Current Nutrition & Food Science - Volume 2, Issue 2, 2006

Malnutrition is a common complication of chronic liver disease (CLD). Standard anthropometric techniques available to assess nutritional status in children with CLD are noted to be inadequate but more sophisticated methods are all limited to research. Nutritional interventions in a few case studies have shown to improve the outcome of children after liver transplantation, but there remains a lack of systematic studies on this subject. What has been established is the relationship between poor nutritional status and growth failure, which sometimes continues following transplantation. The mechanisms underlying growth failure relate to disturbances in the GH/IGF axis and the effects of immunosuppression after liver transplantation. Current methods of trying to improve nutritional status prior to transplantation include intensive nasogastric feeding and in extreme cases parenteral nutrition. These are based on recommendations made in the late 1980's and early 1990's. Since this time there have been no advances in nutritional therapy for children with CLD. While review articles on the subject repeatedly call for more investigations into the use of growth hormone, zinc, and other novel substrates; research into nutritional support in these subjects lays dormant. While transplantation may offer a way of reversing the signs of poor nutritional status, growth failure continues to be a problem, which is a distressing consequence for affected children.

As a whole, biological research has recently shifted its focus from reductionism to holistic approaches to study complex systems, a strategy often termed "systems biology". Nutritional research has progressed similarly, incorporating phenotype, genotype, genomics, and bioinformatics into an integrative molecular nutrition research model to study the impact of nutritional status on health and disease. Given the importance of livestock and companion animals as large animal models for humans, many of these genomes including that of the dog, cow, cat, and chicken have been sequenced or are being sequenced by the National Institutes of Health (NIH). Ongoing projects to sequence the canine genome and create a SNP map, in addition to the phenotypic and genotypic similarities and unique breed structure of domestic dogs, continue to increase the experimental power of the dog model. While anatomical and physiological similarities have deemed the dog a useful model for gastrointestinal research for decades, economical and ethical concerns have recently decreased their use in this research field. This review aims to reiterate the importance of the dog model in gastrointestinal research, including the study of prebiotics and aging on intestinal health, analyzing gene expression profiles to better understand intestinal diseases such as inflammatory bowel disease, and performing whole genome association studies to identify genetic loci contributing to complex intestinal diseases.

It is now commonly accepted that white adipocytes actively secrete a wide range of bioactive molecules including leptin, adiponectin, resistin and many other signals. These adipose-derived factors are mainly influenced by nutritional transitions. This review addresses essentially the differential regulation and role of animal adipose-secreted products in regulating metabolic, endocrine and behavioral responses during prolonged fasting. When reaching a low adiposity threshold, animals enter late fasting characterized by elevated rates of protein degradation while lipid utilization decreases. Low NEFA levels in late fasting could affect PPAR activation and the management of body reserves, thus promoting food seeking behavior. Low leptin levels are also likely involved in the efficient mobilization of energy stores and in the induction of strong rises in hypothalamic orexigenic neuropeptides in late fasting. This effect is prevented by leptin perfusion. During fasting, adiponectin reduced levels could be related to its ability to signal nutritional and/or metabolic changes, to promote energy preservation or to prepare the body to efficiently restore body weight in case of refeeding while resistin low levels could constitute an adipose status sensor and/or improve glucose homeostasis. The fasting-induced changes of other signals during the fed/fasted/refed transitions are also briefly discussed.

Obesity is correlated with low-grade inflammation, which provides a potential link between insulin resistance and the endothelial dysfunction present in the early stages of the atherosclerotic process. Adipose tissue has been considered until recently, just a depot for energy storage, which has the sole function of accretion in the form of triacylglycerols of excess energy. However, adipose tissue is now considered an active endocrine organ that releases a wide range of endocrine, paracrine and metabolic signals. Although obesity increases in adipose tissue the expression of genes is related with inflammation and immunity (and, conversely, caloric restriction improves this inflammatory profile), these genes are expressed mainly in the cells of the stromal vascular fraction of the adipose tissue rather than in the adipocytes. Adipose tissue structure is not uniform. More than half of the adipose tissue cells belong to a heterogeneous stromal vascular fraction, which includes stem cells, preadipocytes, endothelial cells, and macrophages. The strong relationship between adipose tissue, macrophage content and the indicators of adiposity hit at their implication in the increased adipose tissue production of proinflammatory molecules and acute phase proteins associated with obesity. The growing knowledge of the implication of adipose tissue in inflammation, response to immune challenge, and tissue proliferation may be directly traced to cell types not directly related to the energy storage function. Thus, we can conclude that white adipose tissue is something more than simply adipocytes.

