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Open AccessJournal ArticleDOI

Sex and Death: What Is the Connection?

Linda Partridge, +2 more
- 25 Feb 2005 - 
- Vol. 120, Iss: 4, pp 461-472
TLDR
In this paper, the link between lifespan and fecundity is not inevitable, and the molecular basis of the cost of reproduction is informed by elucidation of the mechanisms by which dietary restriction and insulin/IGF signaling affect these two traits.
About
This article is published in Cell.The article was published on 2005-02-25 and is currently open access. It has received 427 citations till now. The article focuses on the topics: Fecundity.

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Citations
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Promoting Health and Longevity through Diet: From Model Organisms to Humans

TL;DR: Findings indicate that meal timing is crucial, with both intermittent fasting and adjusted diurnal rhythm of feeding improving health and function, in the absence of changes in overall intake.
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Mechanisms of Life Span Extension by Rapamycin in the Fruit Fly Drosophila melanogaster

TL;DR: It is shown here that feeding rapamycin to adult Drosophila produces the life span extension seen in some TOR mutants, and analysis of the underlying mechanisms revealed thatRapamycin increased longevity specifically through the TORC1 branch of the TOR pathway, through alterations to both autophagy and translation.
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Lifespan and reproduction in Drosophila: New insights from nutritional geometry

TL;DR: The use of recent techniques in nutrition research to quantify the detailed relationship between diet, nutrient intake, lifespan, and reproduction in Drosophila melanogaster indicates a role for both direct costs of reproduction and other deleterious consequences of ingesting high levels of protein.
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Stem cells, ageing and the quest for immortality.

TL;DR: Unravelling distinct contributions to the aged phenotype will be critical to the success of any therapeutic application of stem cells in the emerging field of regenerative medicine with respect to tissue injury, degenerative diseases or normal functional declines that accompany ageing.
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Amino-acid imbalance explains extension of lifespan by dietary restriction in Drosophila.

TL;DR: Reduced activity of the insulin/insulin-like growth factor signalling pathway extends lifespan in diverse organisms, and it is found that it also protects against the shortening of lifespan with full feeding.
References
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A C. elegans mutant that lives twice as long as wild type

TL;DR: Finding that mutations in the gene daf-2 can cause fertile, active, adult Caenorhabditis elegans hermaphrodites to live more than twice as long as wild type raises the possibility that the longevity of the dauer is not simply a consequence of its arrested growth, but instead results from a regulated lifespan extension mechanism that can be uncoupled from other aspects of dauer formation.
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Mice carrying null mutations of the genes encoding insulin-like growth factor I (Igf-1) and type 1 IGF receptor (Igf1r)

TL;DR: In addition to generalized organ hypoplasia in Igf1r(-/-) embryos, including the muscles, and developmental delays in ossification, deviations from normalcy were observed in the central nervous system and epidermis.
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Role of Insulin-like Growth Factors in Embryonic and Postnatal Growth

TL;DR: Postnatal growth curves indicated that surviving Igf-1(-/-) mutants, which are infertile and exhibit delayed bone development, continue to grow with a retarded rate after birth in comparison with wild-type littermates and become 30% of normal weight as adults.
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daf-2, an Insulin Receptor-Like Gene That Regulates Longevity and Diapause in Caenorhabditis elegans

TL;DR: Life-span regulation by insulin-like metabolic control is analogous to mammalian longevity enhancement induced by caloric restriction, suggesting a general link between metabolism, diapause, and longevity.
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