1,721,080 research outputs found
Nutrigenomics and inflammation
No full textDiet is one of the main factors that can impact gene expression and gut microbiota diversity and it provides the functional groups required for epigenome modulation. Starting from early life, the exposome (e.g. diet, xenobiotics, drugs, etc.) is responsible for specific epigenetics marks [1,2]. A maternal high fat diet and food pesticide exposure during the pre- and post-natal period of live can promote inflammatory responses in offspring that may influence organ development promoting a healthy/unhealthy phenotype in adulthood. High protein and carbohydrate (e.g. fructose, glucose) intake in adult age can play a key role in the development of chronic low-grade systemic inflammation [3]. Of particular concern is that epigenetic marks of diseases may be inherited, hence they can mediate epigenetic inheritance of diseases [4,5]. In this context, nutrigenomics mediated by bioactive compounds and a balanced nutrient intake can actively control inflammation and maintain the cellular redox homeostasis. A summary of data on how and when nutrigenomics can modulate inflammatory responses through healthy dietary choices to prevent the main inflammatory-related metabolic diseases occurring across life will be presented. References 1. Gabbianelli R, Damiani E. J Nutr Biochem. 2018; 57:1-13. 2. Bordoni L, Gabbianelli R. Biochimie. 2019; 160:156-171. 3. Yamashita A.S. et al., Mediators of Inflammation 2018; Article ID 8261432. 4. Bordoni L, et al. Oxid Med Cell Longev. 2019:1472623. 5. Sun W et al. Adv Sci (Weinh). 2019;16;6(11):1900275
Nutri-epigenomics: can we program health?
No full textEpigenetics regulates imprinting which modulates embryonic development and cell specific functions as well as gene expression across life; specific cell functions due to differentiation are maintained by “epigenetic memory” and inherited during replication. This mechanism depends on the availability of functional groups that can be obtained from food oxidation. The exposome, consisting in the exposure to factors like food, environment and stress etc., significantly modulates our epigenome, and in specific period of life ( i.e. neonatal period, pregnancy), these epigenetic changes can impact health at adult age and they might be inherited by progenies. A link between early life epigenetics and the development of obesity and cardiovascular diseases later in life has been observed in offspring born from malnourished mothers (1). Similarly, stress and xenobiotic exposure during neonatal age can modify neuronal development in sensitive subjects (2,3). Nutri-epigenomics studies the impact of micro- and macro-nutrients on gene expression; functional groups (i.e. methyl, acetyl, phosphate, etc) deriving from food oxidation can link with aminoacidic residues at histone tails modify chromatin structure. Furthermore, cytosine methylation at CpG island can modulate gene expression and inhibits transposon mobility, resulting in a proper functionality and genome stability. Studies on experimental models highlight that high fat or low protein diet can lead to disease development in exposed parents and in their offspring due to epigenetic changes; disease can be controlled inhibiting epigenetic inheritance linked to the observed disorder (4). Epigenetic biomarkers (i.e. RXRA) at umbilical cord tissue have been identified and correlated to the increased susceptibility to obesity in adolescents and other diseases at adult age (5). Referenze 1. Tobi EW et al., Human Molecular Genetics, 2009;18 (21): 4046-4053 2. Bordoni L, Gabbianelli R. Biochimie 2019; 160:156-171. 3. Bordoni L, et al. Oxid Med Cell Longev. 2019:1472623. 4. Guida MC et al., Nature Communications (2019)10:193 | https://doi.org/10.1038/s41467-018-08128-3. 5. Godfrey KM, et al. Diabetes. 2011;60(5):1528–1534. doi:10.2337/db10-0979
NuGOweek 2021
No full textImmuno-nutrigenomics: How to feed the immune system
The 17th edition of the NuGOweek will be held online from 6-8 September 2021. In those 3 (half) days the following thematic sessions will be organised:
Immunometabolism – From mechanisms to human interventions
How to feed the immune system – the role of nutrients and food bioactives for the immune system
Nutrigenomics (precision nutrition) of the immune system (inflammation
Early life stress
No full textEpigenetic mechanisms involve chemical modifications of the DNA (e.g., DNA methylation) or proteins compacting it (e.g., histones). These modifications can regulate gene expression and be maintained after cell divisions. Epigenetic inheritance describes the maintenance of epigenetic patterns after cell divisions (mitotic inheritance) or the consequences of epigenetic changes (generally in the germ line) across generations (transgenerational inheritance). Several factors are among the environmental influences reported to interfere with epigenetic programming during early development, among them endocrine disrupting or inorganic chemicals, nutritional compounds, or stressful conditions. Early developmental exposure to endocrine disruptors is shown to affect reproduction and metabolism in the subsequent generations in rodents. Stress have also been reported to produce developmental and transgenerational effects in animal models, including mammals and chickens. Importantly, these epigenetic modifications are detected both in the CNS and in peripheral cells. Because in birds red blood cells are nucleated, unlike in mammals, and sperm collection can be performed without sacrificing the animal, the chicken model provides unique features to perform longitudinal and transgenerational studies on the effects of stress.
