Search

Abstract The literature is full of claims regarding the consumption of polyphenol or polyamine-rich foods that offer some protection from developing cardiovascular disease (CVD). This is achieved by preventing cardiac hypertrophy and protecting blood vessels through improving the function of endothelium. However, do these interventions work in the aged human hearts? Cardiac aging is accompanied by an increase in left ventricular hypertrophy, along with diastolic and systolic dysfunction. It also confers significant cardiovascular risks for both sexes. The incidence and prevalence of CVD increase sharply at an earlier age in men than women. Furthermore, the patterns of heart failure differ between sexes, as do the lifetime risk factors. Do caloric restriction (CR)-mimetics, rich in polyphenol or polyamine, delay or reverse cardiac aging equally in both men and women? This review will discuss three areas: (1) mechanisms underlying age-related cardiac remodeling; (2) gender-related differences and potential mechanisms underlying diminished cardiac response in older men and women; (3) we select a few polyphenol or polyamine rich compounds as the CR-mimetics, such as resveratrol, quercetin, curcumin, epigallocatechin gallate and spermidine, due to their capability to extend health-span and induce autophagy. We outline their abilities and issues on retarding aging in animal hearts and preventing CVD in humans. We discuss the confounding factors that should be considered for developing therapeutic strategies against cardiac aging in humans.

Digestive tract-related cancers account for four of the top ten high-risk cancers worldwide. In recent years, cancer immunotherapy, which exploits the innate immune system to attack tumors, has led to a paradigm shifts in cancer treatment. Gut microbiota modification has been widely used to regulate cancer immunotherapy. Dietary compounds and traditional Chinese medicine (TCM) can alter the gut microbiota and its influence on toxic metabolite production, such as the effect of iprindole on lipopolysaccharide (LPS), and involvement in various metabolic pathways that are closely associated with immune reactions. Therefore, it is an effective strategy to explore new immunotherapies for gastrointestinal cancer to clarify the immunoregulatory effects of different dietary compounds/TCMs on intestinal microbiota. In this review, we have summarized recent progress regarding the effects of dietary compounds/TCMs on gut microbiota and their metabolites, as well as the relationship between digestive cancer immunotherapy and gut microbiota. We hope that this review will act as reference, providing a theoretical basis for the clinical immunotherapy of digestive cancer via gut microbiota modulation.

CRISPR-dCas9 (dead Cas9 protein) technology, combined with chemical molecules and light-triggered genetic switches, offers customizable control over gene perturbation. However, these simple ON/OFF switches cannot precisely determine the sophisticated perturbation process. Here, we developed a resveratrol and protocatechuic acid-programmed CRISPR-mediated gene remodeling biocomputer (REPA CRISPR ) for conditional endogenous transcriptional regulation of genes in vitro and in vivo. Two REPA CRISPR variants, REPA CRISPRi and REPA CRISPRa , were designed for the logic control of gene inhibition and activation, respectively. We successfully demonstrated the digital computations of single or multiplexed endogenous gene transcription by using REPA CRISPRa . We also established mathematical models to predict the dose-responsive transcriptional levels of a target endogenous gene controlled by REPA CRISPRa . Moreover, high levels of endogenous gene activation in mice mediated by the AND logic gate demonstrated computational control of CRISPR-dCas9-based epigenome remodeling in mice. This CRISPR-based biocomputer expands the synthetic biology toolbox and can potentially advance gene-based precision medicine. A record of this paper's transparent peer review process is included in the supplemental information., Competing Interests: Declaration of interests The authors declare no competing interests., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Traditional Chinese medicine (TCM) and dietary compounds have a profound influence on the regulation of gut microbiota (GM) in hepatic fibrosis (HF). Certain substances found in both food and herbs that are edible and medicinal, such as dietary fiber, polyphenols, and polysaccharides, can generate beneficial metabolites like short-chain fatty acids (SCFAs), bile acids (BAs), and tryptophan (Trp). These compounds contribute to regulate the GM, reduce levels of endotoxins in the liver, and alleviate fibrosis and inflammation in the liver. Furthermore, they enhance the composition and functionality of GM, promoting the growth of beneficial bacteria while inhibiting the proliferation of harmful bacteria. These mechanisms mitigate the inflammatory response in the intestines and maintain the integrity of the intestinal barrier. The purpose of this review is to analyze how the GM regulates the pathogenesis of HF, evaluate the regulatory effect of TCM and dietary compounds on the intestinal microflora, with a particular emphasis on modulating flora structure, enhancing gut barrier function, and addressing associated pathogenic factors, thereby provide new insights for the treatment of HF., Competing Interests: The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.AbbreviationsAbbreviationFull TermAbbreviationFull TermAhRAryl hydrocarbon receptorIFN-γInterferon-γALTAlanine aminotransferaseIFNsInterferonsAMPKAdenosine monophosphate-activated protein kinaseIL-1βInterleukin-1betaASTAspartate aminotransferaseIL-6Interleukin-6BAsBile acidsIL-8Interleukin 8BBRBerberineLDLRLow-density lipoprotein receptorCACholic acidLPSLipopolysaccharidesCDCAChenodeoxycholic acidLOXLipoxygenaseCOXCyclooxygenaseMIP-1αMacrophage inflammatory protein-1 alphaCSFsColony-stimulating factorsNF-κBNuclear factor kappa BDCADeoxycholic acidNLRsNod-like receptorsECMExtracellular matrixNONitric oxideEREndoplasmic reticulumPAMPsPathogen-associated molecular patternsFXRsFarnesoid X receptorsPGE2Prostaglandin E2GCAGlycocholic acidPLA2Phospholipase A2GMGut microbiotaPPARγPeroxisome proliferator-activated receptor γGPCRsG protein-coupled receptorsROSReactive oxygen speciesHFDHigh-fat dietSCD1Stearoyl-Coenzyme A desaturase 1HFHepatic fibrosisSCFAsShort-chain fatty acidsHFHCHigh fat and high cholesterolSTAT5Signal Transducer and Activator of Transcription 5HSCsHepatic stellate cellsTCTotal cholesterolHDACHistone deacetylaseTCATricarboxylic acid cycle, (© 2024 The Authors. Published by Elsevier Ltd.)

