZDs), which are synthetic PPARgamma ligands, on the expression and secretion of adiponectin in humans and rodents in vivo and in vitro. The administration of TZDs significantly increased the plasma adiponectin concentrations in insulin resistant humans and rodents without affecting their body weight. Adiponectin mRNA expression was normalized or increased by TZDs in the adipose tissues of obese mice. In cultured 3T3-L1 adipocytes, TZD derivatives enhanced the mRNA expression and secretion of adiponectin in a dose- and time-dependent manner. Furthermore, these effects were mediated through the activation of the promoter by the TZDs. On the other hand, TNF-alpha, which is produced more in an insulin-resistant condition, dose-dependently reduced the expression of adiponectin in adipocytes by suppressing its promoter activity. TZDs restored this inhibitory effect by TNF-alpha. TZDs might prevent atherosclerotic vascular disease in insulin-resistant patients by inducing the production of adiponectin through direct effect on its promoter and antagonizing the effect of TNF-alpha on the adiponectin promoter.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0012-1797
pubmed:author
pubmed:issnType
Print
pubmed:volume
50
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2094-9
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:11522676-3T3 Cells, pubmed-meshheading:11522676-Adipocytes, pubmed-meshheading:11522676-Adiponectin, pubmed-meshheading:11522676-Adipose Tissue, pubmed-meshheading:11522676-Animals, pubmed-meshheading:11522676-Blood, pubmed-meshheading:11522676-Female, pubmed-meshheading:11522676-Humans, pubmed-meshheading:11522676-Intercellular Signaling Peptides and Proteins, pubmed-meshheading:11522676-Ligands, pubmed-meshheading:11522676-Male, pubmed-meshheading:11522676-Mice, pubmed-meshheading:11522676-Mice, Inbred C57BL, pubmed-meshheading:11522676-Middle Aged, pubmed-meshheading:11522676-Osmolar Concentration, pubmed-meshheading:11522676-Proteins, pubmed-meshheading:11522676-Receptors, Cytoplasmic and Nuclear, pubmed-meshheading:11522676-Thiazoles, pubmed-meshheading:11522676-Thiazolidinediones, pubmed-meshheading:11522676-Transcription Factors, pubmed-meshheading:11522676-Tumor Necrosis Factor-alpha
pubmed:year
2001
pubmed:articleTitle
PPARgamma ligands increase expression and plasma concentrations of adiponectin, an adipose-derived protein.
pubmed:affiliation
Department of Internal Medicine and Molecular Science (B5), Graduate School of Medicine, Osaka University, Osaka, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't