Excessive specialization and high production requirements place high demands on the metabolism of poultry. A number of metabolic problems, such as disturbances of energy metabolism (affecting mainly hens) and mineral balance (affecting mainly laying hens), affect performance. Nearly all these problems are multifactorial in nature, but diet, and in particular the interaction between diet and phenotype, plays an important role. The problem of ascites in broiler hens is discussed in relation to external and genetic causative factors. Genetic factors can be further subdivided into structural and functional causative factors. This distinction has important consequences. For example, sudden death syndrome can be distinguished as a separate entity. Fatty liver syndrome in laying hens, and gout and urolithiasis in chicks and hens are briefly discussed. Finally, some of the most important or most common skeletal problems affecting poultry, namely, tibial dyschondroplasia, battery fatigue, rickets, and chondrodystrophy, are briefly discussed in the context of the dietary factors that underlie these disorders or which can be used as treatment.
Peptides are currently vital components in nutrition with physiological advantages beyond a basic diet. This systematic review aims to explain their significance in metabolic, behavioral, and musculoskeletal health, focusing on their therapeutic benefits, molecular mechanisms, and bioactivities. This systematic review analyzed clinical trials from PubMed and Scopus databases in the time range of 2019 to 2024, following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) standards, that investigated the role of peptides in human nutrition. Eight randomized clinical trials (RCTs) met the predefined metabolic, behavioral, and musculoskeletal health inclusion criteria. Peptides are derived from various sources, including milk, fish, and plants, and show various bioactive characteristics such as anti-inflammatory effect, improved muscle protein synthesis, and immune modulation. Some important findings emphasize their potential to govern metabolic processes, defend against chronic diseases, and enhance gut health. For instance, glucagon-like peptide (GLP-1) controls taste perception and appetite stimulation, and collagen peptides strengthen the musculoskeletal system. Peptides display intriguing potential as nutrients for addressing global health challenges, including behavioral responses, aging, and metabolic syndrome. Future investigations would focus on bioavailability, optimizing dosage, and demographic-specific treatments.
Circadian rhythms integrate a finely tuned network of biological processes recurring every 24 h, intricately coordinating the machinery of all cells. This self-regulating system plays a pivotal role in synchronizing physiological and behavioral responses, ensuring an adaptive metabolism within the environmental milieu, including dietary and physical activity habits. The systemic integration of circadian homeostasis involves a balance of biological rhythms, each synchronically linked to the central circadian clock. Central to this orchestration is the temporal dimension of nutrient and food intake, an aspect closely interwoven with the neuroendocrine circuit, gut physiology, and resident microbiota. Indeed, the timing of meals exerts a profound influence on cell cycle regulation through genomic and epigenetic processes, particularly those involving gene expression, DNA methylation and repair, and non-coding RNA activity. These (epi)genomic interactions involve a dynamic interface between circadian rhythms, nutrition, and the gut microbiota, shaping the metabolic and immune landscape of the host. This research endeavors to illustrate the intricate (epi)genetic interplay that modulates the synchronization of circadian rhythms, nutritional signaling, and the gut microbiota, unravelling the repercussions on metabolic health while suggesting the potential benefits of feed circadian realignment as a non-invasive therapeutic strategy for systemic metabolic modulation via gut microbiota. This exploration delves into the interconnections that underscore the significance of temporal eating patterns, offering insights regarding circadian rhythms, gut microbiota, and chrono-nutrition interactions with (epi)genomic phenomena, thereby influencing diverse aspects of metabolic, well-being, and quality of life outcomes.
