Abstract
The nematode Caenorhabditis elegans has been subjected to DR by food ( Escherichia coli) dilution, growth in axenic medium and using animals having defects in feeding behavior or in specific nutrient transporter proteins. There is evidence that DR causes increased resistance against environmental stressors but no decrease of metabolic rate. The insulin/IGF-1 signaling pathway does not mediate the longevity effect of DR in this species, but TOR signaling may be involved. The metabolic stability–longevity theory offers a plausible explanation of the longevity effect of DR but needs experimental validation.
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