Showing papers in "Annual Review of Nutrition in 2001"
TL;DR: This chapter reviews the inhibition of tumorigenesis by phenolic acids and derivatives, tea and catechins, isoflavones and soy preparations, quercetin and other flavonoids, resveratrol, and lignans as well as the mechanisms involved based on studies in vivo and in vitro.
Abstract: Plants consumed by humans contain thousands of phenolic compounds. The effects of dietary polyphenols are of great current interest due to their antioxidative and possible anticarcinogenic activities. A popular belief is that dietary polyphenols are anticarcinogens because they are antioxidants, but direct evidence for this supposition is lacking. This chapter reviews the inhibition of tumorigenesis by phenolic acids and derivatives, tea and catechins, isoflavones and soy preparations, quercetin and other flavonoids, resveratrol, and lignans as well as the mechanisms involved based on studies in vivo and in vitro. Polyphenols may inhibit carcinogenesis by affecting the molecular events in the initiation, promotion, and progression stages. Isoflavones and lignans may influence tumor formation by affecting estrogen-related activities. The bioavailability of the dietary polyphenols is discussed extensively, because the tissue levels of the effective compounds determine the biological activity. Understanding the bioavailability and blood and tissue levels of polyphenols is also important in extrapolating results from studies in cell lines to animal models and humans. Epidemiological studies concerning polyphenol consumption and human cancer risk suggest the protective effects of certain food items and polyphenols, but more studies are needed for clear-cut conclusions. Perspectives on the application of dietary polyphenols for the prevention of human cancer and possible concerns on the consumption of excessive amounts of polyphenols are discussed.
1,315 citations
TL;DR: The peroxisomal β-oxidation system consists of a classical peroxysome proliferator-inducible pathway capable of catalyzing straight-chain acyl-CoAs by fatty acyl CoA oxidase, L-bifunctiona.
Abstract: ▪ Abstract β-Oxidation occurs in both mitochondria and peroxisomes. Mitochondria catalyze the β-oxidation of the bulk of short-, medium-, and long-chain fatty acids derived from diet, and this pathway constitutes the major process by which fatty acids are oxidized to generate energy. Peroxisomes are involved in the β-oxidation chain shortening of long-chain and very-long-chain fatty acyl-coenzyme (CoAs), long-chain dicarboxylyl-CoAs, the CoA esters of eicosanoids, 2-methyl-branched fatty acyl-CoAs, and the CoA esters of the bile acid intermediates di- and trihydroxycoprostanoic acids, and in the process they generate H2O2. Long-chain and very-long-chain fatty acids (VLCFAs) are also metabolized by the cytochrome P450 CYP4A ω-oxidation system to dicarboxylic acids that serve as substrates for peroxisomal β-oxidation. The peroxisomal β-oxidation system consists of (a) a classical peroxisome proliferator–inducible pathway capable of catalyzing straight-chain acyl-CoAs by fatty acyl-CoA oxidase, L-bifunctiona...
805 citations
TL;DR: Vitamin A deficiency diminishes antibody-mediated responses directed by Th2 cells, although some aspects of Th1-mediated immunity are also diminished, presumably account for the increased mortality seen in vitamin A-deficient infants, young children, and pregnant women in many areas of the world today.
Abstract: In populations where vitamin A availability from food is low, infectious diseases can precipitate vitamin A deficiency by decreasing intake, decreasing absorption, and increasing excretion. Infectious diseases that induce the acute-phase response also impair the assessment of vitamin A status by transiently depressing serum retinol concentrations. Vitamin A deficiency impairs innate immunity by impeding normal regeneration of mucosal barriers damaged by infection, and by diminishing the function of neutrophils, macrophages, and natural killer cells. Vitamin A is also required for adaptive immunity and plays a role in the development of T both-helper (Th) cells and B-cells. In particular, vitamin A deficiency diminishes antibody-mediated responses directed by Th2 cells, although some aspects of Th1-mediated immunity are also diminished. These changes in mucosal epithelial regeneration and immune function presumably account for the increased mortality seen in vitamin A-deficient infants, young children, and pregnant women in many areas of the world today.
697 citations
TL;DR: Experimental and field studies on the effects of protein, energy, zinc, vitamin A, and iron deficiencies on gastrointestinal nematodes of humans, livestock, and laboratory rodents are reviewed and the Th2 arm of the immune system is highlighted as a component of primary importance in the association between malnutrition and GI nematode infections.
