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Apple processing results in peel, stem, seeds, and pulp being left as a waste product known as apple pomace. This review comprehensively assessed apple pomace composition for nutritional value and bioactive substances and evaluated potential health benefits and safety. Apple pomace is a rich source of health-benefitting nutrients, including minerals, dietary fiber, antioxidants, and ursolic acid, which suggests it has potential use as a dietary supplement, functional food, and/or food additive. Preclinical studies have found apple pomace and its isolated extracts improved lipid metabolism, antioxidant status, and gastrointestinal function and had a positive effect on metabolic disorders (eg, hyperglycemia, insulin resistance, etc.). Safety studies have shown apple pomace to be a safe livestock feed additive and to have pesticide concentrations within safety thresholds established for human consumption. Commercial development of apple pomace for human consumption requires more research focusing on standardized methods of nutrient reporting, mechanistic studies, and human clinical trials. [ABSTRACT FROM AUTHOR]

The fetal origins of health and disease framework has identified extremes in fetal growth and birth weight as factors associated with the lifelong generation of chronic diseases such as obesity, diabetes, cardiovascular disease, and hypertension. Maternal nutrition plays a critical role in fetal and placental development, in part by providing the methyl groups required to establish the fetus's genome structure and function, notably through DNA methylation. The goal of this narrative review is to describe the role of maternal dietary methyl donor (methionine, folate, and choline) and cofactor (zinc and vitamins B2, B6, and B12) intake in one-carbon metabolism and DNA methylation in the fetus and placenta, as well as their impacts on fetal growth and lifelong health outcomes, with specific examples in animals and humans. Based on the available evidence, it is concluded that intake of different amounts of dietary methyl donors and cofactors during pregnancy may alter fetal growth and development, thus establishing a major link between early environmental exposure and disease development in the offspring later in life. [ABSTRACT FROM AUTHOR]

Neuroinflammation has been implicated in the pathology of various psychiatric and neurodegenerative disorders. Accumulating evidence suggests that food components can modulate inflammatory processes, and therefore it could be hypothesized that such nutrients might exhibit therapeutic efficacy against these brain diseases. Rice bran is often discarded as a waste product, although it contains a wide range of potentially useful substances. Several rice fiber components from rice bran have been described as having antiinflammatory properties. This review summarizes the evidence supporting a modulatory effect of rice fiber components on symptoms in several animal models for neuroinflammation. In vitro studies on immune cells and in vivo studies on nutritional intervention in animal models of central and peripheral inflammation are discussed in the context of the potential use of rice fiber components for prevention and treatment of brain diseases in which neuroinflammation is involved. [ABSTRACT FROM AUTHOR]

Protein malnutrition is one of the most serious nutritional problems worldwide, affecting 794 million people and costing up to $3.5 trillion annually in the global economy. Protein malnutrition primarily affects children, the elderly, and hospitalized patients. Different degrees of protein deficiency lead to a broad spectrum of signs and symptoms of protein malnutrition, especially in organs in which the hematopoietic system is characterized by a high rate of protein turnover and, consequently, a high rate of protein renewal and cellular proliferation. Here, the current scientific information about protein malnutrition and its effects on the hematopoietic process is reviewed. The production of hematopoietic cells is described, with special attention given to the hematopoietic microenvironment and the development of stem cells. Advances in the study of hematopoiesis in protein malnutrition are also summarized. Studies of protein malnutrition in vitro, in animal models, and in humans demonstrate several alterations that impair hematopoiesis, such as structural changes in the extracellular matrix, the hematopoietic stem cell niche, the spleen, the thymus, and bone marrow stromal cells; changes in mesenchymal and hematopoietic stem cells; increased autophagy; G0/G1 cell-cycle arrest of progenitor hematopoietic cells; and functional alterations in leukocytes. Structural and cellular changes of the hematopoietic microenvironment in protein malnutrition contribute to bone marrow atrophy and nonestablishment of hematopoietic stem cells, resulting in impaired homeostasis and an impaired immune response. [ABSTRACT FROM AUTHOR]

Context: Oligosaccharides are the third largest solid component in human milk. These diverse compounds are thought to have numerous beneficial functions in infants, including protection against infectious diseases. The structures of more than 100 oligosaccharides in human milk have been elucidated so far. Objective: The aim of this review was to identify the main factors that affect the concentrations of oligosaccharides in human milk and to determine whether it is possible to calculate representative and reliable mean concentrations. Data Sources: A comprehensive literature search on oligosaccharide concentrations in human milk was performed in 6 electronic databases: BIOSIS, Current Contents Search, Embase, Lancet Titles, MEDLINE and PubMed. Study Selection: The initial search resulted in 1363 hits. After the elimination of duplicates, the literature was screened. The application of strict inclusion criteria resulted in 21 articles selected. Data Extraction: Oligosaccharide concentrations, both mean values and single values, reported in the literature were sorted by gestational age, secretor status of mothers, and defined lactation periods. Results: Mean concentrations, including confidence limits, of 33 neutral and acidic oligosaccharides reported could be calculated. Concentrations of oligosaccharides in human milk show variations that are dependent on both the secretor type of the mother and the lactation period as examined by analyses of variance. In addition, large interlaboratory variations in the data were observed. Conclusions: Worldwide interlaboratory quantitative analyses of identical milk samples would be required to identify the most reliable methods of determining concentrations of oligosaccharides in human milk. The data presented here contribute to the current knowledge about the composition and quantities of oligosaccharides in human milk and may foster greater understanding of the biological functions of these compounds. [ABSTRACT FROM AUTHOR]

