bluuebunny/crossref_metadata_2025 huggingface dataset:
The role of iodine in brain development
Authors: Delange François
Published: February 2011

I is required for the synthesis of thyroid hormones. These hormones, in turn, are required for brain development, which occurs during fetal and early postnatal life. The present paper reviews the impact of I deficiency (1) on thyroid function during pregnancy and in the neonate, and (2) on the intellectual development of infants and children. All extents of I deficiency (based on I intake (μg/d); mild 50–99, moderate 20–49, severe > 20) affect the thyroid function of the mother and neonate, and the mental development of the child. The damage increases with the extent of the deficiency, with overt endemic cretinism as the severest consequence. This syndrome combines irreversible mental retardation, neurological damage and thyroid failure. Maternal hypothyroxinaemia during early pregnancy is a key factor in the development of the neurological damage in the cretin. Se deficiency superimposed on I deficiency partly prevents the neurological damage, but precipitates severe hypothyroidism in cretins. I deficiency results in a global loss of 10–15 intellectual quotient points at a population level, and constitutes the world’s greatest single cause of preventable brain damage and mental retardation.
Nutrition in paediatric human immunodeficiency virus infection
Authors: Miller Tracie L.
Published: February 2011

The nutritional condition of children with human immunodeficiency virus (HIV) infection continues to be a problem both in developed and developing countries. HIV-infected children grow below normal standards in both height and weight when compared with HIV-exposed non-infected children. These patterns persist over time. It is possible that acute infectious episodes and increased HIV viral burden contribute to decrements in all growth variables. Potential aetiologies for abnormal growth include inadequate dietary intake, gastrointestinal malabsorption, increased energy utilization and psycho-social problems. It is likely that all these factors contribute to the growth problems of these children to some extent. With the development of protease inhibitor anti-retroviral therapy and highly-active anti-retroviral treatment regimens, children with HIV infection in developed countries are living longer with a chronic illness. New nutritional problems have arisen with the development of the fat redistribution syndrome or lipodystrophy. Emerging problems are now being recognized, with the development of insulin resistance and truncal obesity which may potentially lead to premature cardiovascular disease.
Assessment of individual fatty acid intake
Authors: Cantwell Marie M.
Published: February 2011

Dietary assessment of individual fatty acid intake is difficult due to a number of limitations. Information regarding the type, quantity and brand-name of fat used in cooking and at the table is required. In addition, margarine manufacturers may change the component oils used for reasons of cost, which changes the fatty acid composition of their products from season-to-season. Independent markers of fatty acid intake are required, therefore, to compensate for these limitations. Adipose tissue concentrations have been used as a measure of habitual intake of fatty acid groups and individual fatty acids in numerous studies. Saturated (SFA) and monounsaturated fatty acids (MUFA) are generally poorly correlated with adipose tissue concentrations, which can be explained partly by endogenous synthesis. In general, adipose tissue concentrations of exogenously-produced fatty acids (n-3 andn-6 polyunsaturated fatty acids (PUFA)) are well correlated with estimates of habitual intake. Correlations between dietarytransunsaturated fatty acids (TUFA) and adipose tissue concentrations vary between countries, which may be due to differences in dietary sources. Correlations may be affected by differences in bioavailability or selective retention of fatty acids in certain tissue lipids.
Interactions between physical activity and diet in the regulation of body weight
Authors: Moore Melanie S.
Published: February 2011

The increasing worldwide prevalence of obesity suggests that there is a chronic positive energy balance. This situation implies poor coupling between energy intake and energy expenditure, but the contribution of each of these factors remains unclear. Epidemiological data suggests that physical activity has a role in the prevention of weight gain, although there is little evidence that it has a beneficial role in weight loss. High-fat diets have also been implicated, evidence from a variety of sources suggests that diets high in fat undermine appetite regulatory mechanisms. There has been much research to investigate the coupling between energy expenditure and energy intake in the short term in an attempt to elucidate some of the mechanisms involved. However, mechanisms regulating appetite are very complex, and it is currently unclear at which points physical activity and diet may have an influence.
Energy expenditure in disease: time to revisit?
Authors: Gibney Eileen R.
Published: February 2011

Knowledge of energy expenditure is especially important in disease, and may in fact help in the understanding of the pathophysiology of wasting associated with disease. Energy requirements in a clinical setting are often ‘prescribed’ by health professionals, either directly through enteral or parenteral feeding, or perhaps controlled through a hospital diet. Studies initially suggested an increase in energy expenditure, and thus energy requirements, as a direct result of an increase in basal metabolic rate often seen in disease. However, many problems exist in the measurement of BMR in a disease situation, due to the effects of drugs, clinical practice, feeding or possibly anxiety either as a cause of the disease or the measurement itself. These problems could in themselves contribute to the rise in metabolism seen in disease. More recently, however, with the use of tracer techniques such as doubly-labelled water and the bicarbonate–urea method, more accurate estimates of energy expenditure, and thus energy requirements, have been made. Some such measurements have in fact shown that even with an elevated BMR, free-living total energy expenditure can in fact be reduced in many disease situations, suggesting a reduced rather than an increased energy requirement. The present review investigates measurements of total energy expenditure in disease to explore the hypothesis that energy expenditure in disease, even with an elevated BMR, can in fact be reduced due to a concurrent reduction in physical activity.
Long-term physiological and economic consequences of growth retardation in children and adolescents
Authors: Norgan N. G.
Published: February 2011

