Dietary restriction-influenced biological performance is found in many animal species. Pardosa pseudoannulata is a dominant spider species in agricultural fields and is important for controlling pests. In this study, three groups – a control group (CK group), a re-feeding group (RF group), and a dietary restriction group (RT group) – were used to explore development, mating, reproduction, and the expression levels of Vg (vitellogenin) and VgR (vitellogenin receptor) genes in the spider. The findings indicated that when subjected to dietary restriction, the carapace size, weight of the spiderlings, and weight of the adults exhibited a decrease. Furthermore, the preoviposition period and egg stage were observed to be prolonged, while the number of spiderlings decreased. It was also observed that re-feeding reduced cannibalism rates and extended the preoviposition period. Dietary restriction also affected the expression of the Vg-3 gene in the spider. These results will contribute to the understanding of the impact of dietary restriction in predators of pest control, as well as provide a theoretical foundation for the artificial rearing and utilisation of the dominant spider in the field.

The way in which animals are fed is an important aspect of their welfare. Not only does food provide the energy and nutrients vital for survival, but feeding is also associated with a number of other factors contributing to the well-being of animals. The feeding method can determine the animals’ abilities to fulfil basic behavioural needs, such as foraging. The aim of this paper is to review and discuss the dilemma of choosing between ad libitum feeding (AL) and dietary restriction (DR). AL can produce obese individuals with severe health problems, though it does appear to be compatible with welfare-friendly management systems. On the other hand, DR is often associated with improved physical health and longevity but can leave animals suffering from hunger, frustration or aggression. The species discussed are the laboratory rat, pigs and poultry all of which are omnivores sharing many characteristics in their eating habits. The welfare implications of different feeding methods depend upon the definition of welfare used. Based on a definition of welfare in terms of functioning, DR could be considered the best way to feed animals, because it results in improved physical health and longevity. If welfare is defined in terms of natural living, it is also a requirement for the animal to be able to engage in natural foraging behaviours. From the feelings-based approach, DR can be viewed as preferable only in circumstances when animals are anticipated to live so long that they would otherwise suffer from the negative long-term consequences of AL. It is argued that incentives are needed to make farmers spend resources to ensure that farm animals are allowed to have their foraging-related needs fulfilled. Feeding of laboratory animals creates special dilemmas when it is important either to under- or over-nourish the animals for experimental purposes, in such instances there is a need for Refinement.

Life expectancy in most developed countries has been rising over the past century. In the UK alone, there are about 12 million people over 65 years old and centenarians have increased by 85% in the past 15 years. As a result of the ageing population, which is due mainly to improvements in medical treatments, public health, improved housing and lifestyle choices, there is an associated increase in the prevalence of pathological conditions, such as metabolic disorders, type 2 diabetes, cardiovascular and neurodegenerative diseases, many types of cancer and others. Statistics suggest that nearly 54% of elderly people in the UK live with at least two chronic conditions, revealing the urgency for identifying interventions that can prevent and/or treat such disorders. Non-pharmacological, dietary interventions such as energetic restriction (ER) and methionine restriction (MR) have revealed promising outcomes in increasing longevity and preventing and/or reversing the development of ageing-associated disorders. In this review, we discuss the evidence and mechanisms that are involved in these processes. Fibroblast growth factor 1 and hydrogen sulphide are important molecules involved in the effects of ER and MR in the extension of life span. Their role is also associated with the prevention of metabolic and cognitive disorders, highlighting these interventions as promising modulators for improvement of health span.

Aging is the major risk factor for a constellation of multifactorial diseases, including insulin resistance, diabetes and cardiovascular complications. Dietary restriction has been shown to delay or prevent the manifestation of age-related health decline, extending lifespan in most species tested to date. Given the scarce willingness of human subjects to adhere to chronic dietary restriction exercises, there has been an interest in deciphering the molecular mechanisms triggering the adaptations to dietary restriction. In this context, Sirtuin 1 (SIRT1), a NAD+-dependent deacetylase enzyme, has been proposed to act as a key mediator of the adaptations to nutrient deprivation in eukaryotes, and SIRT1 activating compounds have been often referred to as ‘dietary restriction mimetic’ molecules. Here, we will discuss the convergences and divergences between the effects of dietary restriction and SIRT1 activation, based on the recent advances in the field. As of now, most evidences indicate that SIRT1 is required, but not sufficient to trigger dietary-restriction induced adaptations.