Aspartame is a synthetic dipeptide artificial sweetener, frequently used in foods, medications, and beverages, notably carbonated and powdered soft drinks. Since 1981, when aspartame was first approved by the US Food and Drug Administration, researchers have debated both its recommended safe dosage (40mg/kg/d) and its general safety to organ systems. This review examines papers published between 2000 and 2016 on both the safe dosage and higher-thanrecommended dosages and presents a concise synthesis of current trends. Data on the safe aspartame dosage are controversial, and the literature suggests there are potential side effects associated with aspartame consumption. Since aspartame consumption is on the rise, the safety of this sweetener should be revisited. Most of the literature available on the safety of aspartame is included in this review. Safety studies are based primarily on animal models, as data from human studies are limited. The existing animal studies and the limited human studies suggest that aspartame and its metabolites, whether consumed in quantities significantly higher than the recommended safe dosage or within recommended safe levels, may disrupt the oxidant/antioxidant balance, induce oxidative stress, and damage cell membrane integrity, potentially affecting a variety of cells and tissues and causing a deregulation of cellular function, ultimately leading to systemic inflammation. [ABSTRACT FROM AUTHOR]

The worldwide prevalence of diabetes mellitus is expected to reach 439 million by 2030. Diabetes increases the risk for developing secondary complications such as nephropathy and cardiovascular disease, critical factors that dictate the survival rate of diabetes patients. Compelling evidence has indicated that the positive impact of fermentable carbohydrates in obesity-related diabetes is mediated by the production of short-chain fatty acids and the modulation of colonic microbiota. This review summarizes the potential implications of dietary resistant starch, a class of fermentable fiber, in glucose homeostasis and kidney health in obesityassociated diabetes and examines the mechanisms underlying the protective effect of resistant starch. Though extensive clinical studies are still warranted, replacement of simple carbohydrates with resistant starch could be a highly effective alternative dietary strategy to prevent secondary complications resulting from hyperglycemia. [ABSTRACT FROM AUTHOR]

The mammalian gastrointestinal tract harbors trillions of commensal microorganisms, collectively known as the microbiota. The microbiota is a critical source of environmental stimuli and, thus, has a tremendous impact on the health of the host. The microbes within the microbiota regulate homeostasis within the gut, and any alteration in their composition can lead to disorders that include inflammatory bowel disease, allergy, autoimmune disease, diabetes, mental disorders, and cancer. Hence, restoration of the gut flora following changes or imbalance is imperative for the host. The low-molecular-weight compounds and nutrients such as short-chain fatty acids, polyamines, polyphenols, and vitamins produced by microbial metabolism of nondigestible food components in the gut actively participate in various epigenomic mechanisms that reprogram the genome by altering the transcriptional machinery of a cell in response to environmental stimuli. These epigenetic modifications are caused by a set of highly dynamic enzymes, notably histone acetylases, deacetylases, DNA methylases, and demethylases, that are influenced by microbial metabolites and other environmental cues. Recent studies have shown that host expression of histone acetylases and histone deacetylases is important for regulating communication between the intestinal microbiota and the host cells. Histone acetylases and deacetylases influence the molecular expression of genes that affect not only physiological functions but also behavioral shifts that occur via neuroepigenetic modifications of genes. The underlying molecular mechanisms, however, have yet to be fully elucidated and thus provide a new area of research. The present review provides insights into the current understanding of the microbiota and its association with mammalian epigenomics as well as the interaction of pathogens and probiotics with host epigenetic machinery. [ABSTRACT FROM AUTHOR]

Microbial colonization of the gastrointestinal tract is an essential process that modulates host physiology and immunity. Recently, researchers have begun to understand how and when these microorganisms colonize the gut and the earlylife factors that impact their natural ecological establishment. The vertical transmission of maternal microbes to the offspring is a critical factor for host immune and metabolic development. Increasing evidence also points to a role in the wiring of the gut-brain axis. This process may be altered by various factors such as mode of delivery, gestational age at birth, the use of antibiotics in early life, infant feeding and hygiene practices. In fact, these early exposures that impact the intestinal microbiota have been associated with the development of diseases such as obesity, type 1 diabetes, asthma, allergies and even neurodevelopmental disorders. The present review summarizes the impact of cesarean birth on the gut microbiome and the health status of the developing infant and discusses possible preventative and restorative strategies to compensate for early-life microbial perturbations. [ABSTRACT FROM AUTHOR]

Short-chain fatty acids (SCFAs), mainly acetate, propionate and butyrate, produced by microbial fermentation of undigested food substances are believed to play a beneficial role in human gut health. Short-chain fatty acids influence colonic health through various mechanisms. In vitro and ex vivo studies show that SCFAs have anti-inflammatory and anticarcinogenic effects, play an important role in maintaining metabolic homeostasis in colonocytes and protect colonocytes from external harm. Animal studies have found substantial positive effects of SCFAs or dietary fiber on colonic disease, but convincing evidence in humans is lacking. Most human intervention trials have been conducted in the context of inflammatory bowel disease. Only a limited number of those trials are of high quality, showing little or no favorable effect of SCFA treatment over placebo. Opportunities for future research include exploring the use of combination therapies with anti-inflammatory drugs, prebiotics or probiotics; the use of prodrugs in the setting of carcinogenesis; or the direct application of SCFAs to improve mucosal healing after colonic surgery. [ABSTRACT FROM AUTHOR]