Dietary compounds significantly affected starch enzymatic digestion. However, effects of dietary compounds on starch digestion and their underlying mechanisms have been not systematically discussed yet. This review summarized the effects of dietary compounds including cell walls, proteins, lipids, non-starchy polysaccharides, and polyphenols on starch enzymatic digestion. Cell walls, proteins, and non-starchy polysaccharides restricted starch disruption during hydrothermal treatment and the retained ordered structures limited enzymatic binding. Moreover, they encapsulated starch granules and formed physical barriers for enzyme accessibility. Proteins, non-starchy polysaccharides along with lipids and polyphenols interacted with starch and formed ordered assemblies. Furthermore, non-starchy polysaccharides and polyphenols showed robust abilities to reduce activities of α-amylase and α-glucosidase. Accordingly, it can be concluded that dietary compounds lowered starch digestion mainly by three modes: (i) prevented ordered structures from disruption and formed ordered assemblies chaperoned with these dietary compounds; (ii) formed physical barriers and prevented enzymes from accessing/binding to starch; (iii) reduced enzymes activities. Dietary compounds showed great potentials in lowering starch enzymatic digestion, thereby modulating postprandial glucose response to food and preventing or treating type II diabetes disease.

Modifications of the activity of Cytochrome 450 (CYP) enzymes by compounds in food might impair medical treatments. These CYP-mediated food–drug interactions (FDI) play a major role in drug clearance in the intestine and liver. Inter-individual variation in both CYP expression and structure is an important determinant of FDI. Traditional targeted approaches have highlighted a limited number of dietary inhibitors and single-nucleotide variations (SNVs), each determining personal CYP activity and inhibition. These approaches are costly in time, money and labor. Here, we review computational tools and databases that are already available and are relevant to predicting CYP-mediated FDIs. Computer-aided approaches such as protein–ligand interaction modeling and the virtual screening of big data narrow down hundreds of thousands of items in databanks to a few putative targets, to which the research resources could be further directed. Structure-based methods are used to explore the structural nature of the interaction between compounds and CYP enzymes. However, while collections of chemical, biochemical and genetic data are available today and call for the implementation of big-data approaches, ligand-based machine-learning approaches for virtual screening are still scarcely used for FDI studies. This review of CYP-mediated FDIs promises to attract scientists and the general public. [ABSTRACT FROM AUTHOR]