Stress often does not only affect individuals and organisms directly exposed but can also have an impact on the progeny`s health. It can thereby potentially explain in part the missing heritability of disease that evolves around the fact that many complex diseases have a strong heritable component that cannot be attributed to single genetic factors. We and others have described a range of behavioral and metabolic effects of early life stress on the male line offspring in mice. We pinpointed specific epigenetic alterations including DNA methylation, histone post translational modifications and small and long non-coding RNA in the brain and the germline as mediators. We have recently identified an interesting contribution of circulating blood metabolites in the induction of crucial germline alterations that was also reflected in a cohort of children exposed to early life stress. This indicates that our findings are potentially also relevant to human disease risk heritability.
Essential hypertension is a complex condition of unknown pathogeneses. Recent advances in the field of developmental origins of increased blood pressure add another layer of complexity. Complications during pregnancy that program increased blood pressure in the offspring are varied and can include preeclampsia, parental smoking or alcohol consumption, maternal stress, or poor perinatal nutrition. Low birth weight serves as a crude proxy for impaired fetal growth indicative of intrauterine growth restriction (IUGR) and numerous experimental models of IUGR are utilized to examine the link between adverse events in early life and increased cardiovascular risk. These experimental models provide proof of principle that birth weight is inversely associated with blood pressure and indicate that despite the method of maternal/fetal insult, mutual mechanistic pathways contribute to the etiology of increased blood pressure in IUGR offspring. The renin angiotensin system, the sympathetic nervous system, endothelin, oxidative stress and vascular dysfunction are all implicated as contributors to increased blood pressure that has its origins in early life. Sex and age also effect the long-term consequences of IUGR on blood pressure control
Lifestyle Genomics: Selected Abstracts from the Published online: July 13, 2018 3rd European Summer School on Nutrigenomics
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Primers on nutrigenetics and nutri(epi)genomics: Origins and development of precision nutrition
Full text linkUnderstanding the relationship between genotype and phenotype is a central goal not just for genetics but also for medicine and biological sciences. Despite outstanding technological progresses, genetics alone is not able to completely explain phenotypes, in particular for complex diseases. Given the existence of a “missing heritability”, growing attention has been given to non-mendelian mechanisms of inheritance and to the role of the environment. The study of interaction between gene and environment represents a challenging but also a promising field with high potential for health prevention, and epigenetics has been suggested as one of the best candidate to mediate environmental effects on the genome. Among environmental factors able to interact with both genome and epigenome, nutrition is one of the most impacting. Not just our genome influences the responsiveness to food and nutrients, but vice versa, nutrition can also modify gene expression through epigenetic mechanisms. In this complex picture, nutrigenetics and nutrigenomics represent appealing disciplines aimed to define new prospectives of personalized nutrition. This review introduces to the study of gene-environment interactions and describes how nutrigenetics and nutrigenomics modulate health, promoting or affecting healthiness through life-style, thus playing a pivotal role in modulating the effect of genetic predispositions
Antioxidants in Oxidative Stress Diseases
No full textReactive oxygen species (ROS), including free radicals, are involved in many physiological and pathological events, and the control of their production is modulated by endogenous and exogenous systems, whose final goal is to maintain the redox equilibrium. Several diseases (e.g., neurodegeneration, cancer, cardiovascular diseases, etc.) are associated with an imbalance in this redox control, and biomarkers of oxidation have been correlated with the development of several age-related diseases. In this context, the use of antioxidants, either through dietary intake or supplementation, has been proposed to counterbalance ROS-induced oxidation. The key point, however, is that to date, the proper quantity of antioxidants required to achieve a personalized protective biological response without any pro-oxidant effects is still poorly defined. Furthermore, several human intervention trials with antioxidant supplementation have shown no conclusive evidence to support the use of vitamins and antioxidant supplements for the prevention of redox-related diseases. With this in mind, this Special Issue aims to publish original research papers, systematic reviews, and meta-analyses that contribute to better clarify the complexity related to dose/gender/age responses on antioxidant-protection against the most common diseases linked with oxidative stress
Epigenetics in ageing and development
No full textThe idea that a universal epigenetic program, which is reset during embryogenesis and influenced by diet and other environmental factors, can drive not only development but also ageing is gaining recognition, and embodies the idea that this is a major target for the future development of therapeutic strategies to improve health and longevity.