The application of a lifespan perspective in human biology in recent years has shown that a number of early environmental factors influencing human growth and development have long-term biological or psycho-social consequences. Human growth is characterized by prolonged infancy, an extended childhood phase and high rates of growth during the adolescent growth spurt. It is unlikely that these characteristics would have evolved without having advantages, and curtailments have the potential for disadvantage. The present paper examines the evidence for long-term physiological and economic consequences of growth retardation in children and adolescents. The emphasis is the biological and economic imperatives of survival, subsistence, reproduction and production rather than aspects of metabolic competence. Many of the consequences of growth retardation are determined by the direct effect on body size, but many other consequences arise from the conditions that cause the growth retardation. Catch up of retarded growth can occur, but does not usually do so because of the continued presence of the retarding agents. Basal metabolism and physical work capacity are usually commensurate with the size of the individual; mechanical efficiency of physical work is unchanged, but falls in activity levels may occur along with a reduction in the pace of activity. Growth retardation in childhood is associated with a higher disease and mortality risk in adulthood, with decreased productivity and employment and promotion prospects. Studies are showing that relative deprivation and the accumulation of socially patterned exposures are important in some societies. Height and growth retardation have proved invaluable in reflecting these factors, but the next generation of studies may require more discriminating indices.
Food allergy and nutrition in early life: implications for later health
Authors: Chandra Ranjit Kumar
Published: February 2011

Allergic diseases are a common cause of illness in most industrialized countries. Diet during early childhood is an important determinant of the development of allergy, particularly in high-risk infants who have a parental history of atopy. Maternal avoidance of highly-allergenic foods during pregnancy and lactation, prolonged exclusive breast-feeding, the use of a hydrolysed milk formula, and delayed introduction of dairy products, eggs, fish, nuts and soyabean are associated with a lower incidence of allergic symptoms and signs. These beneficial effects are observed for as long as 18 years of age. Similarly, nutrition and physical growth are important factors that influence immunocompetence and morbidity due to infections. Small-for-gestational age low-birth-weight infants show prolonged impairment of cell-mediated immunity, antibody responses and phagocyte function. Recent studies indicate the beneficial effect of moderate amounts of Zn given in the first 6 months of life. Thus, diet and nutrition in early life are crucial for the development of allergic and infectious disease throughout childhood and into adulthood.
Measurement of dietary intake in children
Authors: Livingstone M. B. E. , Robson P. J.
Published: February 2011

When children and adolescents are the target population in dietary surveys many different respondent and observer considerations surface. The cognitive abilities required to self-report food intake include an adequately developed concept of time, a good memory and attention span, and a knowledge of the names of foods. From the age of 8 years there is a rapid increase in the ability of children to self-report food intake. However, while cognitive abilities should be fully developed by adolescence, issues of motivation and body image may hinder willingness to report. Ten validation studies of energy intake data have demonstrated that mis-reporting, usually in the direction of under-reporting, is likely. Patterns of under-reporting vary with age, and are influenced by weight status and the dietary survey method used. Furthermore, evidence for the existence of subject-specific responding in dietary assessment challenges the assumption that repeated measurements of dietary intake will eventually obtain valid data. Unfortunately, the ability to detect mis-reporters, by comparison with presumed energy requirements, is limited unless detailed activity information is available to allow the energy intake of each subject to be evaluated individually. In addition, high variability in nutrient intakes implies that, if intakes are valid, prolonged dietary recording will be required to rank children correctly for distribution analysis. Future research should focus on refining dietary survey methods to make them more sensitive to different ages and cognitive abilities. The development of improved techniques for identification of mis-reporters and investigation of the issue of differential reporting of foods should also be given priority.
Secular trends in growth
Authors: Cole T. J.
Published: February 2011

Since the 19th century there have been clearly documented secular trends to increasing adult height in most European countries, with current rates of 10–30 mm / decade. Over the same period menarcheal age has also fallen steeply, but has now stabilized at approximately 13 years and may be rising again. Height trends tend to be greater in childhood than in adulthood due to the associated advance in maturation, but no trends are apparent before the age of 2 years. In particular, birth-weight trends are small and different in shape from height trends. The adult height trend matches that at age 2 years, so that the increment in adult height has already been achieved by age 2 years. To try to identify factors relating to the secular trend, increased height gain in late infancy is hypothesized to be equivalent to a reduction in stunting, and stunting is thought to be caused by impaired growth in the long bones of the leg in later infancy. Leg growth may be regulated by the expression of growth-hormone receptors on the growth plates, which it is hypothesized are susceptible to the interaction between concurrent nutrition and the nominal growth rate set during pregnancy. The timing of menarche is also likely to be determined by some growth factor operating near the time of birth, which also affects later weight, but not height.
The acquisition of obesity: insights from cellular and genetic research
Authors: Wabitsch Martin
Published: February 2011

