Having it all: historical energy intakes do not generate the anticipated trade-offs in fecundity

Author:

Johnston S.L12,Grune T3,Bell L.M1,Murray S.J1,Souter D.M1,Erwin S.S1,Yearsley J.M4,Gordon I.J45,Illius A.W6,Kyriazakis I7,Speakman J.R182

Affiliation:

1. Division of Energy Balance and Obesity, Rowett Research InstituteGreenburn Road, Bucksburn, Aberdeen AB21 9SB, UK

2. Aberdeen Centre for Energy Regulation and Obesity (ACERO)Aberdeen AB21 9SB, UK

3. Research Institute for Environmental Medicine at the Heinrich Heine University Duesseldorf, Molecular Ageing ResearchAuf'm Hennekamp 50, 40225 Duesseldorf, Germany

4. Macaulay InstituteCraigiebuckler, Aberdeen AB15 8QH, UK

5. Sustainable Ecosystems, CSIRO—Davies LaboratoryPMB PO Aitkenvale, Queensland 4814, Australia

6. School of Biological Sciences, Institute of Evolutionary BiologyUniversity of Edinburgh, West Mains Road, Edinburgh EH9 3JT, UK

7. Animal Nutrition & Health Department, Scottish Agricultural CollegeKings Buildings, West Mains Road, Edinburgh EH9 3JG, UK

8. School of Biological Sciences, University of AberdeenAberdeen AB24 2TZ, UK

Abstract

An axiom of life-history theory, and fundamental to our understanding of ageing, is that animals must trade-off their allocation of resources since energy and nutrients are limited. Therefore, animals cannot ‘have it all’—combine high rates of fecundity with extended lifespans. The idea of life-history trade-offs was recently challenged by the discovery that ageing may be governed by a small subset of molecular processes independent of fitness. We tested the ‘trade-off’ and ‘having it all’ theories by examining the fecundities of C57BL/6J mice placed onto four different dietary treatments that generated caloric intakes from −21 to +8.6% of controls. We predicted body fat would be deposited in relation to caloric intake. Excessive body fat is known to cause co-morbidities that shorten lifespan, while caloric restriction enhances somatic protection and increases longevity. The trade-off model predicts that increased fat would be tolerated because reproductive gain offsets shortened longevity, while animals on a restricted intake would sacrifice reproduction for lifespan extension. The responses of body fat to treatments followed our expectations, however, there was a negative relationship between reproductive performance (fecundity, litter mass) and historical intake/body fat. Our dietary restricted animals had lower protein oxidative damage and appeared able to combine life-history traits in a manner contrary to traditional expectations by having increased fecundity with the potential to have extended lifespans.

Publisher

The Royal Society

Subject

General Agricultural and Biological Sciences,General Environmental Science,General Immunology and Microbiology,General Biochemistry, Genetics and Molecular Biology,General Medicine

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