The literature is full of claims regarding the consumption of polyphenol or polyamine-rich foods that offer some protection from developing cardiovascular disease (CVD). This is achieved by preventing cardiac hypertrophy and protecting blood vessels through improving the function of endothelium. However, do these interventions work in the aged human hearts? Cardiac aging is accompanied by an increase in left ventricular hypertrophy, along with diastolic and systolic dysfunction. It also confers significant cardiovascular risks for both sexes. The incidence and prevalence of CVD increase sharply at an earlier age in men than women. Furthermore, the patterns of heart failure differ between sexes, as do the lifetime risk factors. Do caloric restriction (CR)-mimetics, rich in polyphenol or polyamine, delay or reverse cardiac aging equally in both men and women? This review will discuss three areas: (1) mechanisms underlying age-related cardiac remodeling; (2) gender-related differences and potential mechanisms underlying diminished cardiac response in older men and women; (3) we select a few polyphenol or polyamine rich compounds as the CR-mimetics, such as resveratrol, quercetin, curcumin, epigallocatechin gallate and spermidine, due to their capability to extend health-span and induce autophagy. We outline their abilities and issues on retarding aging in animal hearts and preventing CVD in humans. We discuss the confounding factors that should be considered for developing therapeutic strategies against cardiac aging in humans. [ABSTRACT FROM AUTHOR]

Gut microbiota, a group of microorganisms that live in the gastrointestinal tract, plays important roles in health and disease. One mechanism that gut microbiota in modulation of the functions of hosts is achieved through synthesizing and releasing a series of metabolites such as short-chain fatty acids. In recent years, increasing evidence has indicated that dietary compounds can interact with gut microbiota. On one hand, dietary compounds can modulate the composition and function of gut microbiota; on the other hand, gut microbiota can metabolize the dietary compounds. Although there are several reviews on gut microbiota and diets, there is no focused review on the effects of dietary compounds on gut microbiota-derived metabolites. In this review, we first briefly discussed the types of gut microbiota metabolites, their origins, and the reasons that dietary compounds can interact with gut microbiota. Then, focusing on gut microbiota-derived compounds, we discussed the effects of dietary compounds on gut microbiota-derived compounds and the following effects on health. Furthermore, we give our perspectives on the research direction of the related research fields. Understanding the roles of dietary compounds on gut microbiota-derived metabolites will expand our knowledge of how diets affect the host health and disease, thus eventually enable the personalized diets and nutrients.

The circadian rhythm regulates the daily cycles of various physiological activities. Accumulating evidences revealed that circadian rhythm plays an important role in regulating metabolic homeostasis, and disruptions of circadian rhythms resulting in metabolic disorder. Peripheral clocks are not only controlled by the central clock but also entrained by external cues. Dietary pattern and compounds derived from food are found to play multiple roles in regulating metabolic processes through resetting peripheral clocks. Here we review the recent advance of effects and mechanisms of dietary pattern and compounds modulating peripheral clocks and regulating metabolic processes. Multiple molecular mechanisms linked dietary pattern and compounds with circadian rhythm and metabolism were summarized. Elaboration of crosstalk between diet and circadian rhythm may provide targets for the prevention of metabolic disorder. The exact mechanisms that feeding pattern and dietary compounds linked metabolic process and circadian rhythm need to be further investigated.

The relationship between diet and disease has been widely studied. The majority of studies have focused on the role and effects of food groups, nutrients or specific compounds, neglecting the wide range of compounds that make up our food. Each compound possesses unique characteristics and exerts distinct effects in the body. Analyzing correlations at the level of food compounds may provide novel insights into the relationship between diet and health. Currently, various publicly available food compounds databases describe types and concentrations of food compounds present in a large variety of food items. In this paper we describe the coupling of two international food compounds databases, FooDB and Phenol-Explorer, to the Dutch food coding system NEVO, to enable quick translation of generic dietary data from Dutch cohort studies to the level of intake of food compounds. The coupling allows a comprehensive analysis of existing and future cohort data focused on diet and health status, with the aim to identify food compounds that play a role in health and disease. • Two food compounds databases were coupled to the Dutch food coding system NEVO. • The coupling allows translation of generic food intake data to food compound level. • Our approach will help to identify compounds that play a role in health and disease. [ABSTRACT FROM AUTHOR]