The acquisition of increased adipose tissue mass in man occurs during prolonged periods of positive energy balance. Normally, energy homeostasis in children and adults is regulated strictly and the energy stores are kept within the defined age-dependent physiological range. Susceptibility to definitive increases in the level of energy balance during times of reduced energy consumption or increased energy intake, leading to changes in body composition and/or changes in relative body weight, seems to be genetically determined. Although at present much information on the regulation of energy homeostasis and related unfavourable factors exists from animal studies, knowledge of the regulation of energy balance in human subjects is still insufficient. Some evidence on relevant factors involved in the regulation of energy balance in man has been obtained from epidemiological data, as well as from studies of patients with rare monogenetic forms of obesity. In the present article a special focus will be put on the regulation of body energy stores at the level of the adipose tissue, with emphasis on the regulation of human adipocyte differentiation. In addition to the currently intensive scientific interest in the central regulation of energy homeostasis in man, there is sufficient evidence to support the idea that the acquisition of an increased adipose tissue mass is also dependent on the susceptibility of pre-adipocytes to proliferate, to differentiate or to enter into apoptosis.
Body-weight regulation: causes of obesity
Authors: Martinez J. Alfredo
Published: February 2011

The aetiology and treatment of obesity have been fraught with disappointment for researchers, because the mechanisms that control fuel homeostasis and adiposity are incompletely understood. It is assumed that regulatory processes match the dietary fuel supply with energy requirements in order to maintain a stable body mass and adiposity. In this context several theories have been proposed to explain the laws of thermodynamics describing the conservation and transformation of energy in living organisms. In the light of new evidence it can now be hypothesized that the control of body weight and composition depends on an axis with three interrelated and self-controlled components: (1) food intake; (2) nutrient turnover and thermogenesis; (3) body fat stores. Complex feedback mechanisms underlie all these components. The major factors involved in obesity seem to be dietary and physical activity habits. These factors are affected by susceptibility genes that in turn may influence energy expenditure, fuel metabolism, muscle fibre function and appetite or food preferences. However, the increasing rates of obesity cannot be explained exclusively by changes in the gene pool, although genetic variants that were previously ‘silent’ are now being triggered by the high availability of energy- and fat-dense foods, and by the increasingly sedentary lifestyle of modern societies. The study of factors such as genetics and lifestyle implicated in weight gain and obesity is crucial for predictions about the future impact of the global epidemic of obesity, and provides a unique opportunity for the implementation of preventive action.
The hypothalamus and the regulation of energy homeostasis: lifting the lid on a black box
Authors: Williams Gareth , Harrold Joanne A. , Cutler David J.
Published: February 2011

The hypothalamus is the focus of many peripheral signals and neural pathways that control energy homeostasis and body weight. Emphasis has moved away from anatomical concepts of ‘feeding’ and ‘satiety’ centres to the specific neurotransmitters that modulate feeding behaviour and energy expenditure. We have chosen three examples to illustrate the physiological roles of hypothalamic neurotransmitters and their potential as targets for the development of new drugs to treat obesity and other nutritional disorders. Neuropeptide Y (NPY) is expressed by neurones of the hypothalamic arcuate nucleus (ARC) that project to important appetite-regulating nuclei, including the paraventricular nucleus (PVN). NPY injected into the PVN is the most potent central appetite stimulant known, and also inhibits thermogenesis; repeated administration rapidly induces obesity. The ARC NPY neurones are stimulated by starvation, probably mediated by falls in circulating leptin and insulin (which both inhibit these neurones), and contribute to the increased hunger in this and other conditions of energy deficit. They therefore act homeostatically to correct negative energy balance. ARC NPY neurones also mediate hyperphagia and obesity in the ob/ob and db/db mice and fa/fa rat, in which leptin inhibition is lost through mutations affecting leptin or its receptor. Antagonists of the Y5 receptor (currently thought to be the NPY ‘feeding’ receptor) have anti-obesity effects. Melanocortin-4 receptors (MC4-R) are expressed in various hypothalamic regions, including the ventromedial nucleus and ARC. Activation of MC4-R by agonists such as α-melanocyte-stimulating hormone (a cleavage product of pro-opiomelanocortin which is expressed in ARC neurones) inhibits feeding and causes weight loss. Conversely, MC4-R antagonists such as ‘agouti’ protein and agouti gene-related peptide (AGRP) stimulate feeding and cause obesity. Ectopic expression of agouti in the hypothalamus leads to obesity in the AVY mouse, while AGRP is co-expressed by NPY neurones in the ARC. Synthetic MC4-R agonists may ultimately find use as anti-obesity drugs in human subjects Orexins-A and -B, derived from prepro-orexin, are expressed in specific neurones of the lateral hypothalamic area (LHA). Orexin-A injected centrally stimulates eating and prepro-orexin mRNA is up regulated by fasting and hypoglycaemia. The LHA is important in receiving sensory signals from the gut and liver, and in sensing glucose, and orexin neurones may be involved in stimulating feeding in response to falls in plasma glucose.
Regulation of lipid metabolism in adipose tissue
Authors: Samra J. S.
Published: February 2011