Abstract: Nutritionists have long understood that intestinal nematode parasites have deleterious effects on host nutritional status, but only recently has the importance of malnutrition as a predisposing factor to intestinal nematodes been recognized. Here we review experimental and field studies on the effects of protein, energy, zinc, vitamin A, and iron deficiencies on gastrointestinal (GI) nematodes of humans, livestock, and laboratory rodents, and draw certain conclusions about the state of our current understanding. In general, malnutrition promotes the establishment, survival, and fecundity of these parasites, but the magnitude of the effect depends on factors such as host species, parasite species, particular infection protocol used, magnitude of the infection, severity of the nutritional deficiency, and presence of single or multiple infections and single or multiple nutritional deficiencies. We highlight the Th2 arm of the immune system as a component of primary importance in the association between malnutrition and GI nematode infections. We summarize what is known about underlying mechanisms that may account for the observed patterns. Finally, we suggest future research directions.
212 citations
TL;DR: The structural, genetic, and functional aspects of megalin and cubilin are summarized and discussed, with emphasis on their function as receptors for uptake of protein-associated vitamins, lipids, and hormones.
Abstract: Polarized epithelia have several functional and morphological similarities, including a high capacity for uptake of various substances present in the fluids facing the apical epithelial surfaces. Studies during the past decade have shown that receptor-mediated endocytosis, rather than nonspecific pinocytosis, accounts for the apical epithelial uptake of many carrier-bound nutrients and hormones. The two interacting receptors of distinct evolutionary origin, megalin and cubilin, are main receptors in this process. Both receptors are apically expressed in polarized epithelia, in which they function as biological affinity matrices for overlapping repertoires of ligands. The ability to bind multiple ligands is accounted for by a high number of replicated low-density lipoprotein receptor type-A repeats in megalin and CUB (complement C1r/C1s, Uegf, and bone morphogenic protein-1) domains in cubilin. Here we summarize and discuss the structural, genetic, and functional aspects of megalin and cubilin, with emphasis on their function as receptors for uptake of protein-associated vitamins, lipids, and hormones.
196 citations
TL;DR: Suggestions for predialysis and dialysis care of patients undergoing maintenance dialysis that can result in improvement in their nutritional status are offered, and whether this improvement will result in a decrease in patient morbidity and mortality is unknown.
Abstract: About 40% of patients undergoing maintenance dialysis suffer from varying degrees of protein-energy malnutrition. This is a problem of substantial importance because many measures of nutritional status correlate with the risk of morbidity and mortality. There are many causes of protein-energy malnutrition in maintenance dialysis patients. Evidence indicates that nutritional decline begins even when the reduction in glomerular filtration rate is modest, and it is likely that the observed decrease in dietary protein and energy intake plays an important role. The nutrient intake of patients receiving maintenance dialysis also is often inadequate, and several lines of evidence suggest that toxins that accumulate with renal failure suppress appetite and contribute to nutritional decline once patients are on maintenance dialysis. Recent epidemiologic studies have suggested that both increased serum levels of leptin and inflammation may reduce nutrient intake and contribute to the development of protein-energy malnutrition. It is likely that associated illnesses, which are highly prevalent, contribute to malnutrition in maintenance dialysis patients. Recent data from the United States Renal Data System registry suggest that in the United States, the mortality rate of dialysis patients is improving. However, it remains high. We offer suggestions for predialysis and dialysis care of these patients that can result in improvement in their nutritional status. Whether this improvement will result in a decrease in patient morbidity and mortality is unknown.
169 citations
TL;DR: It is too soon to use this research as a basis for new interventions directed at pregnant women for the purpose of reducing chronic disease in their offspring, but data from experimental species suggest possible mechanisms for the origin of chronic disease early in life.
Abstract: The "fetal origins" hypothesis postulates that conditions, most likely nutritional, "program" the fetus for the development of chronic diseases in adulthood. Associations between the newborn's size at birth and various determinants or consequences of chronic diseases have been identified in many, but not all, of the available studies. It remains to be established whether these associations are causal. Remarkably little information is available on the specific role of maternal nutritional status. The role of birth weight remains difficult to interpret except as a proxy for events in intrauterine life. Unfortunately, birth weight does not make an important contribution to the population attributable risk of cardiovascular disease; lifestyle factors during adulthood make much greater contributions. Data from experimental species suggest possible mechanisms for the origin of chronic disease early in life. It is too soon to use this research as a basis for new interventions directed at pregnant women for the purpose of reducing chronic disease in their offspring.
162 citations
TL;DR: It is suggested that current low-energy lifestyles are a common denominator for the current high prevalence not only of ID but also of obesity, diabetes, and osteoporosis.
