| pubmed-article:10512363 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:10512363 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:10512363 | lifeskim:mentions | umls-concept:C0332281 | lld:lifeskim |
| pubmed-article:10512363 | lifeskim:mentions | umls-concept:C0013682 | lld:lifeskim |
| pubmed-article:10512363 | lifeskim:mentions | umls-concept:C0392756 | lld:lifeskim |
| pubmed-article:10512363 | lifeskim:mentions | umls-concept:C1256369 | lld:lifeskim |
| pubmed-article:10512363 | lifeskim:mentions | umls-concept:C0205349 | lld:lifeskim |
| pubmed-article:10512363 | pubmed:issue | 10 | lld:pubmed |
| pubmed-article:10512363 | pubmed:dateCreated | 1999-10-19 | lld:pubmed |
| pubmed-article:10512363 | pubmed:abstractText | Recent studies have shown that genetic deficiency of the adipocyte fatty acid-binding protein (aP2) results in minor alterations of plasma lipids and adipocyte development but provides significant protection from dietary obesity-induced hyperinsulinemia and insulin resistance. To identify potential mechanisms responsible for this phenotype, we examined lipolysis and insulin secretion in aP2-/- mice. Beta-adrenergic stimulation resulted in a blunted rise of blood glycerol levels in aP2-/- compared with aP2+/+ mice, suggesting diminished lipolysis in aP2-/- adipocytes. Confirming this, primary adipocytes isolated from aP2-/- mice showed attenuated glycerol and free fatty acid (FFA) release in response to dibutyryl cAMP. The decreased lipolytic response seen in the aP2-/- mice was not associated with altered expression levels of hormone-sensitive lipase or perilipin. The acute insulin secretory response to beta-adrenergic stimulation was also profoundly suppressed in aP2-/- mice despite comparable total concentrations and only minor changes in the composition of systemic FFAs. To address whether levels of specific fatty acids are different in aP2-/- mice, the plasma FFA profile after beta-adrenergic stimulation was determined. Significant reduction in both stearic and cis-11-eicoseneic acids and an increase in palmitoleic acid were observed. The response of aP2-/- mice to other insulin secretagogues such as arginine and glyburide was similar to that of aP2+/+ mice, arguing against generally impaired function of pancreatic beta-cells. Finally, no aP2 expression was detected in isolated pancreatic islet cells. These results provide support for the existence of an adipo-pancreatic axis, the proper action of which relies on the presence of aP2. Consequently, aP2's role in the pathogenesis of type 2 diabetes might involve regulation of both hyperinsulinemia and insulin resistance through its impact on both lipolysis and insulin secretion. | lld:pubmed |
| pubmed-article:10512363 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10512363 | pubmed:language | eng | lld:pubmed |
| pubmed-article:10512363 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:10512363 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:10512363 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:10512363 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:10512363 | pubmed:issn | 0012-1797 | lld:pubmed |
| pubmed-article:10512363 | pubmed:author | pubmed-author:MorganMM | lld:pubmed |
| pubmed-article:10512363 | pubmed:author | pubmed-author:MeyersD SDS | lld:pubmed |
| pubmed-article:10512363 | pubmed:author | pubmed-author:ParkerR ARA | lld:pubmed |
| pubmed-article:10512363 | pubmed:author | pubmed-author:MakowskiLL | lld:pubmed |
| pubmed-article:10512363 | pubmed:author | pubmed-author:HotamisligilG... | lld:pubmed |
| pubmed-article:10512363 | pubmed:author | pubmed-author:SchejaLL | lld:pubmed |
| pubmed-article:10512363 | pubmed:author | pubmed-author:UysalK TKT | lld:pubmed |
| pubmed-article:10512363 | pubmed:author | pubmed-author:WiesbrockS... | lld:pubmed |
| pubmed-article:10512363 | pubmed:author | pubmed-author:ShimshekD RDR | lld:pubmed |
| pubmed-article:10512363 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:10512363 | pubmed:volume | 48 | lld:pubmed |
| pubmed-article:10512363 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:10512363 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:10512363 | pubmed:pagination | 1987-94 | lld:pubmed |
| pubmed-article:10512363 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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| pubmed-article:10512363 | pubmed:meshHeading | pubmed-meshheading:10512363... | lld:pubmed |
| pubmed-article:10512363 | pubmed:year | 1999 | lld:pubmed |
| pubmed-article:10512363 | pubmed:articleTitle | Altered insulin secretion associated with reduced lipolytic efficiency in aP2-/- mice. | lld:pubmed |
| pubmed-article:10512363 | pubmed:affiliation | Department of Nutrition, Harvard School of Public Health, Boston, Massachusetts 02115, USA. | lld:pubmed |
| pubmed-article:10512363 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:10512363 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:10512363 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| entrez-gene:11770 | entrezgene:pubmed | pubmed-article:10512363 | lld:entrezgene |
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