The development of therapeutic approaches aimed at reducing inflammation, improving lipid metabolism and preventing nonalcoholic fatty liver disease holds significant potential in the management of obesity-associated disease. In this review, the recent basic science and clinical research examining dietary sphingolipid intake and the prevention of dyslipidemia and nonalcoholic fatty liver disease is summarized. Dietary sphingolipids have been shown to dose-dependently reduce the acute intestinal absorption of cholesterol, triglycerides and fatty acids in rodents. Overall, studies feeding dietary sphingolipids to rodents typically show reductions in serum lipids. Furthermore, these hypolipidemic effects are also observed in most human studies, although the magnitude of such effects is typically smaller. Dietary sphingolipids also appear useful in preventing hepatic lipid uptake and accumulation and have shown benefits in preventing hepatic steatosis in rodent models. Dietary sphingolipids may affect the gut-liver axis by preventing the translocation of gut bacteria-derived lipopolysaccharide and/or inhibiting its proinflammatory effects. Current evidence from preclinical studies indicates that dietary sphingolipids have lipid-lowering and anti-inflammatory properties, although their potential to prevent human chronic disease has not been fully explored. It will be important to determine if such effects seen in cell and animal models translate to humans. More research is warranted to define how dietary sphingolipids influence lipid metabolism and inflammation. [ABSTRACT FROM AUTHOR]

A growing body of evidence supports the concept of perinatal programming through which the perinatal environment affects the development of the fetus and infant, thereby modifying the risk profile for disease later in life. Increasing attention is focusing on the role of the early environment in the development of chronic intestinal disorders. Epidemiological studies have highlighted the link between perinatal factors, such as breastfeeding, cesarean delivery, and antibiotic use, and an increased risk for inflammatory bowel disease and/or celiac disease. These links are consistent with the concept of perinatal programming of intestinal inflammatory disorders. Animal models have shown that the early-life environment affects the development of the gastrointestinal tract, but further experimental studies are needed to confirm the long-term effects of the perinatal environment on susceptibility to chronic intestinal disorders later in life. Changes in the development and composition of the intestinal microbiota as well as epigenetic changes are emerging as key mechanisms through which the perinatal environment determines susceptibility to intestinal inflammatory disorders. [ABSTRACT FROM AUTHOR]

Pregnancy and infancy comprise the most critical stages for conditioning an individual's health, with a number of implications for subsequent risks of morbidity, mortality, and reproductive health. Nutrition may influence both the overall pregnancy outcome and the growth trajectory and immune system of the fetus and infant, with short- and long-term effects on the health of the offspring. Within this context, leading experts at Expo Milano 2015 in Milan, Italy, discussed up-to-date knowledge while providing suggestions and challenges before, during, and after pregnancy. This narrative review summarizes the key issues raised by the experts concerning the interplay between the nutritional environment from conception to early infancy and the offspring's immediate and lifelong health, with a particular focus on epigenetic mechanisms, probiotics, vitamin D, and breastfeeding. Taken together, the findings strengthen the awareness that nutritional exposures occurring from preconception to the postnatal period may be strong determinants of the offspring's health and may provide supportive evidence for current nutritional recommendations and guidelines for pregnant women and infants. Critical topics to be addressed in future research and translated into recommendations of public health relevance are also highlighted. [ABSTRACT FROM AUTHOR]

Salt sensitivity, which is an increase in blood pressure in response to high dietary salt intake, is an independent risk factor for cardiovascular disease and mortality. It is associated with physiological, environmental, demographic, and genetic factors. This review focuses on the physiological mechanisms of salt sensitivity in populations at particular risk, along with the associated dietary factors. The interplay of mechanisms such as the renin-angiotensin aldosterone system, endothelial dysfunction, ion transport, and estrogen decrease in women contributes to development of salt sensitivity. Because of their effects on these mechanisms, higher dietary intakes of potassium, calcium, vitamin D, antioxidant vitamins, and proteins rich in L-arginine, as well as adherence to dietary patterns similar to the DASH (Dietary Approaches to Stop Hypertension) diet, can be beneficial to salt-sensitive populations. In contrast, diets similar to the typical Western diet, which is rich in saturated fats, sucrose, and fructose, together with excessive alcohol consumption, may exacerbate salt-sensitive changes in blood pressure. Identifying potential mechanisms of salt sensitivity in susceptible populations and linking them to protective or harmful dietary and lifestyle factors can lead to more specific guidelines for the prevention of hypertension and cardiovascular disease. [ABSTRACT FROM AUTHOR]

Human milk oligosaccharides (HMOs) are complex sugars highly abundant in human milk but currently not present in infant formula. Rapidly accumulating evidence from in vitro and in vivo studies, combined with epidemiological associations and correlations, suggests that HMOs benefit infants through multiple mechanisms and in a variety of clinical contexts. Until recently, however, research on HMOs has been limited by an insufficient availability of HMOs. Most HMOs are found uniquely in human milk, and thus far it has been prohibitively tedious and expensive to isolate and synthesize them. This article reviews new strategies to overcome this lack of availability by generating HMOs through chemoenzymatic synthesis, microbial metabolic engineering, and isolation from human donor milk or dairy streams. Each approach has its advantages and comes with its own challenges, but combining the different methods and acknowledging their limitations creates new opportunities for research and application with the goal of improving maternal and infant health. [ABSTRACT FROM AUTHOR]

Optimal iron nutrition in utero is essential for development of the fetus and helps establish birth iron stores adequate to sustain growth in early infancy. In species with hemochorial placentas, such as humans and rodents, iron in the maternal circulation is transferred to the fetus by directly contacting placental syncytiotrophoblasts. Early kinetic studies provided valuable data on the initial uptake of maternal transferrin, an iron-binding protein, by the placenta. However, the remaining steps of iron trafficking across syncytiotrophoblasts and through the fetal endothelium into the fetal blood remain poorly characterized. Over the last 20 years, identification of transmembrane iron transporters and the iron regulatory hormone hepcidin has greatly expanded the knowledge of cellular iron transport and its regulation by systemic iron status. In addition, emerging human and animal data demonstrating comprised fetal iron stores in severe maternal iron deficiency challenge the classic dogma of exclusive fetal control over the transfer process and indicate that maternal and local signals may play a role in regulating this process. This review compiles current data on the kinetic, molecular, and regulatory aspects of placental iron transport and considers new questions and knowledge gaps raised by these advances. [ABSTRACT FROM AUTHOR]