It is widely known that selenium develops its biological activity via an active selenocysteine residue in the catalytically active centre of functional selenoproteins. By its function in glutathione peroxidases and thioredoxin reductases selenium contributes to a remarkable extent to the maintenance of the cellular antioxidative balance when taken up at the recommended dietary level (animals: 0.1 - 0.3 μg/kg diet, humans: 50 - 150 μg Se daily). In recent years an interesting physiological aspect has been found for selenate (selenium oxidation state +VI). High doses of selenate displayed antidiabetic properties when applied to diabetic animals or added to the media of tissue cultures. Thus selenate treatment could be shown to normalise hyperglycaemia as well as changed activities of glycolytic and gluconeogenic marker enzymes. Mechanistically an increased phosphorylation of single proteins of the insulin signalling cascade could be attributed to the insulinomimetic action of selenate. The examination of the antidiabetic features of selenate in type II diabetic animals revealed that the increase in phosphorylation is presumably based on the inhibition of protein tyrosine phosphatases, which act as negative regulators of insulin signalling. In contrast to the antidiabetic features of high selenate doses, selenite administration to diabetic animals showed no effect on diabetes. In a recent study it could even be demonstrated that the overexpression of glutathione peroxidase 1 (the best characterized selenoprotein) in healthy mice led to an increase in insulin resistance and obesity. These results could partially be confirmed by the data of our most recent investigation in which a high expression and activity of glutathione peroxidase, obtained by feeding selenium at the nutritionally recommended level and at a moderately supranutritive level corresponded to an up-regulated expression of proteins whose expression is increased in insulin resistant type 2 diabetes. From studies on the role of selenium in diabetes carried out so far it can be concluded that selenium plays an ambivalent role with regard to diabetes depending on the compound and on the applied concentration. Thus only high doses of selenate evolve antidiabetic properties. Investigations into an even negative influence of moderate supranutritive doses of selenium on diabetes and the molecular events linked to this are necessary. The review summarizes the information currently available on the ambivalent role of selenium in diabetes which seems to depend on the chemical form and the applied concentration. Established facts, recent findings of our own studies using microarray analysis and RT-PCR and perspectives of the role of selenium in diabetes are presented and discussed against the background of selenium metabolism.

General practitioners (GPs) are frequently confronted with patients who suffer from obesity or other nutritionrelated diseases, such as diabetes and coronary heart disease. There is increasing evidence that nutrition communication is effective in changing nutrition behaviour. Moreover, it is widely argued that GPs are ideally placed to provide nutrition information. The aim of this review is to provide an overview of the state of the art regarding nutrition communication in general practice. First, an overview of the occurrence of nutrition communication in general practice is provided. Next, it is established that patients' perceptions regarding nutrition communication are positive. Although there are many opportunities for nutrition communication in general practice, these opportunities are often not taken up. Even though GPs' perceptions regarding nutrition communication were positive, they also perceive barriers, like lack of time and patient non-compliance. For more effective nutrition communication between GPs and patients, GPs' perceived barriers should be overcome and GPs' self-efficacy should be strengthened. Moreover, we recommend that GPs adapt their nutrition communication style, dependent of the specific circumstances.

During the past decade, there has been vast expansion in the research of fructooligosaccharides (FOS), including their chemistry, biochemistry, and enzymology in living organisms, as well as nutritional and health benefits. However, in spite of these considerable advances in FOS science, many other aspects of the mechanisms of FOS behind their involvement in well being have not been fully understood. FOS constitute the major part of the dry matter of edible Alliums, and the knowledge of the mechanisms of their mode of action in human metabolism are of great interest. Important progress has been made in the chemical, nutritional and clinical research areas of Alliums FOS, as well as on other FOS, and in addition to their role as quality attribute, FOS participate in other processes. This paper aims to review the occurrence, chemistry and health benefits of Alliums' FOS including nutritional contribution of FOS in health and well being.

Greater understanding of factors contributing to nutritional deterioration in cancer, as well as patients' expectations and the personal disease impact, are required to devise meaningful nutritional therapy. In a cross-sectional study of 205 patients with cancer of the head-neck, oesophagus, stomach, colon/rectum, nutritional deterioration was multifactorial and mainly determined by the tumour burden. In a larger cohort of 271 patients, although cancer stage and location were the major determinants of the patients' Quality of Life, nutritional deterioration combined with deficiencies in nutritional intake were functionally more relevant than cancer stage. Based on this framework, we tested the potential role of nutritional intervention on patient predefined outcomes: nutritional status, diet intake, morbidity and Quality of Life. Two prospective randomised controlled trials were conducted in patients with cancer of the colon/rectum (n=111) or head-neck (n=75), in both instances patients were stratified for staging. In order to compare nutritional interventions during radiotherapy, each study had 3 arms: intensive dietary counselling vs oral supplements vs ad libitum intake; outcomes were analysed at the end and 3 months after radiotherapy, the latter period without intervention. In both trials, only nutritional interventions positively influenced outcomes during radiotherapy; 3 months after its completion, intensive counselling was the single method capable of sustaining a significant impact on patients' outcomes. Nutrition is central to the improvement of a diversity of patient outcomes in colorectal and head-neck cancer patients.