Adipose tissues are dynamic tissues that play crucial physiological roles in maintaining health and homeostasis. Although white adipose tissue and brown adipose tissue are currently considered key endocrine organs, they differ functionally and morphologically. The existence of the beige or brite adipocytes, cells displaying intermediary characteristics between white and brown adipocytes, illustrates the plastic nature of the adipose tissue. These cells are generated through white adipose tissue browning, a process associated with augmented non-shivering thermogenesis and metabolic capacity. This process involves the upregulation of the uncoupling protein 1, a molecule that uncouples the respiratory chain from Adenosine triphosphate synthesis, producing heat. β-3 adrenergic receptor system is one important mediator of white adipose tissue browning, during cold exposure. Surprisingly, hyperthermia may also induce beige activation and white adipose tissue beiging. Physical exercising copes with increased levels of specific molecules, including Beta-Aminoisobutyric acid, irisin, and Fibroblast growth factor 21 (FGF21), which induce adipose tissue browning. FGF21 is a stress-responsive hormone that interacts with beta-klotho. The central roles played by hormones in the browning process highlight the relevance of the individual lifestyle, including circadian rhythm and diet. Circadian rhythm involves the sleep-wake cycle and is regulated by melatonin, a hormone associated with UCP1 level upregulation. In contrast to the pro-inflammatory and adipose tissue disrupting effects of the western diet, specific food items, including capsaicin and n-3 polyunsaturated fatty acids, and dietary interventions such as calorie restriction and intermittent fasting, favor white adipose tissue browning and metabolic efficiency. The intestinal microbiome has also been pictured as a key factor in regulating white tissue browning, as it modulates bile acid levels, important molecules for the thermogenic program activation. During embryogenesis, in which adipose tissue formation is affected by Bone morphogenetic proteins that regulate gene expression, the stimuli herein discussed influence an orchestra of gene expression regulators, including a plethora of transcription factors, and chromatin remodeling enzymes, and non-coding RNAs. Considering the detrimental effects of adipose tissue browning and the disparities between adipose tissue characteristics in mice and humans, further efforts will benefit a better understanding of adipose tissue plasticity biology and its applicability to managing the overwhelming burden of several chronic diseases.
Post-COVID-19 Condition (PCC), impacting 30-90% of survivors, is characterized by persistent fatigue and metabolic dysfunction, often linked to underlying mitochondrial impairment. This review examines current evidence on mitochondrial-targeted nutrition therapies, with a focus on magnetic resonance spectroscopy (MRS) as a tool for assessing metabolic recovery. Key findings highlight reduced adenosine triphosphate (ATP) production, heightened oxidative stress, and disrupted mitochondrial biogenesis- metabolic abnormalities that closely mirror those seen in chronic fatigue syndromes. While mitochondrial dysfunction is recognized as central, debate continues on whether systemic inflammation or direct viral damage primarily drives these abnormalities. Current evidence supports nutrients, such as, CoQ10, NAC, and creatine for restoring energy metabolism and reducing oxidative stress. MRS biomarkers (τPCr, Qmax), offer valuable tools for monitoring personalized intervention. However, several limitations persist, including variability in nutritional protocols, inconsistencies in MRS methodologies, and limited consideration of microbiome-psychosocial interactions. Most clinical trials focus on short-term outcomes, lacking data on long-term efficacy or stratification based on mitochondrial dysfunction severity. Future research priorities include multi-omics investigations into mitochondrial-epigenetic interactions, the development of targeted antioxidants, and exploration of engineered microbial metabolites. Standardizing MRS protocols, validating composite endpoints, and optimizing nutrient delivery systems require interdisciplinary collaboration. This review advocates for a precision medicine approach, combining MRS-based metabolic profiling with personalized nutritional strategies, to address the multifactorial nature of PCC and advance clinical translation.
Salinity is a global challenge to sustainable agriculture, impacting plant growth at cellular and functional levels. Nevertheless, silicon (Si), a multifunctional micro-element, plays a vital role in restoring and maintaining growth and development during unfavourable abiotic conditions such as high salinity exposure. Therefore, in the current research, two salinity levels [S1; 1 M (1000 mM) NaCl and S2; 2 M (2000 mM) NaCl] were used to assess the effects of exogenous Si (Si-1; 150 mg/L and Si-2; 250 mg/L) on key biological characteristics and especially the metabolite profiles of Panicum turgidum plants. Our findings revealed that the salt stress negatively affected the plants through high salt content (Na+ and Cl−) that further antagonized the essential nutrient balance in tissues; increased NH4+, but lowered NO3− and K+ in both roots and leaves. The excessive production of NH4+ led to over-accumulation of methylglyoxal (MG), resulting in the hyper-accumulation of sugars and altering the concentrations of amino acids, thereby inducing diabetes-like symptoms in P. turgidum plants. Interestingly, Si application restored the growth of P. turgidum plants by reducing oxidative damage thereby modifying the nutritional status, metabolic and biochemical characteristics of the plants. Specifically, the application of Si-2 showed improvement of key biological indictors in leaves and roots under both salinity levels. The current study also demonstrated that Si substantially reduced the NH4+-mediated MG-induced stress by lowering the concentration of MG, up-regulating the antioxidant capacity of various enzymes glyoxalase I (Gly-I), glyoxalase II (Gly-II), glutathione (GSH), glutamine: 2-oxoglutarate aminotransferase (GOGAT), nitrate reductase (NR), glutamine synthetase (GS), glutamate dehydrogenase (GDH); with concomitant changes in the levels of sugar/carbohydrates in roots and leaves of P. turgidum.