Indeed, multiple and progressive epigenetic changes have emerged as key hallmarks of ageing. These changes include patterns of DNA methylation and histone posttranslational modifications, altered noncoding RNA expression, replacement of canonical histones with histone variants and reduced bulk levels of the core histones (Pal and Tyler, 2016). While part of these changes act like an epigenetic clock and are tightly related to chronological age (Horvath, 2013), others diverge (age-dependently) from chronological age likely reflecting the increasing inter-individual variation in health of old organisms (Slieker and van Iterson, 2016). Reasons for these variations, are not well understood, but they seem to occur in all tissues and cells regardless of their developmental potential.
The impact of epigenetic changes in reflected by altered gene expression, reactivation of endogenous retroelements and genomic instability that can have systemic effects on ageing from cellular to the organismal level.
In this special issue of Mechanisms of Ageing and Development, the hot topics around the role of epigenetic changes in ageing and development are covered by critical reviews or original research manuscripts provided by major experts in the field.
While DNA methylation is currently the most promising biomarker of ageing, the mechanisms underlying age-related DNA methylation changes remain mostly undiscovered. A focused review shows how the dynamics of chromatin structure and histone posttranslational modifications are related to variations of methylcytosine and its oxidative modifications (Ciccarone and Tagliatesta, 2017). How epigenetic clock signature could be used as a lifestyle management tool to monitor healthy ageing, as well as to evaluate the effects of interventions against chronic ageing disorders and to extend healthy lifespan is the focus of another manuscript of this special issue (Declerck and Vanden Berghe, 2018).
CpG DNA methylation is among the epigenetic control mechanisms used by the cell to counteract the risk of genomic instability represented by endogenous retroelements. Indeed, these repetitive elements carry most of the methylated CpG sites of our genome. A dedicated manuscript (Cardelli, 2018) describes how epigenetic changes and endogenous retroelements are tightly related and discuss the relevance of their interaction in ageing research.
How nutrition affects global DNA methylation and how these changes can be transmitted to successive generation (epigenetic inheritance) is a highly discussed topic in ageing research. An original research manuscript (Guarasci and D’Aquila, 2018) provide here evidence that a low-calorie diet in rats affect the offspring’s epigenetic status, in particular when administered during the maternal pre-gestational period. Fetal epigenetics has a key impact on telomere lengths and telomere loss dynamics, and both can control health and lifespan. A review describes how different nutrients and oxygen supplied to the fetus can impact the length and dynamicity of telomeres, highlighting the way in which early environmental factors can have long term effects on healthy and unhealthy ageing (Ravlić and Škrobot Vidaček, 2017).
An interesting manuscript explains ferrosenescence; how iron can promote neurodegeneration and ageing. Early biomarkers in iron dyshomeostasis has been identified, and new strategies to control iron levels suggested. To this aim the microRNA-29 family might lower neuronal iron and could represent a new strategy in the control of ferrosenenscene (Sfera and Bullock, 2017). Another two review manuscripts describe how nutrition and physical exercise can be included among those interventions able to modulate epigenetic changes with a potential benefit in cardiovascular health (Wallace and Twomey, 2017) and in particular neurodegenerative diseases (e.g. Alzhiemer) (Robinson and Grabowski, 2017).
