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N-acylethanolamine signalling mediates the effect of diet on lifespan in Caenorhabditis elegans

Mark Lucanic, Jason M. Held, Maithili C. Vantipalli, Ida M. Klang, Jill B. Graham, Bradford W. Gibson, Gordon J. Lithgow and Matthew S. Gill ()
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Mark Lucanic: Buck Institute for Research on Aging, 8001 Redwood Boulevard
Jason M. Held: Buck Institute for Research on Aging, 8001 Redwood Boulevard
Maithili C. Vantipalli: Buck Institute for Research on Aging, 8001 Redwood Boulevard
Ida M. Klang: Buck Institute for Research on Aging, 8001 Redwood Boulevard
Jill B. Graham: Buck Institute for Research on Aging, 8001 Redwood Boulevard
Bradford W. Gibson: Buck Institute for Research on Aging, 8001 Redwood Boulevard
Gordon J. Lithgow: Buck Institute for Research on Aging, 8001 Redwood Boulevard
Matthew S. Gill: Buck Institute for Research on Aging, 8001 Redwood Boulevard

Nature, 2011, vol. 473, issue 7346, 226-229

Abstract: Lipid signals and lifespan extension Dietary restriction can extend lifespan in model organisms such as the nematode Caenorhabditis elegans. Although a number of key players in lifespan extension have been identified, little is known about the signals that coordinate the metabolic response of the organism. The endocannabinoid system is one candidate for the role, as it is known to regulate nutrient intake and energy balance in mammals. These pathways, and cannabinoid receptors, are absent in C. elegans, but a possible alternative has now been identified in this important model for ageing studies. Abundance of a class of lipid-derived signalling molecules, the N-acylethanolamines (NAEs), is reduced in C. elegans by dietary restriction, and NAE deficiency alone is sufficient to extend lifespan. In mammals, an arachidonic acid containing NAE elicits many — though not all — of its effects through cannabinoid receptors.

Date: 2011
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DOI: 10.1038/nature10007

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