Annual review of nutrition最新文献

The reactions of the tricarboxylic acid (TCA) cycle allow the controlled combustion of fat and carbohydrate. In principle, TCA cycle intermediates are regenerated on every turn and can facilitate the oxidation of an infinite number of nutrient molecules. However, TCA cycle intermediates can be lost to cataplerotic pathways that provide precursors for biosynthesis, and they must be replaced by anaplerotic pathways that regenerate these intermediates. Together, anaplerosis and cataplerosis help regulate rates of biosynthesis by dictating precursor supply, and they play underappreciated roles in catabolism and cellular energy status. They facilitate recycling pathways and nitrogen trafficking necessary for catabolism, and they influence redox state and oxidative capacity by altering TCA cycle intermediate concentrations. These functions vary widely by tissue and play emerging roles in disease. This article reviews the roles of anaplerosis and cataplerosis in various tissues and discusses how they alter carbon transitions, and highlights their contribution to mechanisms of disease.

The gut microbiome plays an integral role in health and disease, and diet is a major driver of its composition, diversity, and functional capacity. Given the dynamic development of the gut microbiome in infants and children, it is critical to address two major questions: (a) Can diet modify the composition, diversity, or function of the gut microbiome, and (b) will such modification affect functional/clinical outcomes including immune function, cognitive development, and overall health? We synthesize the evidence on the effect of nutritional interventions on the gut microbiome in infants and children across 26 studies. Findings indicate the need to study older children, assess the whole intestinal tract, and harmonize methods and interpretation of findings, which are critical for informing meaningful clinical and public health practice. These findings are relevant for precision health, may help identify windows of opportunity for intervention, and may inform the design and delivery of such interventions.

Proper timing of critical care nutrition has long been a matter of controversy. Critical illness waxes and wanes in stages, creating a dynamic flux in energy needs that we have only begun to examine. Furthermore, response to nutrition support likely differs greatly at the level of the individual patient in regard to genetic status, disease stage, comorbidities, and more. We review the observational and randomized literature concerning timing in nutrition support, discuss mechanisms of harm in feeding critically ill patients, and highlight the role of precision nutrition for moving the literature beyond the realm of blunt population averages into one that accounts for the patient-specific complexities of critical illness and host genetics.

Vitamin A, acting through its metabolite, all-trans-retinoic acid, is a potent transcriptional regulator affecting expression levels of hundreds of genes through retinoic acid response elements present within these genes. However, the literature is replete with claims that consider vitamin A to be an antioxidant vitamin, like vitamins C and E. This apparent contradiction in the understanding of how vitamin A acts mechanistically within the body is a major focus of this review. Vitamin E, which is generally understood to act as a lipophilic antioxidant protecting polyunsaturated fatty acids present in membranes, is often proposed to be a transcriptional regulator. The evaluation of this claim is another focus of the review. We conclude that vitamin A is an indirect antioxidant, whose indirect function is to transcriptionally regulate a number of genes involved in mediating the body's canonical antioxidant responses. Vitamin E, in addition to being a direct antioxidant, prevents the increase of peroxidized lipids that alter both metabolic pathways and gene expression profiles within tissues and cells. However, there is little compelling evidence that vitamin E has a direct transcriptional mechanism like that of vitamin A. Thus, we propose that the term antioxidant not be applied to vitamin A, and we discourage the use of the term transcriptional mediator when discussing vitamin E.

Countries worldwide have implemented mandatory or voluntary front-of-package nutrition labeling systems. We provide a narrative review of (a) real-world evaluations of front-of-package nutrition labels that analyze objective sales data and (b) studies that objectively assess product reformulation in response to a front-of-package nutrition label implementation. We argue that there is sufficient scientific evidence to recommend that governments implement mandatory front-of-package nutrition labeling systems to improvepopulation health. We also present a conceptual framework to describe front-of-package label influence and provide recommendations for the optimal label design, emphasizing that labeling systems should be highly visible and salient, be simple and easy to understand, leverage automatic associations, and integrate informational and emotional messaging. The existing research suggests that Guideline Daily Amount labels should be avoided and that the Health Star Rating and Nutri-Score systems are promising but that systems with warning labels like the one in Chile are likely to produce the largest public health benefits.