The molecular clock is vital for regulating circadian rhythms in various physiological processes, and its dysregulation is associated with multiple diseases. As such, the use of small molecule modulators to regulate the molecular clock presents a promising therapeutic approach. In this study, we generated a homology model of the human circadian locomotor output cycles kaput (CLOCK) protein to evaluate its ligand binding sites. Using molecular docking, we obtained further insights into the binding mode of the control compound CLK8 and explored a selection of dietary compounds. Our investigation of dietary compounds was guided by their potential interactions with the retinoic acid-related orphan receptors RORα/γ, which are involved in circadian regulation. Through the molecular similarity and docking analyses, we identified oleanolic acid demethyl, 3-epi-lupeol, and taraxasterol as potential ROR-interacting compounds. These compounds may exert therapeutic effects through their modulation of RORα/γ activity and subsequently influence the molecular clock. Overall, our study highlights the potential of small molecule modulators in regulating the molecular clock and the importance of exploring dietary compounds as a source of such modulators. Our findings also provide insights into the binding mechanisms of CLK8 and shed light on potential compounds that can interact with RORs to regulate the molecular clock. Future investigations could focus on validating the efficacy of these compounds in modulating the molecular clock and their potential use as therapeutic agents. [Display omitted] • Evidence indicates the potential of dietary ligands in treating circadian disorders. • Homology model of the human CLOCK-BMAL1 complex was generated. • A potential ligand binding site was predicted in the CLOCK protein hollow region. • Identified dietary compounds interacting with the ROR ligand-binding domains. • Sterols and triterpenic acids shared molecular similarity with known ROR ligands. [ABSTRACT FROM AUTHOR]

Nutritional quality and the well-being of the body system are directly linked aspects of human survival. From the unborn foetus to adulthood, the need for sustainable access to micronutrient-rich foods is pertinent and the global consumption of banana and plantain fruits, in effect, contributes to the alleviation of the scourge of malnutrition. This review is particularly aimed at evaluating the pharmacological dimensions through the biological mechanisms of Musa fruits in the body, which represent correlations with their constituent micronutrient factors and dietary polyphenolic constituents such as minerals, vitamin members, anthocyanins, lutein, α-,β- carotenes, neoxanthins and cryptoxanthins, epi- and gallo catechins, catecholamines, 3-carboxycoumarin, β-sitosterol, monoterpenoids, with series of analytical approaches for the various identified compounds being highlighted therein. Derivative value-products from the compartments (flesh and peel) of Musa fruits are equally highlighted, bringing forth the biomedicinal and nutritional relevance, including the potentials of Musa species in dietary diversification approaches.

Phenylephrine (PE) has low and variable oral bioavailability in humans, due in part to presystemic metabolism by sulfation. LS180 cells were used as a model of the human intestinal epithelium to examine phenylephrine metabolism and its inhibition by generally recognized as safe (GRAS) and dietary compounds. Curcumin, zingerone, resveratrol, guaiacol, pterostilbene and isoeugenol significantly inhibited phenylephrine disappearance, while vanillin, propylparaben and eugenol did not. However, when propylparaben was combined with either vanillin or eugenol, the phenylephrine disappearance was significantly inhibited. These data suggest that these compounds or combinations thereof may have potential to improve phenylephrine oral bioavailability. [ABSTRACT FROM AUTHOR]

Human brown adipose tissue (BAT) was re-discovered in 2009 by several independent groups, who showed that it is present and active in adults, as judged from the profound uptake of the glucose analogue radiotracer 18F-fluorodeoxyglucose in positron-emission tomography and computed tomography scan analysis after cold exposure. A potential clinical implication of activating BAT relates to its high metabolic activity and its potential role in stimulating energy expenditure (i.e. resting energy expenditure, meal-induced thermogenesis, and cold-induced thermogenesis), which makes it an attractive target to reduce adiposity. Moreover, due to its ability to oxidise glucose and lipids, BAT activation may also potentially exert beneficial metabolic and cardiovascular effects through reducing glucose and lipid levels, respectively. This review describes the potential role of human BAT in the prevention and treatment of obesity, metabolism, and cardiovascular disease focusing on its impact on energy expenditure and management of body fat accumulation as well as on glucose and lipid metabolism. This article also summarises the strategies that are currently being studied to activate human BAT. [ABSTRACT FROM AUTHOR]