Abstract: Nutritional iron deficiency (ID) is caused by an intake of dietary iron insufficient to cover physiological iron requirements. Studies on iron absorption from whole diets have examined relationships between dietary iron bioavailability/absorption, iron losses, and amounts of stored iron. New insights have been obtained into regulation of iron absorption and expected rates of changes of iron stores or hemoglobin iron deficits when bioavailability or iron content of the diet has been modified and when losses of iron occur. Negative effects of ID are probably related to age, up to about 20 years, explaining some of earlier controversies. Difficulties in establishing the prevalence of mild ID are outlined. The degree of underestimation of the prevalence of mild ID when using multiple diagnostic criteria is discussed. It is suggested that current low-energy lifestyles are a common denominator for the current high prevalence not only of ID but also of obesity, diabetes, and osteoporosis.
116 citations
TL;DR: It is found that healthy normolipidemic individuals with this trait show a greater reduction in LDL cholesterol and particle number in response to low-fat, high-carbohydrate diets than do unaffected individuals (subclass pattern A).
Abstract: We have tested whether differences in distribution and dietary responsiveness of low-density lipoprotein (LDL) subclasses contribute to the variability in the magnitude of LDL-cholesterol reduction induced by diets low in total and saturated fat and high in carbohydrate. Our studies have focused on a common, genetically influenced metabolic profile, characterized by a predominance of small, dense LDL particles (subclass pattern B), that is associated with a two- to threefold increase in risk for coronary artery disease. We have found that healthy normolipidemic individuals with this trait show a greater reduction in LDL cholesterol and particle number in response to low-fat, high-carbohydrate diets than do unaffected individuals (subclass pattern A). Moreover, such diets result in reduced LDL particle size, with induction of pattern B in a substantial proportion of pattern A men. Recent studies have indicated that this response is under genetic influence. Future identification of the specific genes involved may lead to improved targeting of dietary therapies aimed at reducing cardiovascular disease risk.
107 citations
TL;DR: In general, food frequency questionnaires overestimated total energy intake and were better at ranking, than quantifying, nutrient intake than food recalls, which both overestimated and underestimated energy intake.
Abstract: Accurate assessment of dietary intake among preschool-aged children is important for clinical care and research, for nutrition monitoring and evaluating nutrition interventions, and for epidemiologic research. We identified 25 studies published between January 1976 and August 2000 that evaluated the validity of food recalls (n = 12), food frequency questionnaires (n = 9), food records (n = 2), or other methods (n = 2). We identified four studies that evaluated the reproducibility of food frequency questionnaires. Validity studies varied in validation standard and study design, making comparisons between studies difficult. In general, food frequency questionnaires overestimated total energy intake and were better at ranking, than quantifying, nutrient intake. Compared with the validation standard, food recalls both overestimated and underestimated energy intake. When choosing a method to estimate diet, both purpose of the assessment and practicality of the method must be considered, in addition to the vali...
104 citations
TL;DR: The yeast Saccharomyces cerevisiae is a valuable model system for elucidation of gene-function relationships in such eukaryotic processes as fatty acid metabolism, and recent genes encoding core and auxiliary enzymes of peroxisomal beta-oxidation have been identified.
Abstract: Long-chain fatty acids are a vital metabolic energy source and are building blocks of membrane lipids. The yeast Saccharomyces cerevisiae is a valuable model system for elucidation of gene-function relationships in such eukaryotic processes as fatty acid metabolism. Yeast degrades fatty acids only in the peroxisome, and recently, genes encoding core and auxiliary enzymes of peroxisomal beta-oxidation have been identified. Mechanisms involved in fatty acid induction of gene expression have been described, and novel fatty acid-responsive genes have been discovered via yeast genome analysis. In addition, a number of genes essential for synthesis of the variety of fatty acids in yeast have been cloned. Advances in understanding such processes in S. cerevisiae will provide helpful insights to functional genomics approaches in more complex organisms.
TL;DR: Glucose-6-phosphate dehydrogenase (G6PD) is unique in this group of enzymes in that it participates in multiple metabolic pathways: reductive biosynthesis, including lipogenesis; protection from oxidative stress; and cellular growth.
Abstract: The family of enzymes involved in lipogenesis is a model system for understanding how a cell adapts to dietary energy in the form of carbohydrate versus energy in the form of triacylglycerol. Glucose-6-phosphate dehydrogenase (G6PD) is unique in this group of enzymes in that it participates in multiple metabolic pathways: reductive biosynthesis, including lipogenesis; protection from oxidative stress; and cellular growth. G6PD activity is enhanced by dietary carbohydrates and is inhibited by dietary polyunsaturated fats. These changes in G6PD activity are a consequence of changes in the expression of the G6PD gene. Nutrients can regulate the expression of genes at both transcriptional and posttranscriptional steps. Most lipogenic enzymes undergo large changes in the rate of gene transcription in response to dietary changes; however, G6PD is regulated at a step subsequent to transcription. This step is involved in the rate of synthesis of the mature mRNA in the nucleus, specifically regulation of the efficiency of splicing of the nascent G6PD transcript. Understanding the mechanisms by which nutrients alter nuclear posttranscriptional events will help uncover new information on the breadth of mechanisms involved in gene regulation.