Recent research has highlighted potential important interaction between metabolism and inflammation, within the context of metabolic health and nutrition, with a view to preventing diet-related disease. In addition to this, there is a paucity of evidence in relation to accurate biomarkers that are capable of reflecting this important biological interplay or relationship between metabolism and inflammation, particularly in relation to diet and health. Therefore the objective of this review is to highlight the potential role of transcriptomic approaches as a tool to capture the mechanistic basis of metabolic inflammation. Within this context, this review has focused on the potential of peripheral blood mononuclear cells transcriptomic biomarkers, because they are an accessible tissue that may reflect metabolism and subacute chronic inflammation. Also these pathways are often dysregulated in the common diet-related diseases obesity, type 2 diabetes, and cardiovascular disease, thus may be used as markers of systemic health. The review focuses on fatty acids and polyphenols, two classes of nutrients/nonnutrient food components that modulate metabolism/inflammation, which we have used as an example of a proof-of-concept with a view to understanding the extent to which transcriptomic biomarkers are related to nutritional status and/or sensitive to dietary interventions. We show that both nutritional components modulate inflammatory markers at the transcriptomic level with the capability of profiling pro- and anti-inflammatory mechanisms in a bidirectional fashion; to this end transcriptomic biomarkers may have potential within the context of metabolic inflammation. This transcriptomic biomarker approach may be a sensitive indicator of nutritional status and metabolic health.
To promote sustainable aquaculture, the formulation of Atlantic salmon (Salmo salar) feeds has changed in recent decades, focusing on replacing standard marine-based ingredients with plant-based alternatives, increasingly demonstrating successful outcomes in terms of fish performance. However, little is known about how these plant-based diets may impact the gut microbiota at first feeding and onwards. Nutritional programming (NP) is one strategy applied for exposing fish to a plant-based (V) diet at an early stage in life to promote full utilisation of plant-based ingredients and prevent potential adverse impacts of exposure to a plant-rich diet later in life. We investigated the impact of NP on gut microbiota by introducing fish to plant ingredients (V fish) during first feeding for a brief period of two weeks (stimulus phase) and compared those to fish fed a marine-based diet (M fish). Results demonstrated that V fish not only maintained growth performance at 16 (intermediate phase) and 22 (challenge phase) weeks post first feeding (wpff) when compared to M fish but also modulated gut microbiota. PERMANOVA general effects revealed gut microbiota dissimilarity by fish group (V vs. M fish) and phases (stimulus vs. intermediate vs. challenge). However, no interaction effect of both groups and phases was demonstrated, suggesting a sustained impact of V diet (nutritional history) on fish across time points/phases. Moreover, the V diet exerted a significant cumulative modulatory effect on the Atlantic salmon gut microbiota at 16 wpff that was not demonstrated at two wpff, although both fish groups were fed the M diet at 16 wpff. The nutritional history/dietary regime is the main NP influencing factor, whereas environmental and host factors significantly impacted microbiota composition in M fish. Microbial metabolic reactions of amino acid metabolism were higher in M fish when compared to V fish at two wpff suggesting microbiota played a role in digesting the essential amino acids of M feed. The excessive mucin O-degradation revealed in V fish at two wpff was mitigated in later life stages after NP, suggesting physiological adaptability and tolerance to V diet. Future studies are required to explore more fully how the microbiota functionally contributes to the NP.