Background The links between gut microbiota and obesity are complex and multidirectional. A large number of studies have demonstrated the provoking effect of microbiota as the main environmental factor on the metabolic, and physiology status of its human host, as well as energy harvest. Dietary compounds are a source of energy and metabolites for gut bacteria. Dietary compounds also change the composition of gut microbiota and can influence the production of their metabolites. Impact of intestinal microbiota composition and metabolic interaction, including interaction with dietary components are the key issue in human health and obesity. Scope and approach Gut microecology could help fulfill the gap between obesity and energy intake throughout altering the processing of nutrients and energy storage in the body, revealing diet-related and age-related changes in the human intestinal microbiome and their consequences. Therefore, it is of critical importance in the prevention of obesity to understand how different types of food can influence gut mucosal integrity. Key findings and conclusions The association between gut microbiota and host metabolism could help explain promising therapeutic approaches throughout gut microbiota regulation in preventing and treating obesity. [ABSTRACT FROM AUTHOR]

After birth, the intestinal immune system enters a critical developmental stage, in which tolerogenic and pro-inflammatory cells emerge to contribute to the overall health of the host. The neonatal health is continuously challenged by microbial colonization and food intake, first in the form of breast milk or formula and later in the form of solid food. The microbiota and dietary compounds shape the newborn immune system, which acquire the ability to induce tolerance against innocuous antigens or induce pro-inflammatory immune responses against pathogens. Disruption of these homeostatic mechanisms might lead to undesired immune reactions, leading to intestinal disorders such as food allergies and inflammatory bowel disease. Hence, a proper education and maturation of the intestinal immune system is likely important to maintain life-long intestinal homeostasis. In this review, the most recent literature regarding the effects of dietary compounds in the development of the intestinal immune system are discussed.

Abstract: Background: Obesity is considered as one of the risk factors for breast cancer. Leptin has been found to be involved in breast cancer progression. Therefore, novel approaches to antagonize biological effects of leptin are much needed. The objective of this study was to evaluate the protective effects of six dietary compounds (quercetin, curcumin, gallic acid, epigallocatechin gallate (EGCG), ascorbic acid and catechin) and assess the phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2) in leptin-stimulated MCF-7 breast cancer cells in vitro. Methods: MCF-7 cells were exposed to leptin, leptin and compound and compound alone for 48 h. Cell viability was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide MTT and fluorometric assays after 48 h incubation. Phosphorylation of ERK1/2 was quantified by ELISA. Results: Only quercetin, curcumin and EGCG showed significant protective effects against leptin-induced proliferation of MCF-7 cells. Increase in ERK1/2 phosphorylation in response to leptin was reduced by the addition of quercetin, curcumin and EGCG. Conclusions: Considering the high prevalence of obesity, this observation provides a rationale for use of curcumin, quercetin and EGCG as antagonists of leptin in the treatment of obese breast cancer patients.

Digestive tract-related cancers account for four of the top ten high-risk cancers worldwide. In recent years, cancer immunotherapy, which exploits the innate immune system to attack tumors, has led to a paradigm shifts in cancer treatment. Gut microbiota modification has been widely used to regulate cancer immunotherapy. Dietary compounds and traditional Chinese medicine (TCM) can alter the gut microbiota and its influence on toxic metabolite production, such as the effect of iprindole on lipopolysaccharide (LPS), and involvement in various metabolic pathways that are closely associated with immune reactions. Therefore, it is an effective strategy to explore new immunotherapies for gastrointestinal cancer to clarify the immunoregulatory effects of different dietary compounds/TCMs on intestinal microbiota. In this review, we have summarized recent progress regarding the effects of dietary compounds/TCMs on gut microbiota and their metabolites, as well as the relationship between digestive cancer immunotherapy and gut microbiota. We hope that this review will act as reference, providing a theoretical basis for the clinical immunotherapy of digestive cancer via gut microbiota modulation., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Feng, Li, Guo and Hu.)

Background: Our daily intake of food provides nutrients for the maintenance of health, growth, and development. The field of nutrigenomics aims to link dietary intake/nutrients to changes in epigenetic status and gene expression., Summary: Although the relationship between our diet and our genes in under intense investigation, there is still a significant aspect of our genome that has received little attention with regard to this. In the past 15 years, the importance of genome organization has become increasingly evident, with research identifying small-scale local changes to large segments of the genome dynamically repositioning within the nucleus in response to/or mediating change in gene expression. The discovery of these dynamic processes and organization maybe as significant as dynamic plate tectonics is to geology, there is little information tying genome organization to specific nutrients or dietary intake., Key Messages: Here, we detail key principles of genome organization and structure, with emphasis on genome folding and organization, and link how these contribute to our future understand of nutrigenomics., (© 2022 The Author(s). Published by S. Karger AG, Basel.)