Adipose tissue is a major source of metabolic fuel. This metabolic fuel is stored in the form of triacylglycerol. Lipolysis of triacylglycerol yields non-esterified fatty acids and glycerol. In human subjectsin vivostudies of the regulation of lipid metabolism in adipose tissue have been difficult because of the heterogeneous nature of the tissue and lack of a vascular pedicle. In the last decade the methodology of study of adipose tissue has improved with the advent of the anterior abdominal wall adipose tissue preparation technique and microdialysis. These techniques have demonstrated that lipid metabolism in adipose tissue is finely coordinated during feeding and fasting cycles, in order to provide metabolic fuel when required. Lipolysis takes place both in extracellular and intracellular space. The extracellular lipolysis is regulated by lipoprotein lipase and the intracellular lipolysis is regulated by hormone-sensitive lipase. In pathophysiological conditions such as trauma, sepsis and starvation profound changes are induced in the regulation of lipid metabolism. The increased mobilization of lipid fuel is brought about by the differential actions of various counter-regulatory hormones on adipose tissue blood flow and adipose tissue lipolysis through lipoprotein lipase and hormone-sensitive lipase, resulting in increased availability of non-esterified fatty acids as a source of fuel. In recent years, it has been demonstrated that adipose tissue produces various cytokines and these cytokines can have paracrine and endocrine effects. It would appear that adipose tissue has the ability to regulate lipid metabolism locally as well as at distant sites such as liver, muscle and brain. In future, it is likely that the mechanisms that lead to the secondary effects of lipid metabolism on atheroma, immunity and carcinogenesis will be demonstrated.
All-trans-retinoic acid and polyriboinosinoic : polyribocytidylic acid cooperate to elevate anti-tetanus immunoglobulin G and immunoglobulin M responses in vitamin A-deficient Lewis rats and Balb/c mice
Authors: DeCicco Kathleen L. , Ross A. Catharine
Published: February 2011

Vitamin A (VA) deficiency compromises antibody responses to T-cell-dependent antigens such as tetanus toxoid, but this effect can be reversed through administration of retinol or retinoic acid (RA). To test whether RA and polyriboinosinioc : polyribocytidylic acid (PIC), a known inducer of several forms of interferon (IFN), can cooperate to increase specific immunoglobulin (Ig)G and IgM production during VA deficiency, rats and mice were made VA-deficient, immunized with TT and treated with all-trans-RA, PIC or their combination. VA-deficient rats produced low primary and secondary anti-tetanus IgG responses (VA-deficient controlsv. VA-sufficient controlsP< 0·001), although total IgG was slightly elevated when compared with VA-sufficient control rats. Although RA administered alone elevated antibody production during VA deficiency to control levels, RA combined with PIC synergistically enhanced these responses (RA and PIC groupv. all other groupsP< 0·0001). In contrast, Balb/c mice maintained on a VA-deficient diet and immunized in a similar fashion showed no impairment in antigen-specific IgG levels, but treatment with a combination of RA and PIC still evoked an additive enhancement in antigen-specific antibody production. Additionally, RA and PIC administration to VA-sufficient mice resulted in elevated antibody responses, suggesting that this combination should be evaluated further for its immuno-stimulatory effects.
The scientific basis of immunonutrition
Authors: Suchner U. , Kuhn K. S. , Fürst P.
Published: February 2011