Infants born to diabetic mothers have a higher frequency of impaired neurodevelopment. The omega-3 or n-3 fatty acid docosahexaenoic acid (DHA) is an important structural component of neural tissue and is critical for fetal brain development. Maternal DHA supplementation during pregnancy is linked to better infant neurodevelopment; however, maternal--fetal transfer of DHA is reduced in women with diabetes. Evidence of mechanisms explaining altered maternal--fetal DHA transfer in this population is limited. This review explores existing evidence underpinning reduced maternal--fetal DHA transfer in maternal fuel metabolism in this population. Further research is necessary to evaluate the role of peroxisome proliferator- activated receptors in modulating placental fatty acid binding and maternal--fetal DHA transfer. Considerations for clinical practice include a diet high in DHA and/or provision of supplemental DHA to obstetric diabetic patients within minimum guidelines. [ABSTRACT FROM AUTHOR]

Glutamine, reviewed extensively in the last century, is a key substrate for the splanchnic bed in the whole body and is a nutrient of particular interest in gastrointestinal research. A marked decrease in the plasma glutamine concentration has recently been observed in neonates and adults during acute illness and stress. Although some studies in newborns have shown parenteral and enteral supplementation with glutamine to be of benefit (by decreasing proteolysis and activating the immune system), clinical trials have not demonstrated prolonged advantages such as reductions in mortality or risk of infections in adults. In addition, glutamine is not able to combat the muscle wasting associated with disease or age-related sarcopenia. Oral glutamine supplementation initiated before advanced age in rats increases gut mass and improves the villus height of mucosa, thereby preventing the gut atrophy encountered in advanced age. Enterocytes from very old rats continuously metabolize glutamine into citrulline, which allowed, for the first time, the use of citrulline as a noninvasive marker of intestinal atrophy induced by advanced age. [ABSTRACT FROM AUTHOR]

Vitamin consumption prior to and during pregnancy has increased as a result of proactive recommendations by health professionals, wide availability of vitamin supplements, and liberal food-fortification policies. Folic acid, alone or in combination with other B vitamins, is the most recommended vitamin consumed during pregnancy because deficiency of this vitamin leads to birth defects in the infant. Folic acid and other B vitamins are also integral components of biochemical processes that are essential to the development of regulatory systems that control the ability of the offspring to adapt to the external environment. Although few human studies have investigated the lasting effects of high vitamin intakes during pregnancy, animal models have shown that excess vitamin supplementation during gestation is associated with negative metabolic effects in both the mothers and their offspring. This research from animal models, combined with the recognition that epigenetic regulation of gene expression is plastic, provides evidence for further examination of these relationships in the later life of pregnant women and their children. [ABSTRACT FROM AUTHOR]

The epidemic of metabolic diseases has raised questions about the interplay between the human diet and the gut and its microbiota. The gut has two vital roles: nutrient absorption and intestinal barrier function. Gut barrier defects are involved in many diseases. Excess energy intake disturbs the gut microbiota and favors body entry of microbial compounds that stimulate chronic metabolic inflammation. In this context, the natural defense mechanisms of gut epithelial cells and the potential to boost them nutritionally warrant further study. One such important defense system is the activation of inducible heat-shock proteins (iHSPs) which protect the gut epithelium against oxidative stress and inflammation. Importantly, various microbial components can induce the expression of iHSPs. This review examines gut epithelial iHSPs as the main targets of microbial signals and nutrients and presents data on diseases involving disturbances of gut epithelial iHSPs. In addition, a broad literature analysis of dietary modulation of gut epithelial iHSPs is provided. Future research aims should include the identification of gut microbes that can optimize gut-protective iHSPs and the evaluation of iHSP-mediated health benefits of nutrients and food components. [ABSTRACT FROM AUTHOR]

Context: Studies suggest that appropriate nutritional modifications can improve the natural conception rate of infertile couples. Objectives: The purpose of this study was to review the human trials that investigated the relation between nutrition and male infertility. Data Sources: A comprehensive systematic review of published human studies was carried out by searching scientific databases. Article selection was carried out in accordance with Preferred Reporting Items for Systematic Reviews and Meta-Analyses. The American Dietetic Association Research Design and Implementation Checklist was also used for quality assessment. Data Extraction: A total of 502 articles were identified, of which 23 studies met the inclusion criteria. Data Synthesis: Results indicated that a healthy diet improves at least one measure of semen quality, while diets high in lipophilic foods, soy isoflavones, and sweets lower semen quality. Conclusion: The role of daily nutrient exposure and dietary quality needs to be highlighted in male infertility. Mechanistic studies addressing the responsible underlying mechanisms of action of dietary modifications are highly warranted. Systematic Review Registration: PROSPERO 2013: CRD42013005953. Available at: http://www.crd.york.ac.uk/PROSPERO/display_record.asp?ID=CRD42013005953. [ABSTRACT FROM AUTHOR]

Post-translational modification is a critical mechanism by which trace mineral transporters rapidly adapt to their environment to homeostatically regulate ion transport. Recently, a novel pathway was described whereby iron stimulates the ubiquitination and proteasomal degradation of the trace mineral transporter ZIP14. Discovery of this pathway suggests the proteasome as a potential therapeutic target for regulation of iron storage. Moreover, these findings contribute to a theoretical framework that can be applied to other ubiquitinated trace mineral transporters. This review will detail the current state of knowledge regarding the ubiquitination of trace mineral transporters, focusing on iron and zinc transporters, and the potential utility of post-translational modification of trace mineral transporters in the treatment of disease. [ABSTRACT FROM AUTHOR]