Beneficial microbes are responsible for the synthesis of nutrients and metabolites that are likely important for the maintenance of mammalian health. Many nutrients and metabolites derived from the gut microbiota by luminal conversion have been implicated in the development, homeostasis and function of innate and adaptive immunity. These factors clearly suggest that intestinal microbiota may influence host immunity via microbial metabolite-dependent mechanisms. We describe how intestinal microbes including probiotics generate microbial metabolites that modulate mucosal and systemic immunity. [ABSTRACT FROM AUTHOR]

After birth, the intestinal immune system enters a critical developmental stage, in which tolerogenic and pro-inflammatory cells emerge to contribute to the overall health of the host. The neonatal health is continuously challenged by microbial colonization and food intake, first in the form of breast milk or formula and later in the form of solid food. The microbiota and dietary compounds shape the newborn immune system, which acquires the ability to induce tolerance against innocuous antigens or induce pro-inflammatory immune responses against pathogens. Disruption of these homeostatic mechanisms might lead to undesired immune reactions, such as food allergies and inflammatory bowel disease. Hence, a proper education and maturation of the intestinal immune system is likely important to maintain life-long intestinal homeostasis. In this review, the most recent literature regarding the effects of dietary compounds in the development of the intestinal immune system are discussed. [ABSTRACT FROM AUTHOR]

Like many malignancies, the development of colorectal carcinoma (CRC) can be considered as an imbalance between the compromised process of programmed cell death (apoptosis) and excessive, uncontrolled proliferation. Several mutations and epigenetic alterations are acquired during colorectal carcinogenesis. These are responsible for the cell cycle regulation, cellular sensitivity to pro- and anti-apoptotic factors, cell proliferation, angiogenesis, invasiveness, as well as metastatic potential. The molecular alterations, along with their morphological expressions, have been recognised in detail, and most of the CRC cases can be attributed to either adenoma-carcinoma or serrated neoplasia pathways: in the first, the anti-apoptotic features prevail; while in the second, the proliferative activity is of the utmost importance. The aim of the work is to discuss the influence of selected drugs and dietary compounds on the proliferation and apoptosis in CRC. [ABSTRACT FROM AUTHOR]

Dietary compounds significantly affected starch enzymatic digestion. However, effects of dietary compounds on starch digestion and their underlying mechanisms have been not systematically discussed yet. This review summarized the effects of dietary compounds including cell walls, proteins, lipids, non-starchy polysaccharides, and polyphenols on starch enzymatic digestion. Cell walls, proteins, and non-starchy polysaccharides restricted starch disruption during hydrothermal treatment and the retained ordered structures limited enzymatic binding. Moreover, they encapsulated starch granules and formed physical barriers for enzyme accessibility. Proteins, non-starchy polysaccharides along with lipids and polyphenols interacted with starch and formed ordered assemblies. Furthermore, non-starchy polysaccharides and polyphenols showed robust abilities to reduce activities of α-amylase and α-glucosidase. Accordingly, it can be concluded that dietary compounds lowered starch digestion mainly by three modes: (i) prevented ordered structures from disruption and formed ordered assemblies chaperoned with these dietary compounds; (ii) formed physical barriers and prevented enzymes from accessing/binding to starch; (iii) reduced enzymes activities. Dietary compounds showed great potentials in lowering starch enzymatic digestion, thereby modulating postprandial glucose response to food and preventing or treating type II diabetes disease., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Chi, Shi, Zhao, Chen, He and Wang.)

• Polyphenols interact with lipids decreasing fat absorption and oxidation. • Polyphenols modify the structure, bioavailability and functionality of proteins. • Polyphenols alter the gelatinization, bioavailability/digestibility of carbohydrates. • Polyphenols exert an anti-nutrient effect on minerals, especially iron. • Polyphenols affect the uptake and bioavailability of vitamins. Polyphenols are plant secondary metabolites, whose biological activity has been widely demonstrated. However, the research in this field is a bit reductive, as very frequently the effect of individual compound is investigated in different experimental models, neglecting more complex, but common, relationships that are established in the diet. This review summarizes the data that highlighted the interaction between polyphenols and other food components, especially macro- (lipids, proteins, carbohydrates and fibers) and micronutrients (minerals, vitamins and organic pigments), paying particular attention on their bioavailability, antioxidant capacity and chemical, physical, organoleptic and nutritional characteristics. The topic of food interaction has yet to be extensively studied because a greater knowledge of the food chemistry behind these interactions and the variables that modify their effects, could offer innovations and improvements in various fields ranging from organoleptic, nutritional to health and economic field. [ABSTRACT FROM AUTHOR]

