Progress in food & nutrition science最新文献

Model-based compartmental analysis was used to interpret data on temporal changes in plasma triglyceride (TG) response to a chronic infusion of chylomicrons (CM) in the rat. Male rats were fed purified diets which varied in fat load [L = 10% (w/w), H = 30%] and P/S ratio (P = 4.6, S = 0.2). Lymph CM isolated from donor rats which were absorbing the P or S fat were infused into recipients for 8 h on 3 consecutive days: on d 1 and 3, CM infusion rate reflected the fat content of the previous diet and on d 2, the other load; the infusion replaced dietary fat. Serial plasma samples from each period were analyzed for TG concentration; TG distribution in plasma lipoproteins and liver lipids was measured after d 3. To describe observed group average data, a compartmental model was developed using the Simulation, Analysis and Modeling computer program. Two compartments were needed in plasma (CM vs nonCM TG); each had 2 outputs: removal of TG-fatty acids by lipoprotein lipase (LPL) and uptake of remnant lipoproteins by the liver. After a delay in the liver, there were 3 fates for TG-derived fatty acids: oxidation, retention, or secretion in very low density lipoproteins. Simulation of changes in the rate constant for total CM TG turnover indicated that the basal level of LPL rose rapidly and dramatically in response to TG infusion; the rise was higher for H vs L. After 3-5 h, apparent LPL activity decreased. Simulation of the rate of CM TG turnover indicated that the turnover rate rose immediately after infusion began to levels higher than the infusion rate, and then came into a slight negative balance. Although the observed data could be qualitatively described based on current understanding of TG metabolism, application of model-based compartmental analysis generated testable hypotheses about quantitative aspects of the system dynamics.

Is frequent reproductive cycling (episodes of pregnancy and/or lactation) in poor women from developing countries a cause of poor maternal nutritional status? This review seeks to examine the evidence available to answer this question. The measurement of reproductive cycling, maternal nutritional status, and the energetic costs of pregnancy and lactation are reviewed. The data available on the anthropometric changes during pregnancy and lactation are described. Against this background, the evidence in support of the hypothesis that repeated reproductive cycling leads to a maternal depletion syndrome is examined. It is concluded that although the data are inadequate to unequivocally establish or rule out the existence of maternal nutritional depletion due to a demanding reproductive history, the data suggest this relationship does exist. Weaknesses of current measurement and study design methodologies are identified and priorities for future research aimed at clarifying the extent to which reproductive cycling affects maternal nutritional status are identified.

The association of toxic substances with human foods has long been recognized. While intrinsic compounds appear during storage as a result of spoilage by chemical processes or by contamination with micro-organisms. In the numerous stages of food production from source to table there are many opportunities for contamination. This article reviews the wide spectrum of food-associated toxicants, outlining the mechanisms by which these substances reach the food products. To illustrate the diversity of these mechanisms, some notable examples of mass contamination of food are quoted. The presence of toxic substances in human food is, and will continue to be, a challenge for toxicologists, and a source of concern for the public, for industry, and for the scientific community.

The role of the genotype in the response to short-term overfeeding was assessed by submitted six pairs of male monozygotic twins to a 4.2 MJ (1000 kcal) per day energy intake surplus for a period of 22 consecutive days. Individual differences in fat mass and fat-free mass gains were observed in response to overfeeding but they were not randomly distributed. Indeed, the within-pair resemblance in the response was striking when compared to the heterogeneity found among the pairs in adiposity and fat-free mass gains. The intrapair resemblance in the response to overfeeding as assessed by the intraclass coefficient computed with the individual changes, reached 0.88 for total fat mass and 0.76 for fat-free mass. A similar trend for a genetically determined pattern of adaptation to overfeeding was observed for resting metabolic rate (intraclass = 0.63), thermic effect of a meal (intraclass = 0.62), and energy cost of submaximal exercise (intraclass = 0.78) when the data were analysed in terms of changes in oxygen uptake. On the other hand, no major alterations in glucose and insulin response to a glucose load or a test meal, in cardio-pulmonary adaptation to submaximal exercise and in maximal exercise tolerance were found with overfeeding. In contrast, the response of suprailiac fat cell lipolysis (intraclass of about 0.7) and heparin releasable adipose tissue lipoprotein lipase (intraclass - 0.82) varied among individuals but was highly homogeneous within genotypes. Similarly, a genotype-overfeeding interaction effect was seen for serum triglycerides (intraclass = 0.69), HDL-cholesterol (intraclass = 0.85), and the HDL-cholesterol to total cholesterol ratio (intraclass = 0.82). Multiple correlation analyses suggest that much of the variance in the response of fat mass (R = 0.65) and fat-free mass (R = 0.81) is accounted for by alterations in the energy expenditure components assessed in the study. If one takes into account the measurement errors always present in such complex studies and the fact that only a limited fraction of the energy expenditure of activity was considered by design, one can conclude that the genotype determines to a large extent the response variation to short-term overfeeding. In particular, the genotype-overfeeding interaction effect for body composition changes seems to be mediated by the various energy expenditure components, themselves characterized by significant genotype-overfeeding interaction effects.(ABSTRACT TRUNCATED AT 400 WORDS)