Studies on centenarians highlight how genetic and epigenetic modulation go hand in hand for a successful ageing. However, the epigenetic responses to the environment in centenarians seems more plastic and powerful then in people that have a less longer life (Puca and Spinelli, 2017). Two reviews focus on age-related diseases; one describes the differences in monozygotic twin pairs underlining the role of epigenetics in amyotrophic lateral sclerosis. The authors summarize some studies that show increased DNA methylation and progressive ageing in some twins affected by amyotrophic lateral sclerosis compared to age-matched controls. Furthermore, similarities in epigenetic biomarkers have been suggested between amyotrophic lateral sclerosis and Alzheimer’s disease (Dolinar and Ravnik-Glavač, 2018). Another review highlights how RYBP nuclear protein, controlling the polycomb group and trithorax group proteins, can influence chromatin condensation in response to stress and growth-related signals. During embryogenesis RYBP modulates the neural tube, neocortex and retinal development, as well as cardiomyocytes differentiation. RYBP has been described capable of influencing normal and pathological development through microRNA regulation and protein ubiquitylation. Interesting are also the evidences supporting the non-epigenetic control of apoptotic activity in mammalian cancer cells (Simoes da Silv and Simón, 2018).
A complex scenario can be described, and early epigenetics plasticity together with environmental epigenetic control throughout life can affect significantly the progression toward a healthy or unhealthy ageing. A graphical scheme resuming the hot topics around epigenetics covered by this special issue is provided in Fig. 1
Effects of Trimethylamine and Trimethylamine Oxide on Human Serum Albumin Observed by Tryptophan Fluorescence and Absorbance Spectroscopies
Full text linkTrimethylamine (TMA) is an aliphatic tertiary amine produced by gut microbiota, starting from dietary precursors such as L-choline, L-carnitine and betaine. TMA and its metabolite trimethylamine-N-oxide (TMAO) are elevated in the plasma of cardiovascular disease (CVD) patients. Despite extensive literature on this topic, the scientific community is still divided on which of the two molecules is responsible for the harmful effects on human health. To assess whether the plasma levels of these molecules are also modulated by interactions with macromolecules present in the plasma, the weak bonds between TMA or/and TMAO with human serum albumin (HSA) were studied via molecular docking and spectrofluorimetric assay. The impact of TMA and TMAO on HSA and low-density lipoproteins (LDL) oxidation was also evaluated. Docking analysis shows three main binding sites for TMA and two for TMAO. Spectrofluorimetric results show interactions of HSA with TMA and TMAO; a significant (p = 0.010) decrease in Trp-214 intrinsic fluorescence of HSA was measured starting from the lowest concentrations of both TMA and TMAO (3.26 nM and 29.2 nM, respectively). Furthermore, at all concentrations tested, no significant effect on the formation of carbonyls in HSA was measured (p > 0.05) in the presence of TMA or TMAO. However, 28.6 mM TMAO significantly increased (p < 0.05) the degree of oxidation of LDL, suggesting that TMAO has a pro-oxidant role on LDL
Biodetoxification and Protective Properties of Probiotics
Full text linkProbiotic consumption is recognized as being generally safe and correlates with multiple and valuable health benefits. However, the mechanism by which it helps detoxify the body and its anti-carcinogenic and antimutagenic potential is less discussed. A widely known fact is that globalization and mass food production/cultivation make it impossible to keep all possible risks under control. Scientists associate the multitude of diseases in the days when we live with these risks that threaten the population’s safety in terms of food. This review aims to explore whether the use of probiotics may be a safe, economically viable, and versatile tool in biodetoxification despite the numerous risks associated with food and the limited possibility to evaluate the contaminants. Based on scientific data, this paper focuses on the aspects mentioned above and demonstrates the probiotics’ possible risks, as well as their anti-carcinogenic and antimutagenic potential. After reviewing the probiotic capacity to react with pathogens, fungi infection, mycotoxins, acrylamide toxicity, benzopyrene, and heavy metals, we can conclude that the specific probiotic strain and probiotic combinations bring significant health outcomes. Furthermore, the biodetoxification maximization process can be performed using probiotic-bioactive compound association
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