Since the rediscovery of brown adipose tissue (BAT) in adult human subjects in 2007, there has been a dramatic resurgence in research interest in its role in heat production and energy balance. This has coincided with a reassessment of the origins of BAT and the suggestion that brown preadipocytes could share a common lineage with skeletal myoblasts. In precocial newborns, such as sheep, the onset of non-shivering thermogenesis through activation of the BAT-specific uncoupling protein 1 (UCP1) is essential for effective adaptation to the cold exposure of the extra-uterine environment. This is mediated by a combination of endocrine adaptations which accompany normal parturition at birth and further endocrine stimulation from the mother's milk. Three distinct adipose depots have been identified in all species studied to date. These contain either primarily white, primarily brown or a mix of brown and white adipocytes. The latter tissue type is present, at least, in the fetus and, thereafter, appears to take on the characteristics of white adipose tissue during postnatal development. It is becoming apparent that a range of organ-specific mechanisms can promote UCP1 expression. They include the liver, heart and skeletal muscle, and involve unique endocrine systems that are stimulated by cold exposure and/or exercise. These multiple pathways that promote BAT function vary with age and between species that may determine the potential to be manipulated in early life. Such interventions could modify, or reverse, the normal ontogenic pathway by which BAT disappears after birth, thereby facilitating BAT thermogenesis through the life cycle.

Increasing evidence from the EU Project EARNEST and many other investigators demonstrates that early nutrition and lifestyle have long-term effects on later health and the risk of common non-communicable diseases (known as ‘developmental programming’). Because of the increasing public health importance and the transgenerational nature of the problem, obesity and associated disorders are the focus of the new EU funded project ‘EarlyNutrition’. Currently, three key hypotheses have been defined: the fuel mediated ‘in utero’ hypothesis suggests that intrauterine exposure to an excess of fuels, most notably glucose, causes permanent changes of the fetus that lead to obesity in postnatal life; the accelerated postnatal weight gain hypothesis proposes an association between rapid weight gain in infancy and an increased risk of later obesity and adverse outcomes; and the mismatch hypothesis suggests that experiencing a developmental ‘mismatch’ between a sub-optimal perinatal and an obesogenic childhood environment is related to a particular predisposition to obesity and corresponding co-morbidities. Using existing cohort studies, ongoing and novel intervention studies and a basic science programme to investigate those key hypotheses, project EarlyNutrition will provide the scientific foundations for evidence-based recommendations for optimal nutrition considering long-term health outcomes, with a focus on obesity and related disorders. Scientific and technical expertise in placental biology, epigenetics and metabolomics will provide understanding at the cellular and molecular level of the relationships between early life nutritional status and the risk of later adiposity. This will help refine strategies for intervention in early life to prevent obesity.

Dieting makes you fat – the title of a book published in 1983 – embodies the notion that dieting to control body weight predisposes the individual to acquire even more body fat. While this notion is controversial, its debate underscores the large gap that exists in our understanding of basic physiological laws that govern the regulation of human body composition. A striking example is the key role attributed to adipokines as feedback signals between adipose tissue depletion and compensatory increases in food intake. Yet, the relative importance of fat depletion per se as a determinant of post-dieting hyperphagia is unknown. On the other hand, the question of whether the depletion of lean tissues can provide feedback signals on the hunger–appetite drive is rarely invoked, despite evidence that food intake during growth is dominated by the impetus for lean tissue deposition, amidst proposals for the existence of protein–static mechanisms for the regulation of growth and maintenance of lean body mass. In fact, a feedback loop between fat depletion and food intake cannot explain why human subjects recovering from starvation continue to overeat well after body fat has been restored to pre-starvation values, thereby contributing to ‘fat overshooting’. In addressing the plausibility and mechanistic basis by which dieting may predispose to increased fatness, this paper integrates the results derived from re-analysis of classic longitudinal studies of human starvation and refeeding. These suggest that feedback signals from both fat and lean tissues contribute to recovering body weight through effects on energy intake and thermogenesis, and that a faster rate of fat recovery relative to lean tissue recovery is a central outcome of body composition autoregulation that drives fat overshooting. A main implication of these findings is that the risk of becoming fatter in response to dieting is greater in lean than in obese individuals.