The aryl hydrocarbon receptor (AhR) is a ligand-activated basic-helix-loop-helix transcription factor that binds structurally diverse ligands and senses cues from environmental toxicants and physiologically relevant dietary/microbiota-derived ligands. The AhR is an ancient conserved protein and is widely expressed across different tissues in vertebrates and invertebrates. AhR signaling mediates a wide range of cellular functions in a ligand-, cell type-, species-, and context-specific manner. Dysregulation of AhR signaling is linked to many developmental defects and chronic diseases. In this review, we discuss the emerging role of AhR signaling in mediating bidirectional host-microbiome interactions. We also consider evidence showing the potential for the dietary/microbial enhancement ofhealth-promoting AhR ligands to improve clinical pathway management in the context of inflammatory bowel diseases and colon tumorigenesis.

After I studied medicine, my career took an early and unusual course when I was offered a clinical research post in Jamaica dealing with childhood malnutrition, of which I knew nothing. My subsequent nutritional explorations allowed gastrointestinal and metabolic analyses to have an impact on several public health policies. The biggest challenges came from unexpected political demands: coping with poor school performers in the Caribbean; addressing UK public health initiatives in health education; breaking the siege of Sarajevo; developing a Food Standards Agency as a sudden need for Tony Blair as incoming prime minister; dealing with widespread bovine spongiform encephalopathy in Europe; and responding to a United Nations request to assess global malnutrition. This last task revealed the need for a lifelong approach to nutrition, which also encompassed pregnancy. But perhaps the biggest challenge was establishing the criteria for obesity assessment, management, and prevention for policy makers across the globe.

Ketone bodies play significant roles in organismal energy homeostasis, serving as oxidative fuels, modulators of redox potential, lipogenic precursors, and signals, primarily during states of low carbohydrate availability. Efforts to enhance wellness and ameliorate disease via nutritional, chronobiological, and pharmacological interventions have markedly intensified interest in ketone body metabolism. The two ketone body redox partners, acetoacetate and D-β-hydroxybutyrate, serve distinct metabolic and signaling roles in biological systems. We discuss the pleiotropic roles played by both of these ketones in health and disease. While enthusiasm is warranted, prudent procession through therapeutic applications of ketogenic and ketone therapies is also advised, as a range of metabolic and signaling consequences continue to emerge. Organ-specific and cell-type-specific effects of ketone bodies are important to consider as prospective therapeutic and wellness applications increase.

This review aims to summarize the effects of intermittent fasting on markers of cardiometabolic health in humans. All forms of fasting reviewed here-alternate-day fasting (ADF), the 5:2 diet, and time-restricted eating (TRE)-produced mild to moderate weight loss (1-8% from baseline) and consistent reductions in energy intake (10-30% from baseline). These regimens may benefit cardiometabolic health by decreasing blood pressure, insulin resistance, and oxidative stress. Low-density lipoprotein cholesterol and triglyceride levels are also lowered, but findings are variable. Other health benefits, such as improved appetite regulation and favorable changes in the diversity of the gut microbiome, have also been demonstrated, but evidence for these effects is limited. Intermittent fasting is generally safe and does not result in energy level disturbances or increased disordered eating behaviors. In summary, intermittent fasting is a safe diet therapy that can produce clinically significant weight loss (>5%) and improve several markers of metabolic health in individuals with obesity.

The ideal of experimental methodology in animal research is the reduction or elimination of environmental variables or consistency in their application. In lab animals, diet has been recognized as a very influential response variable. Reproducibility in research using rodents required the development of a unique diet of consistent ingredient and nutrient composition to allow for cross-comparisons of lab results, spatially and temporally. These diets are commonly referred to as standard reference diets (SRDs). The established validity of published nutritional requirements combined with the cooperation of commercial partners led to species-specific reference diets commonly used by the research community. During the last several decades, zebrafish (Danio rerio) have become a widespread alternative animal model, but specific knowledge of their nutrition is lacking. We present a short-term approach for developing an SRD for zebrafish, similar to that eventually attained for rodents over decades. Imminent development of an open-formulation, commercially produced SRD for zebrafish will notably advance translational biomedical science.