Very preterm infants (<32 weeks' gestation) are at high risk for impaired skeletal development because of factors that limit the provision of extrauterine nutrients. Cumulative net deficiencies of calcium, phosphorus, docosahexaenoic acid (DHA), and arachidonic acid (ARA) are evident in these infants after prolonged administration of total parenteral nutrition (TPN). This is significant because minerals as well as metabolites of DHA and ARA are important modulators of bone cell differentiation, lengthening of bone, and bone matrix deposition. Furthermore, diets containing only precursors of DHA and ARA result in suboptimal skeletal growth. With the emergence of new intravenous lipid emulsions, it is important to understand the impact of fatty acids on bone metabolism in the third trimester in order to optimize the provision of TPN in very preterm infants. The purpose of this review is to evaluate current evidence regarding intravenous lipid emulsions and bone metabolism in very preterm infants receiving prolonged TPN and to identify areas of research needed. [ABSTRACT FROM AUTHOR]

Dietary deficiencies of folate and other B vitamin cofactors involved in one-carbon metabolism, together with genetic polymorphisms in key folate-methionine metabolic pathway enzymes, are associated with increases in circulating plasma homocysteine, reduction in DNA methylation patterns, and genome instability events. All of these biomarkers have also been associated with pre-eclampsia. The aim of this review was to explore the literature and identify potential knowledge gaps in relation to the role of folate at the genomic level in either the etiology or the prevention of pre-eclampsia. A systematic search strategy was designed to identify citations in electronic databases for the following terms: folic acid supplementation AND preeclampsia, folic acid supplementation AND genome stability, folate AND genome stability AND pre-eclampsia, folic acid supplementation AND DNA methylation, and folate AND DNA methylation AND pre-eclampsia. Forty-three articles were selected according to predefined selection criteria. The studies included in the present review were not homogeneous, which made pooled analysis of the data very difficult. The present review highlights associations between folate deficiency and certain biomarkers observed in various tissues of women at risk of pre-eclampsia. Further investigation is required to understand the role of folate in either the etiology or the prevention of pre-eclampsia. [ABSTRACT FROM AUTHOR]

The human body has evolved with a disposition for nutrient storage, allowing for periods of irregular food availability and famine. In contrast, the modern diet is characterized by excessive consumption of fats and sugars, resulting in a surge in the rates of obesity and type 2 diabetes. Although these metabolic disorders arise from a complex interaction of genetic, social, and environmental factors, evidence now points tofundamental changes in nutrient metabolism at the cellular level contributing to the underlying pathology. Taste receptors detect nutrients in the oral cavity and gastrointestinal tract and can influence the hormonal response to nutrients; they may also become maladaptive in conditions of excess fat or sugar consumption. Precise links between taste receptor activity, and downstream effects on energy intake and glycemia are not well defined. This review outlines the candidate taste receptors for carbohydrates and fats in the oral cavity and within the small intestine, highlighting the contributions of underlying genetics (polymorphisms) and sensory challenges (e.g., a high-fat diet) to the development of obesity and type 2 diabetes. [ABSTRACT FROM AUTHOR]

In this review, the influence of fat depots on insulin resistance and the main characteristics of metabolically obese normal-weight and metabolically healthy obese phenotypes are discussed. Medline/PubMed and Science Direct were searched for articles related to the terms metabolically healthy obesity, metabolically obese normal weight, adipose tissue, and insulin resistance. Normal weight and obesity might be heterogeneous in regard to their effects. Fat distribution and lower insulin sensitivity are the main factors defining phenotypes within the same body mass index. Although these terms are interesting, controversies about them remain. Future studies exploring these phenotypes will help elucidate the roles of adiposity and/or insulin resistance in the development of metabolic alterations. [ABSTRACT FROM AUTHOR]

Abnormal expression and/or function of mammalian hexose transporters contribute to the hallmark hyperglycemia of diabetes. Due to different roles in glucose handling, various organ systems possess specific transporters that may be affected during the diabetic state. Diabetes has been associated with higher rates of intestinal glucose transport, paralleled by increased expression of both active and facilitative transporters and a shift in the location of transporters within the enterocyte, events that occur independent of intestinal hyperplasia and hyperglycemia. Peripheral tissues also exhibit deregulated glucose transport in the diabetic state, most notably defective translocation of transporters to the plasma membrane and reduced capacity to clear glucose from the bloodstream. Expression of renal active and facilitative glucose transporters increases as a result of diabetes, leading to elevated rates of glucose reabsorption. However, this may be a natural response designed to combat elevated blood glucose concentrations and not necessarily a direct effect of insulin deficiency. Functional foods and nutraceuticals, by modulation of glucose transporter activity, represent a potential dietary tool to aid in the management of hyperglycemia and diabetes. [ABSTRACT FROM AUTHOR]

It is well known that taste perception influences food intake. After ingestion, gustatory receptors relay sensory signals to the brain, which segregates, evaluates, and distinguishes the stimuli, leading to the experience known as "flavor." It is well accepted that five taste qualities - sweet, salty, bitter, sour, and umami - can be perceived by animals. In this review, the anatomy and physiology of human taste buds, the hormonal modulation of taste function, the importance of genetic chemosensory variation, and the influence of gustatory functioning on macronutrient selection and eating behavior are discussed. Individual genotypic variation results in specific phenotypes of food preference and nutrient intake. Understanding the role of taste in food selection and ingestive behavior is important for expanding our understanding of the factors involved in body weight maintenance and the risk of chronic diseases including obesity, atherosclerosis, cancer, diabetes, liver disease, and hypertension. [ABSTRACT FROM AUTHOR]