Eicosapentaenoic acid (EPA), a long chain fatty acid of the n-3 series, is found in marine foods. Beneficial effects of these foods containing EPA on factors associated with cardiovascular disease risk and arterial thrombosis have been demonstrated. More recently, studies have suggested that EPA may also have a favourable effect on other human diseases such as arthritis, renal disorders, psoriasis and possibly also cancer. EPA is metabolized in a manner generally similar to that of arachidonic acid (AA) although some significant differences between the two are apparent. The metabolic fate of dietary EPA in human subjects is reviewed herein with inclusion of information from animal studies where human data is not available. The metabolism of EPA in the phospholipids of human platelets is emphasized to some extent. Effects of EPA on AA metabolism are also described.

Dental caries and periodontal disease are wide-spread oral illnesses whose etiology is intimately associated with the consumption of carbohydrate sweeteners. Since dental caries is multifactorial in nature, it is reasonable to assume that there is no single method, usable in the foreseeable future, which would lead to its eradication. Consequently, any new caries preventive measures must function coherently with those currently in use, so that the concerted action of all methods would lead to the best cariostatic effect. Strict restriction of sucrose intake without suggestion of alternatives is not realistic. This fact has given rise to attempts to replace sucrose, especially in products consumed between meals, with sweeteners that are less cariogenic. Human clinical trials and several animal experiments have shown promising clinical results obtained by replacing sucrose with certain sugar alcohols (polyols). Among the sugar alcohols, the best results so far have been obtained with xylitol, which is chemically a pentitol containing five carbon atoms. Chewing gums containing xylitol have been shown to be strong instruments against caries in caries-active age-groups and in high-risk subjects. More research is needed to assess the ability of mixtures of xylitol with sorbitol, palatinit, maltitol, other sugar alcohols, and intense sweeteners to prevent oral plaque diseases. Although thorough clinical trials on the relationship between carbohydrate sweeteners and periodontal diseases have not been performed, the available data indicate that dietary polyols may have a restricted dampening effect on periodontal and gingival inflammations.

This review addresses the role of zinc in the metabolism of lipids including cholesterol, phospholipids, triglyceride, fatty acids, lipoproteins, and essential fatty acids and it discusses to a limited extent the role of zinc in membranes as well as zinc's known effects on receptors. The evidence which is compiled demonstrates two main features of the interactions of zinc in lipid and fatty acid metabolism; 1) that zinc intimately affects many aspects of lipid metabolism through established enzymes but also has modulatory effects whose mechanism is not obvious or established, and 2) many of the observations are superficially contradictory and do not lend themselves to ready explanation. These are the features of a field whose time has come and which beckons further research to clarify these issues.

Breast milk is the food most suited for the normal newborn infant. The evolution, complexity and general nutrient composition of this biological fluid is discussed from the perspective of the normal infant's requirements for growth and current knowledge of neonatal nutritional requirements.

Diets were formulated to contain varying concentrations of lactalbumin (3, 6, 9, 12, 15 and 18%), with lactalbumin increased at the expense of the carbohydrate source (Formulation 1) or with the nonprotein composition held constant (Formulation 2). Diets were fed for 21 days to male weanling rats of the Sprague-Dawley strain at three levels of intake (7, 9 or 11 g/day). For each diet formulation, maximum body weight gain (Rmax) was predicted for each intake level by relating body weight gain and protein intake using the saturation kinetics model. Rmax and asymptotic standard errors at intake levels 1, 2 and 3 were 10 +/- 3, 50 +/- 16 and 80 +/- 12 g, respectively, for Formulation 1, and 12 +/- 3, 40 +/- 3 and 69 +/- 4 g, respectively, for Formulation 2. Combining diet formulations, Rmax expressed as percentages of Rmax at intake level 3 were approximately 15 and 60% at intake levels 1 and 2, respectively. Since intakes at levels 1 and 2 were approximately 64 and 82%, respectively, of that at level 3, the results of this study show that the percentage decrease in Rmax is much greater than the percentage decrease in intake. This study has demonstrated that saturation kinetics can be used to model the effects of energy restriction on protein utilization.