Domestication of dogs from wolves is the oldest known example of ongoing animal selection, responsible for generating more than 300 dog breeds worldwide. In order to investigate the taxonomic and functional evolution of the canine gut microbiota, a multi-omics approach was applied to six wild wolves and 169 dog faecal samples, the latter encompassing 51 breeds, which fully covers currently known canine genetic biodiversity. Specifically, 16S rRNA gene and bifidobacterial Internally Transcribed Spacer (ITS) profiling were employed to reconstruct and then compare the canine core gut microbiota to those of wolves and humans, revealing that artificial selection and subsequent cohabitation of dogs with their owners influenced the microbial population of canine gut through loss and acquisition of specific bacterial taxa. Moreover, comparative analysis of the intestinal bacterial population of dogs fed on Bones and Raw Food (BARF) or commercial food (CF) diet, coupled with shotgun metagenomics, highlighted that both bacterial composition and metabolic repertoire of the canine gut microbiota have evolved to adapt to high-protein or high-carbohydrates intake. Altogether, these data indicate that artificial selection and domestication not only affected the canine genome, but also shaped extensively the bacterial population harboured by the canine gut.
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Human mutations in MTHFD1 have recently been identified in patients with severe combined immunodeficiency (SCID). SCID results from inborn errors of metabolism that cause impaired T- and B-cell proliferation and function. One of the most common causes of SCID is adenosine deaminase (ADA) deficiency, which ultimately inhibits DNA synthesis and cell division. MTHFD1 has been shown to translocate to the nucleus during S-phase of the cell cycle; this localization is critical for synthesis of thymidyate (dTMP or the "T" base in DNA) and subsequent progression through the cell cycle and cell proliferation. Identification of MTHFD1 mutations that are associated with SCID highlights the potential importance of adequate dTMP synthesis in the etiology of SCID.
SUMMARY Fungal-induced inaccessibility in oat to Blumeria graminis requires active cell processes. These are reiterative de novo cell processes involved in inherent penetration resistance. Therefore, induced inaccessibility may well involve cellular memory of the initial attack. Phenylpropanoid biosynthesis inhibitors (AOPP and OH-PAS) and phosphate scavengers (DDG and d-mannose) strongly suppressed induced inaccessibility, but silicon nutrition had no effect. Induced accessibility was modulated by the presence of fungal haustoria inside cells. Haustoria actively suppress or reprogram infected plant cells toward a constant state of penetration susceptibility. Neither inhibitor treatments nor silicon nutrition affected fungal-induced accessibility.
The increased prevalence of obesity and related comorbidities is a major public health problem. While genetic factors undoubtedly play a role in determining individual susceptibility to weight gain and obesity, the identified genetic variants only explain part of the variation. This has led to growing interest in understanding the potential role of epigenetics as a mediator of gene-environment interactions underlying the development of obesity and its associated comorbidities. Initial evidence in support of a role of epigenetics in obesity and type 2 diabetes mellitus (T2DM) was mainly provided by animal studies, which reported epigenetic changes in key metabolically important tissues following high-fat feeding and epigenetic differences between lean and obese animals and by human studies which showed epigenetic changes in obesity and T2DM candidate genes in obese/diabetic individuals. More recently, advances in epigenetic methodologies and the reduced cost of epigenome-wide association studies (EWAS) have led to a rapid expansion of studies in human populations. These studies have also reported epigenetic differences between obese/T2DM adults and healthy controls and epigenetic changes in association with nutritional, weight loss, and exercise interventions. There is also increasing evidence from both human and animal studies that the relationship between perinatal nutritional exposures and later risk of obesity and T2DM may be mediated by epigenetic changes in the offspring. The aim of this review is to summarize the most recent developments in this rapidly moving field, with a particular focus on human EWAS and studies investigating the impact of nutritional and lifestyle factors (both pre- and postnatal) on the epigenome and their relationship to metabolic health outcomes. The difficulties in distinguishing consequence from causality in these studies and the critical role of animal models for testing causal relationships and providing insight into underlying mechanisms are also addressed. In summary, the area of epigenetics and metabolic health has seen rapid developments in a short space of time. While the outcomes to date are promising, studies are ongoing, and the next decade promises to be a time of productive research into the complex interactions between the genome, epigenome, and environment as they relate to metabolic disease.