The average salt intake of people in Canada, the United States, and Europe is about 3,400mg of sodium per day, which exceeds the recommended intake levels set by various health organizations. The World Health Organization recommends a worldwide reduction of sodium intake to less than 2,000mg per day. Most research to date has focused on the negative effects of high-sodium intake; however, little information is available on the metabolic effects of low-sodium intakes. This review focuses on the hormonal changes associated with low-sodium diets, specially the hormones involved in metabolism and cardiovascular and renal function. Based largely on rodent studies, low-sodium diets have been associated with changes in glycemic control, energy metabolism, cardiovascular disease risk, cholesterol concentrations, inflammation, and functioning of the renin-angiotensin-aldosterone system. Overall, research has revealed mixed results regarding the impact of dietary sodium intake on various hormones. Further research is required to assess the effects of sodium reduction on hormones and their associated pathways in order to determine the likelihood of any unintended effects. [ABSTRACT FROM AUTHOR]

Epidemiological studies have led scientists to postulate the developmental origins of health and disease hypothesis for noncommunicable diseases such as diabetes, cardiovascular diseases, hypertension, and obesity. However, the cellular and molecular mechanisms involved in the development of these diseases are not well understood. In various animal models, it has been observed that oxidative stress during pregnancy is associated with the early development of endothelial dysfunction in offspring. This phenomenon suggests that endothelial dysfunction may initiate in the uterus and could lead to increased risk of cardiovascular disease later in life. Currently, it is known that many of the fetal adaptive responses to environmental factors are mediated by epigenetic changes in the genome, especially by the degree of methylation in cytosines in the promoter regions of genes. These findings suggest that the establishment of a particular epigenetic pattern in the genome may be generated by oxidative stress. [ABSTRACT FROM AUTHOR]

Visceral fat is strongly associated with the development of specific obesity-related metabolic alterations. Genetic and epigenetic mechanisms seem to be involved in the development of obesity and visceral adiposity. The aims of this review are to identify the single-nucleotide polymorphisms related to central obesity and to summarize the main findings on DNA methylation and obesity. A search of the MEDLINE database was conducted to identify genome-wide association studies, meta-analyses of genome-wide association studies, and gene-diet interaction studies related to central obesity, and, in addition, studies that analyzed DNA methylation in relation to body weight regulation. A total of 8 genome-wide association studies and 9 meta-analyses of genome-wide association studies reported numerous single-nucleotide polymorphisms to be associated with central obesity. Ten studies analyzed gene-diet interactions and central obesity, while 2 epigenome-wide association studies analyzed DNA methylation patterns and obesity. Nine studies investigated the relationship between DNA methylation and weight loss, excess body weight, or adiposity outcomes. Given the development of new sequencing and omics technologies, significantly more knowledge on genomics and epigenomics of obesity and body fat distribution will emerge in the near future. [ABSTRACT FROM AUTHOR]

The role of holocarboxylase synthetase ( HLCS) in catalyzing the covalent binding of biotin to the five biotin-dependent carboxylases in humans is well established, as are the essential roles of these carboxylases in the metabolism of fatty acids, the catabolism of leucine, and gluconeogenesis. This review examines recent discoveries regarding the roles of HLCS in assembling a multiprotein gene repression complex in chromatin. In addition, emerging evidence suggests that the number of biotinylated proteins is far larger than previously assumed and includes members of the heat-shock superfamily of proteins and proteins coded by the ENO1 gene. Evidence is presented linking biotinylation of heat-shock proteins HSP60 and HSP72 with redox biology and immune function, respectively, and biotinylation of the two ENO1 gene products MBP-1 and ENO1 with tumor suppression and glycolysis, respectively. [ABSTRACT FROM AUTHOR]

Human milk is a rich source of oligosaccharides. Acidic oligosaccharides, such as sialyllactose ( SL), contain sialic acid ( SA) residues. In human milk, approximately 73% of SA is bound to oligosaccharides, whereas only 3% is present in free form. Oligosaccharides are highly resistant to hydrolysis in the gastrointestinal tract. Only a small portion of the available oligosaccharides in breast milk is absorbed in the neonatal small intestine. SL and sialylated oligosaccharides are thought to have significant health benefits for the neonate, because of their roles in supporting resistance to pathogens, gut maturation, immune function, and cognitive development. The need for SA to allow proper development during the neonatal period is thought to exceed the endogenous synthesis. Therefore, these structures are important nutrients for the neonate. Based on the potential benefits, SL and sialylated oligosaccharides may be interesting components for application in infant nutrition. Once the hurdle of limited availability of these oligosaccharides has been overcome, their functionality can be explored in more detail, and supplementation of infant formula may become feasible. [ABSTRACT FROM AUTHOR]

Reviewed here is the existing evidence for the effects of ginseng extracts and isolated ginsenosides relevant to cognition in humans. Clinical studies in healthy volunteers and in patients with neurological disease or deficit, evidence from preclinical models of cognition, and pharmacokinetic data are considered. Conditions under which disease modification may indirectly benefit cognition but may not translate to cognitive benefits in healthy subjects are discussed. The number of chronic studies of ginseng effects in healthy individuals is limited, and the results from acute studies are inconsistent, making overall assessment of ginseng's efficacy as a cognitive enhancer premature. However, mechanistic results are encouraging; in particular, the ginsenosides Rg3, Rh1, Rh2, Rb1, Rd, Rg2, and Rb3, along with the aglycones protopanaxadiol and protopanaxatriol, warrant further attention. Compound K has a promising pharmacokinetic profile and can affect neurotransmission and neuroprotection. Properly conducted trials using standardized tests in healthy individuals reflecting the target population for ginseng supplementation are required to address inconsistencies in results from acute studies. The evidence summarized here suggests ginseng has potential, but unproven, benefits on cognition. [ABSTRACT FROM AUTHOR]

