Source:http://linkedlifedata.com/resource/pubmed/id/14651962
Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
|
pubmed:dateCreated |
2003-12-3
|
pubmed:abstractText |
Adiponectin is an adipocyte-derived hormone best known for its insulin-sensitizing ability. The expression and circulating concentration of adiponectin are decreased in type 2 diabetics and increase following treatment with thiazolidinediones. Endothelin-1 (ET-1) is a potent vasoconstrictor peptide whose levels are elevated in numerous disease states, including obesity and diabetes. ET-1 has profound effects on adipose tissue metabolism and alters the release of adipose-derived factors such as leptin and resistin, therefore we investigated the role of ET-1 in adiponectin secretion. 3T3-L1 adipocytes were treated with insulin (100 nM), ET-1 (100 nM), or the appropriate vehicle and adiponectin secretion into the media was determined by immunoblotting and densitometric analysis. Adiponectin secretion significantly increased 1h following insulin or ET-1 treatment, respectively. Pretreatment with ET-1 for 24h significantly inhibited the ability of insulin or ET-1 to acutely stimulate adiponectin secretion. The specific ET(A) receptor antagonist, BQ-610 (1 microM), significantly inhibited ET-1-stimulated adiponectin secretion. In summary, ET-1 acutely stimulates adiponectin secretion through the ET(A) receptor. Chronic exposure to ET-1 dramatically decreases the stimulatory effect of insulin and ET-1 on adiponectin secretion. Our findings suggest vascular factors such as ET-1 may play a role in the regulation of adiponectin secretion and whole body energy metabolism.
|
pubmed:grant | |
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
IM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adiponectin,
http://linkedlifedata.com/resource/pubmed/chemical/Endothelin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Insulin,
http://linkedlifedata.com/resource/pubmed/chemical/Intercellular Signaling Peptides...,
http://linkedlifedata.com/resource/pubmed/chemical/Proteins
|
pubmed:status |
MEDLINE
|
pubmed:month |
Dec
|
pubmed:issn |
0006-291X
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:day |
26
|
pubmed:volume |
312
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
945-9
|
pubmed:dateRevised |
2011-11-17
|
pubmed:meshHeading |
pubmed-meshheading:14651962-3T3-L1 Cells,
pubmed-meshheading:14651962-Adaptation, Physiological,
pubmed-meshheading:14651962-Adiponectin,
pubmed-meshheading:14651962-Animals,
pubmed-meshheading:14651962-Cell Differentiation,
pubmed-meshheading:14651962-Endothelin-1,
pubmed-meshheading:14651962-Gene Expression Regulation,
pubmed-meshheading:14651962-Insulin,
pubmed-meshheading:14651962-Intercellular Signaling Peptides and Proteins,
pubmed-meshheading:14651962-Mice,
pubmed-meshheading:14651962-Proteins,
pubmed-meshheading:14651962-Signal Transduction
|
pubmed:year |
2003
|
pubmed:articleTitle |
Regulation of adiponectin secretion by endothelin-1.
|
pubmed:affiliation |
Department of Anatomy, Physiology and Pharmacology, College of Veterinary Medicine, Auburn University, Auburn, AL 36849-5518, USA.
|
pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|