Substrates with immune-modulating actions have been identified among both macro- and micronutrients. Currently, the modes of action of individual immune-modulating substrates, and their effects on clinical outcomes, are being examined. At present, some enteral formulas are available for the clinical setting which are enriched with selected immune-modulating nutrients. The purpose of the present paper is to review the scientific rationale of enteral immunonutrition. The major aspects considered are mucosal barrier structure and function, cellular defence function and local or systemic inflammatory response. It is notable that in critical illness the mucosal barrier and cellular defence are impaired and a reinforcement with enteral immunonutrition is desirable, while local or systemic inflammatory response should be down regulated by nutritional interventions. The results available from clinical trials are conflicting. Meta-analyses of recent trials show improvements such as reduced risk of infection, fewer days on a ventilator, and reduced length of intensive care unit and hospital stay. Thus, a grade A recommendation was proclaimed for the clinical use of enteral immune-modulating diets. Improvement in outcome was only seen when critical amounts of the immune-modulating formula were tolerated in patients classified as being malnourished. However, in other patients with severe sepsis, shock and organ failure, no benefit or even disadvantages from immunonutrition were reported. In such severe conditions we hypothesize that systemic inflammation might be undesirably intensified by arginine and unsaturated fatty acids, directly affecting cellular defence and inflammatory response. We therefore recommend that in patients suffering from systemic inflammatory response syndrome great caution should be exercised when immune-enhancing substrates are involved which may aggravate systemic inflammation.
Dietary treatments of obesity
Authors: Moloney Mary
Published: February 2011

Numerous dietary treatments that purport to promote something unique for stimulating weight loss have been published. These treatments include fad diets, diets formulated by various commercial slimming clubs, very-low-energy diets (VLCD) and conventional diets. Fad diets may possibly reduce some weight short-term; however, there is no scientific basis to their long-term use. Commercial slimming clubs may be suitable for some individuals but they need to be properly assessed professionally. There are specific guidelines for the use of VLCD, which are only appropriate for short-term use. There is scientific evidence to suggest that conventional diets can produce both short- and long-term weight loss. A successful weight-loss programme depends on a multidisciplinary team approach. Management strategies should be devised for addressing issues such as goals, monitoring, follow-up, relapse and evaluation. Initial assessments should include medical, laboratory and anthropometric data, fitness level and dietary and behavioural attitudes. These results will form the basis of the treatment plan. Frequent visits to the clinic are fundamental in promoting continuing weight loss during the long-term maintenance stage of treatment. The visits should be made worthwhile for the patient. Realistic and attainable goals for diet, exercise and behaviour modification should be made. The diet should have a novel approach and be tailored to the needs of the patient. It should be adequate nutritionally, low in energy and fat. The overall aim should be to promote lifelong changes in lifestyle, improvement in quality of life and health risks.
The role of food ethics in food policy
Authors: Mepham T. Ben
Published: February 2011

Certain developments in the agricultural and food sciences have far-reaching implications for society and the environment, which suggest the need to examine their ethical acceptability as a standard component of technology assessment. Such considerations have led to the emergence of a new academic discipline, food ethics. The present paper describes how ethical theory may be applied to the analysis of the impacts of prospective food biotechnologies to assess potential effects on four 'interest groups', i.e. consumers, producers, treated organisms and the biota (fauna and flora). The principles which structure the framework used, i.e. the ethical matrix, are adapted to the field of agriculture and food from those applied in medical ethics. Use of the ethical matrix is illustrated by applying it to the specific case of bovine somatotrophin, the genetically-engineered protein hormone which is injected into lactating cattle to increase their milk yields. Ethical analysis is seen to depend on a number of critical requirements, i.e. scientific data, non-scientific evidence and predictions, suitably-qualified assessors ('competent moral judges'), the 'world-views' of the assessors and application of the precautionary principle to cope with 'uncertainty'.
Alternative futures for world cereal and meat consumption
Authors: Rosegrant Mark W. , Leach Nancy , Gerpacio Roberta V.
Published: February 2011

Fundamental changes in the global structure of food demand will lead to an extra-ordinary increase in the importance of developing countries in global food markets. Economic growth in developing countries is changing consumption patterns, with slower growth (and in many countries actual declines) in per capita food consumption of grains and rapidly growing per capita and total meat consumption, combined with induced growth in cereal feed consumption. The present paper examines the hypothesis, suggested by some researchers, that high-meat diets in developed countries limit improvement in food security in developing countries. These analysts argue that reduced meat consumption in developed countries would release cereals from livestock feed to food for poorer populations, thus improving food security in developing countries. Using the International Food Policy Research Institute (Washington, DC, USA) global food projections model, the international model for policy analysis of agricultural com-modities and trade (see Rosegrant et al. 1995), we first analyse the implications for future global cereal and meat supply and demand resulting from changes in global income, population growth and other structural changes, then simulate alternative sce-narios to examine the effect of large reductions in meat consumption in developed coun-tries on food consumption and food security in developing countries. The paper shows that while the long-term prospects for food supply, demand and trade indicate a strength-ening of world cereal and livestock markets, the improvement in food security in the developing world will be slow, and changes in the dietary patterns in developed countries are not an effective route to improvement in food security in developing countries.
Meat and colo-rectal cancer
Authors: Hill Michael J.
Published: February 2011

