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Nutrimetabonomics: applications for nutritional sciences, with specific reference to gut microbial interactions
No full textUnderstanding the role of the diet in determining human health and disease is one major objective of modern nutrition. Mammalian biocomplexity necessitates the incorporation of systems biology technologies into contemporary nutritional research. Metabonomics is a powerful approach that simultaneously measures the low-molecular-weight compounds in a biological sample, enabling the metabolic status of a biological system to be characterized. Such biochemical profiles contain latent information relating to inherent parameters, such as the genotype, and environmental factors, including the diet and gut microbiota. Nutritional metabonomics, or nutrimetabonomics, is being increasingly applied to study molecular interactions between the diet and the global metabolic system. This review discusses three primary areas in which nutrimetabonomics has enjoyed successful application in nutritional research: the illumination of molecular relationships between nutrition and biochemical processes; elucidation of biomarker signatures of food components for use in dietary surveillance; and the study of complex trans-genomic interactions between the mammalian host and its resident gut microbiome. Finally, this review illustrates the potential for nutrimetabonomics in nutritional science as an indispensable tool to achieve personalized nutrition
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Nutrimetabonomics: nutritional applications of metabolic profiling
No full textAn individual's metabolic phenotype, and ultimately health, is significantly influenced by complex interactions between their genes and the diet. Studying these associations and their downstream biochemical consequences has proven extremely challenging using traditional hypothesis-led strategies. Metabonomics, a systems biology approach, allows the global metabolic response of biological systems to stimuli to be characterised. Through the application of this approach to nutritional-based research, nutrimetabonomics, the biochemical response to dietary inputs is being investigated at greater levels of resolution. This has allowed novel insights to be gained regarding intricate diet-gene interactions and their consequences for health and disease. In this review, we present some of the latest research exploring how nutrimetabonomics can assist in the elucidation of novel biomarkers of dietary behaviour and provide new perspectives on diet-health relationships. The use of this approach to study the metabolic interplay between the gut microbiota and the host is also explored
The effects of a hydrolyzed protein diet on the plasma, fecal and urine metabolome in cats with chronic enteropathy
No full textHydrolyzed protein diets are extensively used to treat chronic enteropathy (CE) in cats. However, the biochemical effects of such a diet on feline CE have not been characterized. In this study an untargeted 1H nuclear magnetic resonance spectroscopy-based metabolomic approach was used to compare the urinary, plasma, and fecal metabolic phenotypes of cats with CE to control cats with no gastrointestinal signs recruited at the Royal Veterinary College (RVC). In addition, the biomolecular consequences of a hydrolyzed protein diet in cats with CE was also separately determined in cats recruited from the RVC (n = 16) and the University of Bristol (n = 24) and whether these responses differed between dietary responders and non-responders. Here, plasma metabolites related to energy and amino acid metabolism significantly varied between CE and control cats in the RVC cohort. The hydrolyzed protein diet modulated the urinary metabolome of cats with CE (p = 0.005) in both the RVC and Bristol cohort. In the RVC cohort, the urinary excretion of phenylacetylglutamine, p-cresyl-sulfate, creatinine and taurine at diagnosis was predictive of dietary response (p = 0.025) although this was not observed in the Bristol cohort. Conversely, in the Bristol cohort plasma betaine, glycerol, glutamine and alanine at diagnosis was predictive of outcome (p = 0.001), but these same results were not observed in the RVC cohort. The biochemical signature of feline CE in the RVC cohort was consistent with that identified in human and animal models of inflammatory bowel disease. The hydrolyzed protein diet had the same effect on the urinary metabolome of cats with CE at both sites. However, biomarkers that were predictive of dietary response at diagnosis differed between the 2 sites. This may be due to differences in disease severity, disease heterogeneity, factors unrelated to the disease or small sample size at both sites. As such, further studies utilizing larger number of cats are needed to corroborate these findings.</p