It is a well-appreciated fact that in many organisms the process of ageing reacts highly plastically, so that lifespan increases or decreases when the environment changes. The perhaps best-known example of such lifespan plasticity is dietary restriction (DR), a phenomenon whereby reduced food intake without malnutrition extends lifespan (typically at the expense of reduced fecundity) and which has been documented in numerous species, from invertebrates to mammals. For the evolutionary biologist, DR and other cases of lifespan plasticity are examples of a more general phenomenon called phenotypic plasticity, the ability of a single genotype to produce different phenotypes (e.g. lifespan) in response to changes in the environment (e.g. changes in diet). To analyse phenotypic plasticity, evolutionary biologists (and epidemiologists) often use a conceptual and statistical framework based on reaction norms (genotype-specific response curves) and genotype × environment interactions (G × E; differences in the plastic response among genotypes), concepts that biologists who are working on molecular aspects of ageing are usually not familiar with. Here I briefly discuss what has been learned about lifespan plasticity or, more generally, about plasticity of somatic maintenance and survival ability. In particular, I argue that adopting the conceptual framework of reaction norms and G × E interactions, as used by evolutionary biologists, is crucially important for our understanding of the mechanisms underlying DR and other forms of lifespan or survival plasticity.

Epigenetic changes may be causal in the ageing process and may be influenced by diet, providing opportunities to improve health in later life. The aim of this review is to provide an overview of several areas of research relevant to this topic and to explore a hypothesis relating to a possible role of epigenetic effects, mediated by sirtuin 1, in the beneficial effects of dietary restriction, including increased lifespan. Epigenetic features of ageing include changes in DNA methylation, both globally and at specific loci, which differ between individuals. A major focus of research on dietary influences on epigenetic status has been on nutrition in utero, because the epigenome is probably particularly malleable during this life-course window and because epigenetic marking by early exposures is a compelling mechanism underlying effects on lifelong health. We explore the potential of diet during adulthood, including the practice of dietary restriction, to affect the epigenetic architecture. We report progress with respect to deriving data to support our hypothesis that sirtuin 1 may mediate some of the effects of dietary restriction through effects on DNA methylation and note observations that resveratrol affects DNA methylation and other epigenetic features. Disentangling cause and effect in the context of epigenetic change and ageing is a challenge and requires better understanding of the underlying mechanisms and also the development of more refined experimental tools to manipulate the epigenetic architecture, to facilitate hypothesis-driven research to elucidate these links and thus to exploit them to improve health across the full life-course through dietary measures.

Inflammation plays an important role in diabetes mellitus and its complications. In this context, the negative cross-talk between adipose tissue and skeletal muscle leads to disturbances in muscle cell insulin signalling and induces insulin resistance. Because several studies have shown that energy restriction brings some benefits to diabetes, the aim of the present study was to evaluate the effects of dietary restriction on systemic and skeletal muscle inflammatory biomarkers, such C-reactive protein, adipokines and cytokines, and in insulin resistance in Goto-Kakizaki rats. This is an animal model of spontaneous non-obese type 2 diabetes with strongly insulin resistance and without dyslipidaemia. Animals were maintained during 2 months of dietary restriction (50 %) and were killed at 6 months of age. Some biochemical determinations were done using ELISA and Western blot. Data from the present study demonstrate that in Goto-Kakizaki rats the dietary restriction improved insulin resistance, NEFA levels and adipokine profile and ameliorated inflammatory cytokines in skeletal muscle. These results indicate that dietary restriction in type 2 diabetes enhances adipose tissue metabolism leading to an improved skeletal muscle insulin sensitivity.

The aim was to investigate the effects of a 48 h period of fluid, energy or combined fluid and energy restriction on salivary IgA (s-IgA) responses at rest and after exercise. Thirteen healthy males (age 21 (sem 1) years) participated in four randomised 48 h trials. In the control trial participants received their estimated energy (12 154 (sem 230) kJ/d) and water (3912 (sem 140) ml/d) requirements. On fluid restriction (FR) participants received their energy requirements and 193 (sem 19) ml water/d to drink and on energy restriction (ER) participants received their water requirements and 1214 (sem 25) kJ/d. Fluid and energy restriction (F+ER) was a combination of FR and ER. After 48 h, participants performed a 30 min treadmill time trial (TT) followed by rehydration (0–2 h) and refeeding (2–6 h). Unstimulated saliva was collected at 0, 24 and 48 h, post-TT, and 2 and 6 h post-TT. Saliva flow rate (sflw) and s-IgA (ELISA) remained unchanged in control conditions and on ER. However, 48 h on FR decreased sflw (64 %) which most probably accounted for the increase in s-IgA concentration (P < 0·01). Despite a decrease in sflw (54 %), s-IgA concentration did not increase on F+ER, resulting in a decreased s-IgA secretion rate by 24 h (0 h: 20 (sem 2); 24 h: 12 (sem 2) μg/min; P < 0·01). Post-TT s-IgA secretion rate was not lower compared with 48 h on any trial. s-IgA secretion rate returned to within 0 h values by 6 h post-TT on F+ER. In conclusion, a 24–48 h period of combined F+ER decreased s-IgA secretion rate but normalisation occurred upon refeeding.