In early epidemiological studies of diet and cancer the stress was on the search for causal factors. Population (ecological) studies tended to show a strong correlation between meat intake, particularly red meat, and the risk of colo-rectal cancer. They also tended to show meat to be strongly inversely correlated with cancers of the stomach and oesophagus and liver. Early case- control studies tended to support the postulated role for red meat in colo-rectal carcinogenesis, although more recent case-control studies, particularly those from Europe, have tended to show no relationship. The cohort studies in general failed to detect any relationship between meat intake and colo-rectal cancer risk. The available evidence points to the intake of protective factors such as vegetables and whole-grain cereals being the main determinants of colo-rectal cancer risk, with meat intake only coincidentally related.
Nutrition and lung health
Authors: Sridhar Mangalam K.
Published: February 2011

There is an increasing interest in the relationship between nutrition and lung health. Epidemiological studies suggest that dietary habits may have an influence on lung function and the tendency to common lung diseases such as asthma, chronic obstructive pulmonary disease (COPD) and lung cancer. In particular, a diet rich in fresh fruit and fish has been associated with a salutary effect on lung health. End-stage COPD is associated with a state of nutritional depletion which is refractory to conventional nutritional supplementation. In contrast, malnutrition associated with cystic fibrosis is amenable to nutritional therapy, which has been shown to improve prognosis in this disease.
The pulmonary cachexia syndrome: aspects of energy balance
Authors: Congleton Jo
Published: February 2011

The present paper reviews current knowledge of the pulmonary cachexia syndrome with reference to chronic obstructive pulmonary disease (COPD). Aspects of incidence, aetiology and management are discussed. Malnutrition occurs in approximately one-quarter to one-third of patients with moderate to severe COPD. Both fat mass and fat-free mass become depleted. Loss of fat-free mass is the more important and appears to be due to a depression of protein synthesis. Weight loss is an independent prognostic indicator of mortality, and is associated with increased morbidity and decreased health-related quality of life. The aetiology of malnutrition in COPD is not well understood. Reduced food intake does not seem to be the primary cause. Resting energy expenditure (REE) is elevated in a proportion of patients and probably contributes to negative energy balance. Measurement of actual REE is helpful when considering the adequacy of nutritional supplementation. The underlying reason for a hypermetabolic state is not known. Although weight-losing COPD patients are not catabolic, nutritional supplementation alone does not appear to reverse the loss of fat-free mass. Strategies involving nutritional supplementation in combination with a second intervention are being explored, and there are some encouraging results using anabolic hormones.
Manipulating meat quality and composition
Authors: Wood J. D. , Enser M. , Fisher A. V. , Nute G. R. , Richardson R. I. , Sheard P. R.
Published: February 2011

Meat quality describes the attractiveness of meat to consumers. The present paper focuses on two major aspects of meat quality, tenderness and flavour. Both aspects of quality can be influenced by nutrition, principally through its effects on the amount and type of fat in meat. In several countries, high levels of intramuscular fat (marbling fat), i.e. above 30 g/kg muscle weight inlongissimus, are deemed necessary for optimum tenderness, although poor relationships between fat content and tenderness have generally been found in European studies, where fat levels are often very low, e.g. below 10 g/kg in UK pigs. Muscle lipid may be a marker for red oxidative (type 1) muscle fibres which are found at higher concentrations in tender muscles and carcasses. Nutritional treatment can be used to manipulate the fatty acid content of muscle to improve nutritional balance, i.e. increase the polyunsaturated (PUFA) : saturated fatty acid value and reduce then−6 :n−3 PUFA value. Increasing PUFA levels may also change flavour because of their greater susceptibility to oxidative breakdown and the generation of abnormal volatile compounds during cooking. This situation particularly applies to then−3 PUFA which are the most unsaturated meat lipids. In pigs, a concentration of 3 mg α-linolenic acid (18 : 3)/100 mg in muscle and fat tissue fatty acids can easily be achieved by including whole linseed in the diet. This level has led to abnormal odours and flavours in some studies, but not in others. In cattle and sheep, feeding whole linseed raised 18 : 3 concentrations in muscle fatty acids from about 0.7 mg/100 mg to > 1 mg/100 mg. As with pigs, this diet also increased levels of long-chainn−3 PUFA formed from 18 : 3, including eicosapentaenoic acid (20 : 5). Although this increase led to greater oxidative breakdown of lipids during storage and the generation of large quantities of lipid-derived volatile compounds during cooking, there were no deleterious effects on odour or flavour. When 18 : 3 levels are raised in lamb and beef because of grass feeding, the intensity of the flavours increases in comparison with grain-fed animals which consume and deposit relatively more linoleic acid (18 : 2). In ruminants, very high levels of 18 : 2 produced by feeding protected oil supplements cause the cooked beef to be described as oily, bland or pork-like.
Defining optimal body iron
Authors: Cook James D.
Published: February 2011