Nowadays, nutrition focuses on improving health of individuals through diet. Current nutritional research aims at health promotion, disease prevention, and performance improvement. Modern analytical platforms allow the simultaneous measurement of multiple metabolites providing new insights in the understanding of the functionalities of cells and whole organisms. Metabonomics, "the quantitative measurement of the dynamic multiparametric metabolic response of living systems to pathophysiological stimuli or genetic modifications", provides a systems approach to understanding global metabolic regulations of organisms. This concept has arisen from various applications of NMR and MS spectroscopies to study the multicomponent metabolic composition of biological fluids, cells, and tissues. The generated metabolic profiles are processed by multivariate statistics to maximize the recovery of information to be correlated with well-determined stimuli such as dietary intervention or with any phenotypic data or diet habits. Metabonomics is thus uniquely suited to assess metabolic responses to deficiencies or excesses of nutrients and bioactive components. Furthermore, metabonomics is used to characterize the metabolic phenotype of individuals integrating genetic polymorphism, metabolic interactions with commensal and symbiotic partners such as gut microflora, as well as environmental and behavioral factors including dietary preferences. This paper reports several experimental key aspects in nutritional metabonomics, reviews its applications employing targeted and holistic approach analysis for the study of the metabolic responses following dietary interventions. It also reports the assessment of intra- and inter-individual variability in animal and human populations. The potentialities of nutritional metabonomics for the discovery of new biomarkers and the characterization of metabolic phenotypes are discussed in a context of their possible utilizations for personalized nutrition to provide health maintenance at the individual level.
The metabolic syndrome is a very common disease associated with an increased risk of type 2 diabetes mellitus (T2DM) and CVD. The clinical characteristics of the metabolic syndrome include insulin resistance, dyslipidaemia, abdominal obesity and hypertension. The diverse clinical characteristics illustrate the complexity of the disease process, which involves several dysregulated metabolic pathways. Thus, multiple genetic targets must be involved in the pathogenesis and progression of the metabolic syndrome. Nevertheless, the human genome has not changed markedly in the last decade but the prevalence of the metabolic syndrome has increased exponentially, which illustrates the importance of gene-environmental interactions. There is good evidence that nutrition plays an important role in the development and progression of the metabolic syndrome. Indeed, obesity is a key aetiological factor in the development of the metabolic syndrome. Understanding the biological impact of gene-nutrient interactions will provide a key insight into the pathogenesis and progression of diet-related polygenic disorders, including the metabolic syndrome. The present paper will explore the interactions between genetic background and dietary exposure or nutritional therapy, focusing on the role of dietary fatty acids within the context of nutrient regulation of gene expression and individual responsiveness to dietary therapy. Only with a full understanding of gene-gene, gene-nutrient and gene-nutrient-environment interactions can the molecular basis of the metabolic syndrome be solved to minimise the adverse health effects of obesity and reduce the risk of the metabolic syndrome, and subsequent T2DM and CVD.
Endocrine homeostasis and metabolic diseases have been the subject of extensive research in recent years. The development of new techniques and insights has led to a deeper understanding of the mechanisms underlying these conditions and opened up new avenues for diagnosis and treatment. In this review, we discussed the rise of metabolic diseases, especially in Western countries, the genetical, psychological, and behavioral basis of metabolic diseases, the role of nutrition and physical activity in the development of metabolic diseases, the role of single-cell transcriptomics, gut microbiota, epigenetics, advanced imaging techniques, and cell-based therapies in metabolic diseases. Finally, practical applications derived from this information are made.
Today, there is a growing awareness about the importance of eating nutritious foods and fish is gaining momentum as a result of its unique nutritional benefits. Fish are considered as nutritionally valuable part of the human diet because of the presence of both macronutrients (proteins, lipids and ash) and micronutrients (vitamins and minerals). These nutrients are indispensable in human nutrition and have proven to be involved in several metabolic functions. The nutritional content can be used to rank different fish species based on their nutritional and functional benefits, allowing consumers to make better decisions according to their requirements. Proximate composition of fish includes determination of moisture, protein, fat and ash contents, which constitutes about 96%-98% of the total constituents of the fish body. The study of these components gives us a clear understanding in assessing the energy value of the fishes. In the present study, an attempt has been made to provide a concise review about the proximate composition of various fish species from different parts of the world in order to evaluate the high-protein, low-fat food with excellent nutritional values and to enlighten the different exogenous and endogenous factors that are actually responsible for their variation. The review also provides an insight into the characteristics of the chemical composition of various fish species, which are gaining importance for the sector involving fish and fishery products for domestic and foreign trade and for appreciating as animal feed all over the world.