TL;DR: Advancing the understanding of the molecular mechanism of action of C/EBPs will undoubtedly further the authors' appreciation for the role these transcription factors play in both health and disease.
Abstract: C/EBPs are a family of transcription factors that play important roles in energy metabolism. Although initially thought to be constitutive regulators of transcription, an increasing amount of evidence indicates that their transactivating capacity within the cell can be modulated by nutrients and hormones. There are several mechanisms whereby this occurs. First, hormones/nutrients are known to directly alter the expression of C/EBPs. Second, hormones/nutrients may cause an alteration in the phosphorylation state of C/EBPs, which can affect their DNA-binding activity or transactivating capacity. Third, C/EBPs can function as accessory factors on gene promoters within a hormone response unit, interacting with other transcription factors to enhance the degree of responsiveness to specific hormones. Given their role in regulating genes involved in a wide variety of metabolic events, advancing our understanding of the molecular mechanism of action of C/EBPs will undoubtedly further our appreciation for the role these transcription factors play in both health and disease.
TL;DR: The thesis proposed in this paper is that realistic estimations of dietary zinc requirements by a factorial approach require attention to the dynamic interrelationships between major variables of zinc homeostasis.
Abstract: Currently, estimates of human zinc requirements depend primarily on a factorial approach. The availability of tracer techniques employing zinc stable isotopes has facilitated the acquisition of data on major variables of zinc homeostasis in addition to those that can be measured with careful metabolic balance techniques. These data have promising potential to facilitate and improve the factorial approach. The thesis proposed in this paper is that realistic estimations of dietary zinc requirements by a factorial approach require attention to the dynamic interrelationships between major variables of zinc homeostasis. This applies especially to the positive relationship between endogenous fecal zinc and total absorbed zinc, which is the essential starting point in estimating physiologic and, from there, dietary requirements.
TL;DR: In this article, the formation of chylomicrons acts as a signal for the induction of intestinal apo-A-IV synthesis and is also enhanced by a factor from the ileum, probably peptide tyrosine-tyrosine.
Abstract: Apolipoprotein A-IV (apo A-IV) is a glycoprotein synthesized by the human intestine. In rodents, both the small intestine and liver secrete apo A-IV, but the small intestine is the major organ responsible for the circulating apo A-IV. Intestinal apo A-IV synthesis is markedly stimulated by fat absorption and appears not to be mediated by the uptake or reesterification of fatty acids to form triglycerides. Rather, the formation of chylomicrons acts as a signal for the induction of intestinal apo A-IV synthesis. Intestinal apo A-IV synthesis is also enhanced by a factor from the ileum, probably peptide tyrosine-tyrosine. The inhibition of food intake by apo A-IV is mediated centrally. The stimulation of intestinal synthesis and the secretion of apo A-IV by lipid absorption are rapid; thus, apo A-IV likely plays a role in the short-term regulation of food intake. Other evidence suggests that apo A-IV may also be involved in the long-term regulation of food intake and body weight. Chronic ingestion of a high-fat diet blunts the intestinal apo A-IV response to lipid feeding and may explain why the chronic ingestion of a high-fat diet predisposes both animals and humans to obesity.
TL;DR: Public health efforts must focus not only on eradicating undernutrition in West Africa and the Caribbean but also on preventing obesity, hypercholesterolemia, and their consequences.
Abstract: Along with their foods and dietary customs, Africans were carried into diaspora throughout the Americas as a result of the European slave trade. Their descendants represent populations at varying stages of the nutrition transition. West Africans are in the early stage, where undernutrition and nutrient deficiencies are prevalent. Many Caribbean populations represent the middle stages, with undernutrition and obesity coexisting. African-Americans and black populations in the United Kingdom suffer from the consequences of caloric excess and diets high in fat and animal products. Obesity, non-insulin-dependent diabetes mellitus, hypertension, coronary heart disease, and certain cancers all follow an east-to-west gradient of increasing prevalence. Public health efforts must focus not only on eradicating undernutrition in West Africa and the Caribbean but also on preventing obesity, hypercholesterolemia, and their consequences. Fortunately, a coherent and well-supported set of recommendations exists to promote better nutrition. Implementation of it founders primarily as a result of the influence of commercial and political interests.