Beginning with the early work of McCay and Maynard (1935) who reported a life-prolonging effect of caloric restriction in rats, numerous attempts have been made to study the underlying causes of this obviously general mechanism. It could be shown that a reduction of caloric intake of 30 to 50% prolonged the life of rodents up to 60%. The same results were obtained in young animals and in older adults which received the reduced diet later in life. The results of the studies on rodents could be confirmed in numerous studies on other vertebrates, nematodes and even protozoa (see Masoro, 2000). Evidence for enhanced survival under dietary restriction in insects was provided by studies on waterstriders (Kaitala, 1991), carabid beetles (Ernsting and Isaaks, 1991), and Drosophila (see chapters in this book). Longtime studies using primates started in the eighties and continue up to now, revealing exciting results (Mattison et al., 2003).
The influence of dietary restriction on the organism is manifold. Obviously, the reduction of oxidative stress by reducing the accumulation of reactive oxygen molecules and the protection of the antioxidant system plays a central role.
It is often reported that a dietary restriction leads to a reduction of fertility. It was argued that the energy resources are used for the maintenance of body function instead for reproduction with the result of prolonging the life span. The evolutionary implications of such a life-history strategy were discussed by Shanley and Kirkwood (2000).
Recently the influence of dietary restriction on gene expression has attracted more and more attention. It could be shown that the expression of gluconeogenetic genes was stimulated in rodents after caloric restriction (Spindler, 2001).
Regarding the change in intermediary metabolism, a gene family came into consideration which is called SIR2 (Brachman et al., 1995). Studies with yeast show that the gene product of SIR2 is a NAD-dependent histone deacetylase which inactivates chromosomal regions (Guarente and Kenyon, 2000). With increasing age, a partial loss of inactivation results in errors in gene expression. This process can be delayed by high bioavail-ability of NAD. A reduced glycolytic flow as shown after
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