Lens opacification or cataract reduces vision in over 80 million people worldwide and blinds 18 million. These numbers will increase dramatically as both the size of the elderly demographic and the number of those with carbohydrate metabolism-related problems increase. Preventative measures for cataract are critical because the availability of cataract surgery in much of the world is insufficient. Epidemiologic literature suggests that the risk of cataract can be diminished by diets that are optimized for vitamin C, lutein/zeaxanthin, B vitamins, omega-3 fatty acids, multivitamins, and carbohydrates: recommended levels of micronutrients are salutary. The limited data from intervention trials provide some support for observational studies with regard to nuclear -- but not other types of -- cataracts. Presented here are the beneficial levels of nutrients in diets or blood and the total number of participants surveyed in epidemiologic studies since a previous review in 2007. [ABSTRACT FROM AUTHOR]

Lactose is the preeminent soluble glycan in milk and a significant source of energy for most newborn mammals. Elongation of lactose with additional monosaccharides gives rise to a varied repertoire of free soluble glycans such as 2′-fucosyllactose (2′- FL), which is the most abundant oligosaccharide in human milk. In infants, 2′- FL is resistant to digestion and reaches the colon where it is partially fermented, behaving as soluble prebiotic fiber. Evidence also suggests that portions of small soluble milk glycans, including 2′- FL, are absorbed, thus raising the possibility of systemic biological effects. 2′- FL bears an epitope of the Secretor histo-blood group system; approximately 70-80% of all milk samples contain 2′- FL, since its synthesis depends on a fucosyltransferase that is not uniformly expressed. The fact that some infants are not exposed to 2′- FL has helped researchers to retrospectively probe for biological activities of this glycan. This review summarizes the attributes of 2′- FL in terms of its occurrence in mammalian phylogeny, its postulated biological activities, and its variability in human milk. [ABSTRACT FROM AUTHOR]

Obesity in women is associated with serious reproductive sequelae. Given its prevalence among women of reproductive age, much recent attention has focused on the mechanisms by which obesity affects female reproductive function and fertility. This review summarizes the literature investigating the epidemiology and pathophysiology of obesity in women of reproductive age and proposes research strategies that may help inform approaches to improve reproductive function and outcomes among obese women. [ABSTRACT FROM AUTHOR]

The postnatal feeding practices of obese and overweight mothers may place their children at increased risk for the development of obesity through shared biology and family environments. This article reviews the feeding practices of obese mothers, describes the potential mechanisms linking maternal feeding behaviors to child obesity risk, and highlights the potential avenues of intervention. Strategies important for improving the quality of the eating environment and preventing the intergenerational transmission of obesity include supporting breastfeeding, improving the food choices of obese women, and encouraging the development of feeding styles that are responsive to hunger and satiety cues. [ABSTRACT FROM AUTHOR]

Maternal obesity can profoundly affect offspring phenotype and predisposition to obesity and metabolic disease. Carefully controlled studies in precocial and altricial mammalian species provide insights into the involved mechanisms. These include programming of hypothalamic appetite-regulating centers to increase orexigenic relative to anorexigenic drive; increasing maternal, fetal, and offspring adrenal and peripheral tissue glucocorticoid production; and increasing maternal oxidative stress. Outcomes often show offspring sex differences that may play a role in the differential susceptibility of males and females to later-life obesity and other related metabolic diseases. [ABSTRACT FROM AUTHOR]

In nutrition research, analyzing the relationship between a diet-related chronic disease and impaired metabolism is a common reductionist approach. Meta-analyses have enabled quantification of these relationships. There is, however, a need for more holistic approaches to determine the sequence of connections between diseases and associated physiological mechanisms. The objective of this exhaustive review was to collect scientific evidence - with priority given to quantitative reviews - published between 1950 and 2011 to assess the relationships between major diet-related chronic diseases and deregulated mechanisms. The results revealed that diabetes and obesity are the key diseases that lead to all other diet-related chronic diseases, while cancer, cardiovascular disease, skeletal disease, and sarcopenia are endpoint diseases. Liver disease, kidney disease, digestive disease, and mental illness are consequences as well as causes of other diet-related chronic diseases. All diseases have multifactorial causes, and most result from decreased antioxidant status, acid-base imbalance, increased inflammatory status, impaired carbohydrate/lipid/one-carbon metabolism, impaired functioning of neurons and DNA transcription, hypertension, and/or modified digestive microflora. Nutritional strategies that focus on the prevention of obesity and diabetes should be prioritized in order to reduce the prevalence of other major chronic diseases. [ABSTRACT FROM AUTHOR]

The healthy human gut supports a complex and diverse microbiota, dominated by bacterial phylotypes belonging to Bacteroidetes and Firmicutes. In the inflamed gut, overall diversity decreases, coincident with a greater representation of Proteobacteria. There is growing evidence supporting an important role for human gut bacteria in mucosal immunity; interactions at the level of both intestinal and colonic epithelial cells, dendritic cells, and T and B immune cells have been documented. These interactions influence gut barrier and defense mechanisms that include antimicrobial peptide and secretory IgA synthesis. The functional effects of commensal bacteria on T helper cell differentiation have led to the emerging concept that microbiota composition determines T effector- and T regulatory-cell balance, immune responsiveness, and homeostasis. The importance of this biology in relation to immune homeostasis, inflammatory bowel disease, and the rising incidence of autoimmune diseases will be discussed. The detailed description of the human gut microbiota, integrated with evidence-based mechanisms of immune modulation, provides an exciting platform for the identification of next-generation probiotics and related pharmaceutical products. [ABSTRACT FROM AUTHOR]

Folate is essential for human health in the prevention of megaloblastic anemia and neural tube birth defects and plays important roles in cardiovascular disease and cancer. Therefore, research into environmental factors that may impact folate status, such as solar ultraviolet (UV) radiation, is of great health significance. In vitro studies have shown that UV radiation can degrade folate and folic acid in human blood and this has been confirmed in several human studies. Despite these findings, there is a dearth of epidemiological research into investigating the relationship between folate status and the links to solar UV exposure. [ABSTRACT FROM AUTHOR]