UNLABELLED: The gut microbiota enhances the host's metabolic capacity for processing nutrients and drugs and modulate the activities of multiple pathways in a variety of organ systems. We have probed the systemic metabolic adaptation to gut colonization for 20 days following exposure of axenic mice (n = 35) to a typical environmental microbial background using high-resolution (1)H nuclear magnetic resonance (NMR) spectroscopy to analyze urine, plasma, liver, kidney, and colon (5 time points) metabolic profiles. Acquisition of the gut microbiota was associated with rapid increase in body weight (4%) over the first 5 days of colonization with parallel changes in multiple pathways in all compartments analyzed. The colonization process stimulated glycogenesis in the liver prior to triggering increases in hepatic triglyceride synthesis. These changes were associated with modifications of hepatic Cyp8b1 expression and the subsequent alteration of bile acid metabolites, including taurocholate and tauromuricholate, which are essential regulators of lipid absorption. Expression and activity of major drug-metabolizing enzymes (Cyp3a11 and Cyp2c29) were also significantly stimulated. Remarkably, statistical modeling of the interactions between hepatic metabolic profiles and microbial composition analyzed by 16S rRNA gene pyrosequencing revealed strong associations of the Coriobacteriaceae family with both the hepatic triglyceride, glucose, and glycogen levels and the metabolism of xenobiotics. These data demonstrate the importance of microbial activity in metabolic phenotype development, indicating that microbiota manipulation is a useful tool for beneficially modulating xenobiotic metabolism and pharmacokinetics in personalized health care. IMPORTANCE: Gut bacteria have been associated with various essential biological functions in humans such as energy harvest and regulation of blood pressure. Furthermore, gut microbial colonization occurs after birth in parallel with other critical processes such as immune and cognitive development. Thus, it is essential to understand the bidirectional interaction between the host metabolism and its symbionts. Here, we describe the first evidence of an in vivo association between a family of bacteria and hepatic lipid metabolism. These results provide new insights into the fundamental mechanisms that regulate host-gut microbiota interactions and are thus of wide interest to microbiological, nutrition, metabolic, systems biology, and pharmaceutical research communities. This work will also contribute to developing novel strategies in the alteration of host-gut microbiota relationships which can in turn beneficially modulate the host metabolism.
Fermented food products, especially those derived from cereals and legumes are important contributors to diet diversity globally. These food items are vital to food security and significantly contribute to nutrition. Fermentation is a process that desirably modifies food constituents by increasing the palatability, organoleptic properties, bioavailability and alters nutritional constituents. This review focuses on deciphering possible mechanisms involved in the modification of nutritional constituents as well as nutrient bioavailability during the fermentation of cereals and legumes, especially those commonly consumed in developing countries. Although modifications in these constituents are dependent on inherent and available nutrients in the starting raw material, it was generally observed that fermentation increased these nutritive qualities (protein, amino acids, vitamins, fats, fatty acids, etc.) in cereals and legumes, while in a few instances, a reduction in these constituents was noted. A general reduction trend in antinutritional factors was also observed with a corresponding increase in the nutrient bioavailability and bioaccessibility. Notable mechanisms of modification include transamination or the synthesis of new compounds during the fermentation process, use of nutrients as energy sources, as well as the metabolic activity of microorganisms leading to a degradation or increase in the level of some constituents. A number of fermented products are yet to be studied and fully understood. Further research into these food products using both conventional and modern techniques are still required to provide insights into these important food groups, as well as for an overall improved food quality, enhanced nutrition and health, as well as other associated socioeconomic benefits.
BACKGROUND: Dietary advice remains the cornerstone of prevention and management of type 2 diabetes (T2D). However, understanding the efficacy of dietary interventions is confounded by the challenges inherent in assessing free living diet. Here we profiled dietary metabolites to investigate glycaemic deterioration and cardiometabolic risk in people at risk of or living with T2D. METHODS: score was used to explore the relationships between diet, glycaemic deterioration and cardio-metabolic risk via multiple linear regression models. FINDINGS: score was also associated lower total body adiposity in both cohorts and lower fasting glucose (β=-0.2 mmol/L, 95% CI -0.3, -0.01) and insulin (β=-9.2 pmol/mol, 95% CI -17.9, -0.4) concentrations in cohort 2. INTERPRETATION: Plasma dietary metabolite profiling provides objective measures of diet intake, showing a relationship to glycaemic deterioration and cardiometabolic health. FUNDING: This work was supported by the Innovative Medicines Initiative Joint Undertaking under grant agreement no. 115,317 (DIRECT), resources of which are composed of financial contribution from the European Union's Seventh Framework Programme (FP7/2007-2013) and EFPIA companies.