The effect of a hydrolyzed protein diet on the fecal microbiota in cats with chronic enteropathy
No full textThe effect of a hydrolyzed protein diet on the fecal microbiota has not been studied in feline chronic enteropathy (CE). Our study aimed to (1) compare the fecal microbiota of cats with CE to control cats with no gastrointestinal signs and (2) determine the effect of a hydrolyzed protein diet on the fecal microbiota of cats with CE and whether this differs between dietary responders and non-responders. The fecal microbiome of cats with CE (n = 36) showed decreased α-diversity in terms of genus richness (P = 0.04) and increased β-diversity in terms of Bray-Curtis Dissimilarity (P < 0.001) compared to control cats (n = 14). Clostridium was the only genera significantly over-represented in cats with CE compared to control cats (adjusted P < 0.1). After 6-weeks of feeding the diet, fifteen cats were classified as responders and 18 as non-responders, based on clinical signs. At the genus level, α-diversity was increased in non-responders versus responders at diagnosis, but decreased after dietary intervention in both groups (P < 0.05). At the family level, non-responders became increasingly dissimilar after dietary intervention (P = 0.012). In general, the abundance of bacteria decreased with feeding a hydrolyzed diet, with the genera most significantly affected being more frequently observed in non-responders. Bifidobacterium was the only genus that increased significantly in abundance post-diet and this effect was observed in both responders and non-responders. Both Oscillibacter and Desulfovibrionaceae_unclassified were most abundant in non-responders at diagnosis but were rarely observed post diet in neither responders nor non-responders. Cats with CE had similar microbiota changes to those described in human inflammatory bowel disease. Whether the presence of Oscillibacter and Desulfovibrionaceae_unclassified are indicators of non-response to the diet at diagnosis requires further investigation. Despite the hydrolyzed diet reducing α-diversity in all cats with CE, this did not resolve gastrointestinal signs in some cats. However, responders metabolized the diet in a similar manner, reflected by sustained β-diversity, while the microbiome of non-responders became increasingly dissimilar compared to diagnosis at the family level. Therefore, the microbiome may not be as tightly regulated in cats with CE that are non-responders and therefore, these cats would require additional therapy for remission of clinical signs
Metabolic phenotyping of malnutrition during the first 1000 days of life
No full textNutritional restrictions during the first 1000 days of life can impair or delay the physical and cognitive development of the individual and have long-term consequences for their health. Metabolic phenotyping (metabolomics/metabonomics) simultaneously measures a diverse range of low molecular weight metabolites in a sample providing a comprehensive assessment of the individual's biochemical status. There are a growing number of studies applying such approaches to characterize the metabolic derangements induced by various forms of early-life malnutrition. This includes acute and chronic undernutrition and specific micronutrient deficiencies. Collectively, these studies highlight the diverse and dynamic metabolic disruptions resulting from various forms of nutritional deficiencies. Perturbations were observed in many pathways including those involved in energy, amino acid, and bile acid metabolism, the metabolic interactions between the gut microbiota and the host, and changes in metabolites associated with gut health. The information gleaned from such studies provides novel insights into the mechanisms linking malnutrition with developmental impairments and assists in the elucidation of candidate biomarkers to identify individuals at risk of developmental shortfalls. As the metabolic profile represents a snapshot of the biochemical status of an individual at a given time, there is great potential to use this information to tailor interventional strategies specifically to the metabolic needs of the individual.</p
Author correction: obesity and ethnicity alter gene expression in skin