Gut microbiota, a group of microorganisms that live in the gastrointestinal tract, plays important roles in health and disease. One mechanism that gut microbiota in modulation of the functions of hosts is achieved through synthesizing and releasing a series of metabolites such as short-chain fatty acids. In recent years, increasing evidence has indicated that dietary compounds can interact with gut microbiota. On one hand, dietary compounds can modulate the composition and function of gut microbiota; on the other hand, gut microbiota can metabolize the dietary compounds. Although there are several reviews on gut microbiota and diets, there is no focused review on the effects of dietary compounds on gut microbiota-derived metabolites. In this review, we first briefly discussed the types of gut microbiota metabolites, their origins, and the reasons that dietary compounds can interact with gut microbiota. Then, focusing on gut microbiota-derived compounds, we discussed the effects of dietary compounds on gut microbiota-derived compounds and the following effects on health. Furthermore, we give our perspectives on the research direction of the related research fields. Understanding the roles of dietary compounds on gut microbiota-derived metabolites will expand our knowledge of how diets affect the host health and disease, thus eventually enable the personalized diets and nutrients., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2022 Feng, Liu, Cheng, Zhang, Tan and Peng.)

Abstract: Macrophages, a heterogeneous and ubiquitous cell population representing up to 15% of the cellular content of different types of tissue, are the principal cell mediators in response to pathogens, inflammation process, tissue homeostasis and repair and play a pivotal role in atherosclerosis and insulin resistance because of their capacity to be the major source of inflammatory cytokines, which can function through paracrine and endocrine mechanisms. Recently, differently activated macrophage populations have been described, depending on a large variety of microenvironmental signals, and it is now recognized that their activation plays a crucial role in the development and progression of atherosclerosis. There is good evidence of the ability of conjugated linoleic acids and polyphenolic compounds to modulate inflammation in experimental models involving macrophages. This observation leaves room to the intriguing hypothesis that macrophage polarization could represent one of the unifying mechanisms through which specific food components can exert anti-inflammatory effects in humans, contributing to the prevention of chronic diseases strongly linked to inflammation, such as atherosclerosis. Future studies should be addressed to substantiate this hypothesis, investigating whether or not physiological concentrations of food-derived metabolites can perturb macrophage activation in vitro. On the in vivo side, the evaluation of macrophage populations in tissues, however complex, should be included among the analyses performed in observational and intervention studies, in order to understand if macrophage activation is involved in the anti-inflammatory activity of a specific dietary regimen. [Copyright &y& Elsevier]

Abstract: Recent development of animal models relevant to human prostate cancer (PC) etiopathogenesis has provided important information on the specific functions provided by key gene products altered during disease initiation and progression to locally invasive, metastatic and hormone-refractory stages. Especially, the characterization of transgenic mouse models has indicated that the inactivation of distinct tumor suppressor proteins such as phosphatase tensin homolog deleted on chromosome 10 (PTEN), Nkx3.1, p27KIP1, p53 and retinoblastoma (pRb) may cooperate for the malignant transformation of prostatic stem/progenitor cells into PC stem/progenitor cells and tumor development and metastases. Moreover, the sustained activation of diverse oncogenic signaling elements, including epidermal growth factor receptor (EGFR), sonic hedgehog, Wnt/β-catenin, c-Myc, Akt and nuclear factor-kappaB (NF-κB) also may contribute to the acquisition of more aggressive and hormone-refractory phenotypes by PC stem/progenitor cells and their progenies during disease progression. Importantly, it has also been shown that an enrichment of PC stem/progenitor cells expressing stem cell-like markers may occur after androgen deprivation therapy and docetaxel treatment in the transgenic mouse models of PC suggesting the critical implication of these immature PC cells in treatment resistance, tumor re-growth and disease recurrence. Of clinical interest, the molecular targeting of distinct gene products altered in PC cells by using different dietary compounds has also been shown to counteract PC initiation and progression in animal models supporting their potential use as chemopreventive or chemotherapeutic agents for eradicating the total tumor cell mass, improving current anti-hormonal and chemotherapies and preventing disease relapse. [Copyright &y& Elsevier]