The growing prevalence of metabolic syndrome as well as its impact on public health has garnered increased attention in recent years. As a result, metabolic syndrome is now considered one of the world's leading public health problems. Bioactive peptides deriving from milk proteins may play an important role in the prevention and treatment of metabolic syndrome and its complications via several mechanisms, such as the satiety response, the regulation of insulinemia levels and blood pressure, the uptake of free radicals, and alteration of the lipid profile. These peptides can be incorporated into functional foods or administered via nutraceuticals to decrease the risk of obesity, atherogenesis, arterial hypertension, and type 2 diabetes. Recent findings have generated considerable scientific and commercial interest in milk-derived bioactive peptides, leading to numerous publications on the effectiveness of these substances. This review summarizes the current knowledge on bioactive peptides derived from milk proteins and examines the potential value of these peptides in the treatment and prevention of metabolic syndrome and its complications. [ABSTRACT FROM AUTHOR]

Transcellular models of dietary Ca2+ absorption by the intestine assign essential roles to TRPV6 and calbindin-D9K. However, studies with gene-knockout mice challenge this view. Something fundamental is missing. The L-type channel Cav1.3 is located in the apical membrane from the duodenum to the ileum. In perfused rat jejunum in vivo and in Caco-2 cells, Cav1.3 mediates sodium glucose transporter 1 (SGLT1)-dependent and prolactin-induced active, transcellular Ca2+ absorption, respectively. TRPV6 is activated by hyperpolarization and is vitamin D dependent; in contrast, Cav1.3 is activated by depolarization and is independent of calbindin-D9K and vitamin D. This review considers evidence supporting the idea that Cav1.3 and TRPV6 have complementary roles in the regulation of intestinal Ca2+ absorption as depolarization and repolarization of the apical membrane occur during and between digestive periods, respectively, and as chyme moves from one intestinal segment to another and food transit times increase. Reassessment of current arguments for paracellular flow reveals that key phenomena have alternative explanations within the integrated Cav1.3/TRPV6 view of transcellular Ca2+ absorption. [ABSTRACT FROM AUTHOR]

Oats in a gluten-free diet increase the diet's nutritional value, but their use remains controversial. Contamination with prolamins of other cereals is frequent, and some clinical and experimental studies support the view that a subgroup of celiac patients may be intolerant to pure oats. Thus, this issue is more complex than previously suggested. In order to produce oats that are safe for all celiac patients, the following topics should be addressed: selection of oat cultivars with low avenin content, research on such recombinant varieties of oats, development of assay methods to detect avenins in oat products, guidelines for the agricultural processing of oats and the manufacture of oat products, as well as guidelines for following up with celiac patients who consume oats. [ABSTRACT FROM AUTHOR]

Deficiencies of the vitamins folate, B, and B are associated with neurological and psychological dysfunction and with congenital defects. In the elderly, cognitive impairment and incident dementia may be related to the high prevalence of inadequate B vitamin status and to elevations of plasma homocysteine. Plausible mechanisms include homocysteine neurotoxicity, vasotoxicity, and impaired S-adenosylmethionine-dependent methylation reactions vital to central nervous system function. In light of this, it is imperative to find safe ways of improving vitamin B status in the elderly without exposing some individuals to undue risk. [ABSTRACT FROM AUTHOR]

Dementia is an acquired highly disabling syndrome common among elderly people. Alzheimer's disease is the most frequent type of dementia, and its prevalence is rapidly increasing due to the aging of populations. Therefore, the need to find effective preventive means is pressing. Population studies allow identification of risk/protective factors for dementia/Alzheimer's disease, thus leading to preventive strategies that can be implemented in the general population to reduce the incidence of this disorder. Presented here is an overview of the main findings of epidemiological studies on nutritional factors and nutrition-related pathological conditions, as related to dementia and Alzheimer's disease. [ABSTRACT FROM AUTHOR]

Information regarding several papers discussed at a symposium on the functions and adaptations of the human brain and its relation with age is presented. Topics include the receptor biology of the brain, the impact of environmental factors into the brain, and the secular changes of the brain in aging. The symposium featured several international nutrition experts including Tom Kirkwood, Marshal Folstein, and Richard Wurtman.

Aging contributes to physiological decline and vulnerability to disease. In the brain, even with minimal neuronal loss, aging increases oxidative damage, inflammation, demyelination, impaired processing, and metabolic deficits, particularly during pathological brain aging. In this review, the possible role of docosahexaenoic acid (DHA) in the prevention of age-related disruption of brain function is discussed. High-fat diabetogenic diets, cholesterol, and the omega-6 fatty acid arachidonate and its prostaglandin metabolites have all been implicated in promoting the pathogenesis of Alzheimer's disease. Evidence presented here shows DHA acts to oppose this, exerting a plethora of pleiotropic activities to protect against the pathogenesis of Alzheimer's disease. [ABSTRACT FROM AUTHOR]

Any discussion of the impact of nutrition and environment on the brain is based on the premise that the brain is malleable, but just how malleable is this most complex of all organs? And to what extent does the term 'malleability' extend beyond subtle functional changes into the realms of morphology and connectivity? Recent methodological advances have provided new insight into these issues and have revealed synapse populations that turn over at high rates and synaptic receptors that are continuously on the move. The unveiling of this unsuspected structural plasticity has prompted new research on a class of enzymes (matrix metalloproteinases) that regulate the physical constraints imposed by extracellular matrix molecules. The realization that the brain is more 'softwired' than previously anticipated emphasizes the relevance of current endeavors to explore the impact of nutrition and exercise on brain function and structure. [ABSTRACT FROM AUTHOR]