No full textDaniel Butler was omitted from the author list in the original version of this Article. The Author contributions section now reads: “J.M.W. designed, conducted, and contributed to the writing of the manuscript, prepared Fig. 1. S.G. evaluated and did statistical analysis on the skin and fat samples, prepared Figs. 2–9. J.O.A. evaluated and contributed to writing the manuscript. D.B prepared and sequenced DNA libraries for the skin microbiota data, and wrote the applicable parts of the methods section. C.M. analyzed and wrote up the skin microbiota data, prepared Fig. 10. All authors have read the manuscript and approved its contents. D.D. analyzed and wrote up the skin microbiota data. S.Z. ran and analyzed the skin metabolite data. J.S. assisted in design, analysis and wrote up the skin metabolite data. J.K. assisted in analysis write up of skin and fat data. J.L.B. assisted in analysis, interpretation and writing of the manuscript. P.R.H. designed, analyzed, interpreted the data, and was the primary author of the manuscript.” This has been corrected in the PDF and HTML versions of the Article, and in the accompanying Supplementary Information file.</p
Targeting microbial metabolites to treat autism
No full textA first-in-class therapeutic that targets neuroactive microbial metabolites in the gut shows promising target engagement, safety and behavioral improvements in adolescents with autism spectrum disorder
L-rhamnose as a source of colonic propionate inhibits insulin secretion but does not influence measures of appetite or food intake
Full text linkActivation of free fatty acid receptor (FFAR)2 and FFAR3 via colonic short-chain fatty acids, particularly propionate, are postulated to explain observed inverse associations between dietary fiber intake and body weight. Propionate is reported as the predominant colonic fermentation product from l-rhamnose, a natural monosaccharide that resists digestion and absorption reaching the colon intact, while effects of long-chain inulin on appetite have not been extensively investigated. In this single-blind randomized crossover study, healthy unrestrained eaters (n = 13) ingested 25.5 g/d l-rhamnose, 22.4 g/d inulin or no supplement (control) alongside a standardized breakfast and lunch, following a 6-d run-in to investigate if appetite was inhibited. Postprandial qualitative appetite, breath hydrogen, and plasma glucose, insulin, triglycerides and non-esterified fatty acids were assessed for 420 min, then an ad libitum meal was provided. Significant treatment x time effects were found for postprandial insulin (P = 0.009) and non-esterified fatty acids (P = 0.046) with a significantly lower insulin response for l-rhamnose (P = 0.023) than control. No differences between treatments were found for quantitative and qualitative appetite measures, although significant treatment x time effects for meal desire (P = 0.008) and desire to eat sweet (P = 0.036) were found. Breath hydrogen was significantly higher with inulin (P = 0.001) and l-rhamnose (P = 0.009) than control, indicating colonic fermentation. These findings suggest l-rhamnose may inhibit postprandial insulin secretion, however neither l-rhamnose or inulin influenced appetite.</p
Modeling Enteropathy or Diarrhea with the Top Bacterial and Protozoal Pathogens: Differential Determinants of Outcomes
Full text linkDeveloping effective therapeutics or preventive interventions for important health threats is greatly enhanced whenever accessible models can enable the assessment of clinically important outcomes. While no non-human model is ever perfect, inexpensive in vivo small animal models in such as mice are often of great help in assessing the relevant efficacy of potential interventions. In addition to acute diarrhea, the long-term growth and developmental effects of enteric infections, with or without overt diarrhea, are increasingly recognized. To address these diverse effects, inexpensive animal models are proving to be very helpful. Herein, we review the major clinical concerns with enteric parasitic and bacterial infections that are extremely common worldwide, especially in vulnerable young children living in impoverished areas, and the recently published murine models of these infections and their outcomes. We find that common dietary deficiencies seen in children in developing areas have striking effects on diarrhea and enteropathy outcomes in mice. However, these effects differ with different pathogens. Specifically, the effects of protein or zinc deficiency differ considerably with different major protozoal and bacterial pathogens, suggesting different pathogenetic pathways and intervention effects. The pathogens reviewed are the seven top parasitic and bacterial pathogens seen in children, namely, Cryptosporidium, Giardia, Campylobacter, Shigella, enterotoxigenic Escherichia coli (ETEC), enteroaggregative E. coli (EAEC), and enteropathogenic E. coli (EPEC)
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