There is considerable disagreement regarding what constitutes a healthy diet. Ever since the influential work of Cannon and Richter, it was debated whether the ‘wisdom of the body’ will automatically direct us to the foods we need for healthy lives or whether we must carefully learn to eat the right foods, particularly in an environment of plenty. Although it is clear that strong mechanisms have evolved to prevent consumption of foods that have previously made us sick, it is less clear whether reciprocal mechanisms exist that reinforce the consumption of healthy diets. Here, we review recent progress in providing behavioural evidence for the regulation of intake and selection of proteins, carbohydrates and fats. We examine new developments in sensory physiology enabling recognition of macronutrients both pre- and post-ingestively. Finally, we propose a general model for central neural processing of nutrient-specific appetites. We suggest that the same basic neural circuitry responsible for the homoeostatic regulation of total energy intake is also used to control consumption of specific macro- and micronutrients. Similar to salt appetite, specific appetites for other micro- and macronutrients may be encoded by unique molecular changes in the hypothalamus. Gratification of such specific appetites is then accomplished by engaging the brain motivational system to assign the highest reward prediction to exteroceptive cues previously associated with consuming the missing ingredient. A better understanding of these nutrient-specific neural processes could help design drugs and behavioural strategies that promote healthier eating.

Research with laboratory species suggests that meals can be terminated by peripheral signals carried to brain feeding centres via hepatic vagal afferents, and that these signals are affected by oxidation of fuels. Pre-gastric fermentation in ruminants greatly alters fuels, allowing mechanisms conserved across species to be studied with different types and temporal absorption of fuels. These fuels include SCFA, glucose, lactate, amino acids and long-chain fatty acid (FA) isomers, all of which are absorbed and metabolised by different tissues at different rates. Propionate is produced by rumen microbes, absorbed within the timeframe of meals, and quickly cleared by the liver. Its hypophagic effects are variable, likely due to its fate; propionate is utilised for gluconeogenesis or oxidised and also stimulates oxidation of acetyl-CoA by anapleurosis. In contrast, acetate has little effect on food intake, likely because its uptake by the ruminant liver is negligible. Glucose is hypophagic in non-ruminants but not ruminants and unlike non-ruminant species, uptake of glucose by ruminant liver is negligible, consistent with the differences in hypophagic effects between them. Inhibition of FA oxidation increases food intake, whereas promotion of FA oxidation suppresses food intake. Hypophagic effects of fuel oxidation also vary with changes in metabolic state. The objective of this paper is to compare the type and utilisation of fuels and their effects on feeding across species. We believe that the hepatic oxidation theory allows insight into mechanisms controlling feeding behaviour that can be used to formulate diets to optimise energy balance in multiple species.

ApoE is a key protein in lipid metabolism with three major isoforms. ApoE allele frequencies show non-random global distribution especially in Europe with high apoE ε3 frequency in the Mediterranean area, whereas the apoE ε4 genotype is enriched in Northern Europe. The apoE ε4 genotype is one of the most important genetic risk factors for age-dependent chronic diseases, including CVD and Alzheimer's disease (AD). The apoE polymorphism has been shown to impact on blood lipids, biomarkers of oxidative stress and chronic inflammation, which all may contribute to the isoform-dependent disease risk. Studies in mice and human subjects indicate that the apoE ε3 but not the apoE ε4 genotype may significantly benefit from dietary flavonoids (e.g. quercetin) and n-3 fatty acids. Metabolism of lipid soluble vitamins E and D is likewise differentially affected by the apoE genotype. Epidemiological and experimental evidence suggest a better vitamin D status in apoE ε4 than ε3 subjects indicating a certain advantage of ε4 over ε3. The present review aims at evaluation of current data available on interactions between apoE polymorphism and dietary responsiveness to flavonoids, fat soluble vitamins and n-3 fatty acids. Likewise, distinct geographic distribution and chronic disease risk of the different apoE isoforms are addressed.

The objective of this review is to provide an overview of the implication of amino acids (AA) in important physiological functions. This is done in the context of pig production where the competition for AA utilisation is exacerbated by constraints to maximise productive responses and the necessity to reduce dietary protein input for environmental, economic and sanitary issues. Therefore, there is an opportunity to refine the nutritional recommendations by exploring the physiological roles of AA. For example, methionine and cysteine, either in selenised or sulfur forms, are directly involved in the regulation of the glutathione antioxidative system. In sows, glutathione antioxidative system may contribute to improving ovulation conditions through control of oxidative pressure. Supplementation of sow diets with l-arginine, a precursor of NO and polyamines, may stimulate placental growth, promoting conceptus survival, growth and tissue development. The beneficial effect of arginine supplementation has been also suggested to improve lactation performance. Feed intake is usually the first response that is impacted by an inadequate AA supply. Valine and tryptophan imbalances may act as signals for decreasing feed intake. AA are also important nutrients for maintaining the animal's defence systems. Threonine, one of the main constituents of mucin protein, is important for gut development during the postnatal period. It may exert a protective effect that reduces the impact of weaning on gut morphology and associated disturbances. Finally, tryptophan is involved in the regulation of the defence system through its action as a precursor of antioxidants and its effect on the inflammatory response.