The major liabilities of Fe lack include defects in psychomotor development in infants, impaired educational performance in schoolchildren, increased perinatal morbidity, and impaired work capacity. Few if any of the relevant investigations have demonstrated these abnormalities in the absence of anaemia. Consequently, adequate Fe nutrition can be defined as a normal haemoglobin concentration. On the other hand, optimal Fe nutrition should be regarded as sufficient body Fe to avoid any limitation in tissue Fe supply, termed Fe-deficient erythropoiesis. A variety of laboratory measurements have been used to identify this milder form of Fe deficiency, including serum ferritin, transferrin saturation, erythrocyte protoporphyrin, mean corpuscular volume, and more recently the concentration of the soluble fragment of transferrin receptor in serum. Recent studies indicate that the serum transferrin receptor is the preferred measurement, because enhanced synthesis of the transferrin receptor represent the initial cellular response to a declining Fe supply. Moreover, unlike other methods, it is not affected by chronic inflammation or infection which are often confused with Fe deficiency. In an otherwise normal healthy population the transferrin receptor: ferritin value provides a useful quantitative index of body Fe over a wide spectrum of Fe status, ranging from Fe repletion to Fe-deficiency anaemia. It is concluded that optimal Fe nutrition is best defined as a normal haemoglobin, serum ferritin and transferrin receptor concentration.
Metal ions as regulators of the conformation and function of the tumour suppressor protein p53: implications for carcinogenesis
Authors: Méplan Catherine , Verhaegh Gerald , Richard Marie-Jeanne , Hainaut Pierre
Published: February 2011

The p53 protein is a multi-function nuclear factor that is activated in response to multiple forms of stress and controls the proliferation, survival, DNA repair and differentiation of cells exposed to potentially genotoxic DNA damage. Loss of p53 function by mutation is a frequent event in human cancer, and is thought to result in the capacity of cells to acquire and accumulate oncogenic mutations during the progression of neoplasia. The p53 protein is a metal-binding transcription factor that is inactivated by metal chelation and by oxidation in vitro. In intact cells, p53 protein activity is crucially dependent on the availability of Zn ions and is impaired by exposure to Cd, a metal which readily substitutes for Zn in a number of transcription factors. Inactivation by Cd suppresses the p53-dependent responses to DNA damage. Overall, these findings indicate that regulation by metals plays an important role in the control of p53, and that perturbation of this control may explain the carcinogenic potential of several metal compounds. Résumé La protéine p53 est un facteur nucléaire multi-fonctionnel qui est activé en réponse à de multiples formes de stress et qui contrôle la prolifération, la survie, la réparation de l’ADN et la différenciation de cellules exposées à des agents génotoxiques. La perte de la fonction de p53 par mutation est un évènement fréquent dans les cancers chez l’homme, et l’on considère que cette inactivation a pour conséquence de rendre la cellule susceptible d’accumuler rapidement des mutations oncogéniques au cours de la progression du cancer. La protéine p53 est un facteur de transcription qui lie les métaux et qui peut être inactivée in vitro par chélation des métaux ainsi que par oxydation. Dans des cellules en culture, l’activité biologique de la p53 dépend de la bio-disponibilité en Zn, et est altérée par l’exposition des cellules au Cd, un métal qui se substitue facilement au Zn dans nombre de facteurs de transcription Zn-dépendants. L’inactivation de p53 par le Cd inhibe les réponses p53-dépendantes suite à la formation de lésions de l’ADN. Globalement, ces données suggèrent que la régulation par les métaux joue un rôle important dans le contrôle de la p53, et que des perturbations de ce contrôle pourraient contribuer à expliquer le potentiel carcinogénique de certains composés métalliques.
Micronutrients and ageing: intakes and requirements
Authors: Richard Marie-Jeanne , Roussel Anne-Marie
Published: February 2011

Ageing (and related diseases) may be described as a process which results from impaired immunological, genetic, neurological or endocrinological functions. Oxidative mechanisms may play an important role in the ageing process. It is important, therefore, to emphasize the relationship between health and nutrition in the elderly, particularly with regard to antioxidant micronutrient requirements. Indeed, accelerated ageing may be related to a deficit in the intakes of antioxidant vitamins (tocopherols, carotenoids and vitamin C) and trace elements (Zn and Se), as well as to an impaired adaptative mechanism against oxidative stress. Physiological modifications occurring during the lifetime and environmental influences are significant factors contributing to the impairment of micronutrient status, and these factors have to be considered when defining the specific requirements of the elderly. For Fe there is no evidence of benefit of supplementation in healthy subjects, but in the present state of knowledge combined supplementation, including Zn, Se, vitamins C and E and carotenoids, could be the best way to prevent accelerated ageing and reduce the risk of several common age-related diseases. Résumé De nombreuses théories (immunologique, génétique et neuroendocrinologique) ont été proposées pour expliquer les processus de vieillissement et les pathologies qui s’y rapportent. Les mécanismes oxydatifs pourraient contribuer à ces processus et plus particulièrement à leur accélération. La théorie radicalaire repose sur une modification avec l’âge du rapport prooxydants ou antioxydants dû à une majoration des processus oxydatifs accompagnés d’une diminution des systèmes de défense subséquentes à une carence en un ou plusieurs micronutriments antioxydants. Les modifications physiologiques qui accompagnent le vieillisement et une alimentation sélective contribuent aux modifications d’apport et d’absorption des micronutriments. Ces altérations sont accentuées lors de pathologies chroniques. Il n’existe pas de réel consensus sur les recommandations d’apports en oligoéléments adaptés au sujet âgé. Néanmoins les études récentes montrent qu’une association zinc, sélénium, vitamines antioxydantes (vitamines A et E et caroténodes) pourrait être le moyen le plus efficace de lutte contre les pathologies du grand âge et également de prévention du vieillissement accéléré.
Targets and procedures for altering ruminant meat and milk lipids
Authors: Demeyer D. , Doreau M.
Published: February 2011

