| pubmed-article:17988211 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17988211 | lifeskim:mentions | umls-concept:C0037083 | lld:lifeskim |
| pubmed-article:17988211 | lifeskim:mentions | umls-concept:C1711300 | lld:lifeskim |
| pubmed-article:17988211 | lifeskim:mentions | umls-concept:C0376558 | lld:lifeskim |
| pubmed-article:17988211 | lifeskim:mentions | umls-concept:C0019868 | lld:lifeskim |
| pubmed-article:17988211 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
| pubmed-article:17988211 | lifeskim:mentions | umls-concept:C0678695 | lld:lifeskim |
| pubmed-article:17988211 | lifeskim:mentions | umls-concept:C2347375 | lld:lifeskim |
| pubmed-article:17988211 | lifeskim:mentions | umls-concept:C2700613 | lld:lifeskim |
| pubmed-article:17988211 | pubmed:dateCreated | 2008-2-14 | lld:pubmed |
| pubmed-article:17988211 | pubmed:abstractText | Insulin-like signaling is critical for nutrient homeostasis, growth and survival. However, work with lower metazoans-Caenorhabditis elegans and Drosophila-shows that reduced insulin-like signaling extends life span. In addition, reduced insulin signaling in higher animals-rodents and humans-causes glucose intolerance and hyperinsulinemia that progresses to diabetes and shortens the life span of affected individuals. Hyperinsulinemia usually develops to maintain glucose homeostasis and prevent the progression toward life-threatening type 2 diabetes; however, increased circulating insulin may have negative effects on the brain that promote age-related disease. We discuss the possibility that the brain is the site where reduced insulin-like signaling can consistently extend mammalian life span-just as reduced insulin-like signaling extends the life span of lower metazoans. | lld:pubmed |
| pubmed-article:17988211 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17988211 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:17988211 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:17988211 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17988211 | pubmed:issn | 0066-4278 | lld:pubmed |
| pubmed-article:17988211 | pubmed:author | pubmed-author:WhiteMorris... | lld:pubmed |
| pubmed-article:17988211 | pubmed:author | pubmed-author:TaguchiAkikoA | lld:pubmed |
| pubmed-article:17988211 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17988211 | pubmed:volume | 70 | lld:pubmed |
| pubmed-article:17988211 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17988211 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17988211 | pubmed:pagination | 191-212 | lld:pubmed |
| pubmed-article:17988211 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
| pubmed-article:17988211 | pubmed:meshHeading | pubmed-meshheading:17988211... | lld:pubmed |
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| pubmed-article:17988211 | pubmed:meshHeading | pubmed-meshheading:17988211... | lld:pubmed |
| pubmed-article:17988211 | pubmed:year | 2008 | lld:pubmed |
| pubmed-article:17988211 | pubmed:articleTitle | Insulin-like signaling, nutrient homeostasis, and life span. | lld:pubmed |
| pubmed-article:17988211 | pubmed:affiliation | Howard Hughes Medical Institute, Division of Endocrinology, Children's Hospital Boston, Harvard Medical School, Karp Family Research Laboratories, Boston, MA 02115, USA. | lld:pubmed |
| pubmed-article:17988211 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:17988211 | pubmed:publicationType | Review | lld:pubmed |
| pubmed-article:17988211 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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