Abstract: Epigenetics refers to heritable changes that are not encoded in the DNA sequence itself, but play an important role in the control of gene expression. In mammals, epigenetic mechanisms include changes in DNA methylation, histone modifications and non-coding RNAs. Although epigenetic changes are heritable in somatic cells, these modifications are also potentially reversible, which makes them attractive and promising avenues for tailoring cancer preventive and therapeutic strategies. Burgeoning evidence in the last decade has provided unprecedented clues that diet and environmental factors directly influence epigenetic mechanisms in humans. Dietary polyphenols from green tea, turmeric, soybeans, broccoli and others have shown to possess multiple cell-regulatory activities within cancer cells. More recently, we have begun to understand that some of the dietary polyphenols may exert their chemopreventive effects in part by modulating various components of the epigenetic machinery in humans. In this article, we first discuss the contribution of diet and environmental factors on epigenetic alterations; subsequently, we provide a comprehensive review of literature on the role of various dietary polyphenols. In particular, we summarize the current knowledge on a large number of dietary agents and their effects on DNA methylation, histone modifications and regulation of expression of the non-coding miRNAs in various in vitro and in vivo models. We emphasize how increased understanding of the chemopreventive effects of dietary polyphenols on specific epigenetic alterations may provide unique and yet unexplored novel and highly effective chemopreventive strategies for reducing the health burden of cancer and other diseases in humans. [ABSTRACT FROM AUTHOR]

This study evaluated the ability of common ergogenic supplement components to alter satellite cell proliferative activity in vitro. Compounds studied were cinnamic acid, ferulic acid, L-glutathione, β-hydroxybutyric acid, calcium-β-hydroxy-β-methylbutyrate monohydrate, DL-thioctic acid (α-lipoic acid), and ornithine α-ketoglutarate. Satellite cells were exposed to different levels of ergogenic test compound for a specified amount of time and analyzed by counting mononucleated and multinucleated cells. At the levels evaluated, none of these compounds altered satellite cell proliferation over that of control cultures (p > 0.05). Four of the compounds were shown to alter satellite cell differentiation over control cultures (p < 0.05), but due to the small amounts of fusion, the biological relevance is in question (e.g. differences in small numbers). These data suggest that a few of the ergogenic compounds examined by this laboratory do influence satellite cell activity in vitro. However, additional studies are vital in order to define the biological relevance of our observations. [ABSTRACT FROM AUTHOR]

CYP3A4 is the main human enzyme responsible for phase I metabolism of dietary compounds, prescribed drugs and xenobiotics, steroid hormones, and bile acids. The inhibition of CYP3A4 activity might impair physiological mechanisms, including the endocrine system and response to drug admission. Here, we aimed to discover new CYP3A4 inhibitors from food and dietary supplements. A deep-learning model was built that classifies compounds as either an inhibitor or noninhibitor, with a high specificity of 0.997. We used this classifier to virtually screen ∼60,000 dietary compounds. Of the 115 identified potential inhibitors, only 31 were previously suggested. Many herbals, as predicted here, might cause impaired metabolism of drugs, and endogenous hormones and bile acids. Additionally, by applying Lipinski's rules of five, 17 compounds were also classified as potential intestine local inhibitors. New CYP3A4 inhibitors predicted by the model, bilobetin and picropodophyllin, were assayed in vitro.

The gastrointestinal tract is optimized to efficiently absorb nutrients and provide a competent barrier against a variety of lumen environmental compounds. Different regulatory mechanisms jointly collaborate to maintain intestinal homeostasis, but alterations in these mechanisms lead to a dysfunctional gastrointestinal barrier and are associated to several inflammatory conditions usually found in chronic pathologies such as inflammatory bowel disease (IBD). The gastrointestinal mucus, mostly composed of mucin glycoproteins, covers the epithelium and plays an essential role in digestive and barrier functions. However, its regulation is very dynamic and is still poorly understood. This review presents some aspects concerning the role of mucus in gut health and its alterations in IBD. In addition, the impact of gut microbiota and dietary compounds as environmental factors modulating the mucus layer is addressed. To date, studies have evidenced the impact of the three-way interplay between the microbiome, diet and the mucus layer on the gut barrier, host immune system and IBD. This review emphasizes the need to address current limitations on this topic, especially regarding the design of robust human trials and highlights the potential interest of improving our understanding of the regulation of the intestinal mucus barrier in IBD. [ABSTRACT FROM AUTHOR]