Beef and dairy products suffer from a negative health image, related to the nature of their lipid fraction. Rumen lipid metabolism involves the presence of saturated lipids in ruminant tissues. Lipolysis, fatty acid biohydrogenation and formation of microbial fatty acids in the rumen and their effects on rumen outflow of fatty acids are discussed. Special emphasis is given to the formation of trans-fatty acids and the possibilities of decreasing biohydrogenation. Small differences in intestinal digestibilities of fatty acids are mentioned, followed by a discussion on transfer of absorbed fatty acids into milk and adipose tissue lipids. The preferential retention of polyunsaturated fatty acids as well as the balance between synthesis and incorporation of fatty acids in tissues is described. Dietary means for the modification of milk fat are listed, with special emphasis on the possibilities for enrichment in polyunsaturated fatty acids and the presence of conjugated linoleic acids. A description of the nature and development of fat depots in beef cattle is followed by a discussion of breed, conformation and feed effects on adipose tissue distribution and fatty acid composition. Special emphasis is given to the very lean Belgian Blue double-muscled breed. The review ends with a consideration of the limits to the modification of ruminant fats, involving considerations of consumer acceptance as well as animal welfare and environmental effects.
A genetic dissection of the retinoid signalling pathway in the mouse
Authors: Mark Manuel , Ghyselinck Norbert B. , Wendling Olivia , Dupé Valérie , Mascrez Bénédicte , Kastner Philippe , Chambon Pierre
Published: February 2011

To determine the functions of retinoic acid receptors RAR and RXR, we have systematically knocked-out their genes by homologous recombination in the embryonic stem cells and generated null-mutant mice. This approach has allowed us to perform a genetic dissection of the retinoic acid signalling pathway.
Amino acid limitation regulates gene expression
Authors: Bruhat Alain , Jousse Céline , Fafournoux Pierre
Published: February 2011

In mammals, the plasma concentration of amino acids is affected by nutritional or pathological conditions. For example, an alteration in the amino acid profile has been reported when there is a deficiency of any one or more of the essential amino acids, a dietary imbalance of amino acids, or an insufficient intake of protein. We examined the role of amino acid limitation in regulating mammalian gene expression. Depletion of arginine, cystine and all essential amino acids leads to induction of insulin-like growth factor-binding protein-1 (IGFBP-1) mRNA and protein expression in a dose-dependent manner. Moreover, exposure of HepG2 cells to amino acids at a concentration reproducing the amino acid concentration found in portal blood of rats fed on a low-protein diet leads to a significantly higher (P < 0·0002) expression of IGFBP-1. Using CCAAT/enhancer-binding protein homologous protein (CHOP) induction by leucine deprivation as a model, we have characterized the molecular mechanisms involved in the regulation of gene expression by amino acids. We have shown that leucine limitation leads to induction of CHOP mRNA and protein. Elevated mRNA levels result from both an increase in the rate of CHOP transcription and an increase in mRNA stability. We have characterized two elements of the CHOP gene that are essential to the transcriptional activation produced by an amino acid limitation. These findings demonstrate that an amino acid limitation, as occurs during dietary protein deficiency, can induce gene expression. Thus, amino acids by themselves can play, in concert with hormones, an important role in the control of gene expression.
Free radicals in skin and muscle: damaging agents or signals for adaptation?
Authors: Jackson Malcom J.
Published: February 2011

Much of the current literature regarding the biological effects of antioxidant nutrients has concentrated on their potential role in inhibiting or preventing tissue damage induced by free radical species produced during metabolism. Recent findings indicate that antioxidants may also have more subtle roles, regulating changes in gene expression induced by oxidizing free radical species. There is increasing evidence that free radicals act as signals for cell adaptation in a variety of cell types and the nature of the mechanisms by which free radical species influence gene expression is the subject of much current research. Processes such as these may be particularly important in tissues regularly exposed to varying amounts of oxidative stress as part of their normal physiological functions. Examples of such tissues include skin exposed to u.v. light and skeletal muscle subjected to repeated bouts of exercise.