Display Settings:

Format

Send to:

Choose Destination
Exp Gerontol. 2011 May;46(5):376-81. doi: 10.1016/j.exger.2010.09.003. Epub 2010 Sep 16.

Ageing in Drosophila: the role of the insulin/Igf and TOR signalling network.

Author information

  • 1Institute of Healthy Ageing, London, WC1E 6BT, UK. l.partridge@ucl.ac.uk

Abstract

A remarkable discovery of recent years is that, despite the complexity of ageing, simple genetic interventions can increase lifespan and improve health during ageing in laboratory animals. The pathways involved have often proved to sense nutrients and to match costly activities of organisms, such as growth, metabolism and reproduction, to nutrient status. For instance, the insulin/insulin-like growth factor and Target of Rapamycin signalling network has proved to play a function in ageing, from yeast to mammals, seemingly including humans. In the fruit fly Drosophila, altered activity of several components of this network can increase lifespan and improve locomotor and cardiac function during ageing. The fly brain, fat body (equivalent of mammalian liver and white adipose tissue) and the germ line are important in determination of lifespan, with considerable communication between different tissues. Cellular detoxification pathways, increased autophagy and altered protein synthesis have all been implicated in increased lifespan from reduced IIS/TOR activity, with the role of defence against oxidative stress unresolved. Reduced IIS/TOR signalling can alter or block the response of lifespan to dietary restriction. Reduced IIS can act acutely to lower death rate, implying that it may ameliorate the effects of ageing-related damage, rather than preventing it.

Copyright © 2010 Elsevier Inc. All rights reserved.

PMID:
20849947
[PubMed - indexed for MEDLINE]
PMCID:
PMC3087113
Free PMC Article

Images from this publication.See all images (3)Free text

Fig. 1
Fig. 2
Fig. 3
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Icon for PubMed Central
    Loading ...
    Write to the Help Desk