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The cerebellum has a long, protracted developmental period that spans from the embryonic to postnatal periods; as a result, it is more sensitive to intrauterine and postnatal insults like nutritional deficiencies. Folate is crucial for foetal and early postnatal brain development; however, its effects on cerebellar growth and development are unknown. The aim of this study was to examine the effects of maternal folate intake on the histomorphology and cell density of the developing cerebellum. Twelve adult female rats (rattus norvegicus) were randomly assigned to one of four premixed diet groups: standard (2 mg/kg), folate-deficient (0 mg/kg), folate-supplemented (8 mg/kg) or folate supra-supplemented (40 mg/kg). The rats started their diets 14 days before mating and consumed them throughout pregnancy and lactation. On postnatal days 1, 7, 21 and 35, five pups from each group were sacrificed, and their brains were processed for light microscopic analysis. Histomorphology and cell density of the external granule, molecular, Purkinje and internal granule layers were obtained. The folate-deficient diet group had smaller, dysmorphic cells and significantly lower densities of external granule, molecular, Purkinje and internal granule cells. Although the folate-enriched groups had greater cell densities than the controls, the folate-supplemented group had considerably higher cell densities than the supra-supplemented group. The folate supra-supplemented group had ectopic Purkinje cells in the internal granule cell layer. These findings imply that a folate-deficient diet impairs cellular growth and reduces cell density in the cerebellar cortex. On the other hand, folate supplementation increases cell densities, but there appears to be an optimal dose of supplementation since excessive folate levels may be detrimental., (© 2024 International Society for Developmental Neuroscience.)

Background: Premature infants may suffer from high levels of bilirubin that could lead to neurotoxicity. Bilirubin has been shown to decrease L1-mediated ERK1/2 signaling, L1 phosphorylation, and L1 tyrosine 1176 dephosphorylation. Furthermore, bilirubin redistributes L1 into lipid rafts (LR) and decreases L1-mediated neurite outgrowth. We demonstrate that choline supplementation improves L1 function and signaling in the presence of bilirubin., Methods: Cerebellar granule neurons (CGN) were cultured with and without supplemental choline, and the effects on L1 signaling and function were measured in the presence of bilirubin. L1 activation of ERK1/2, L1 phosphorylation and dephosphorylation were measured. L1 distribution in LR was quantified and neurite outgrowth of CGN was determined., Results: Forty µM choline significantly reduced the effect of bilirubin on L1 activation of ERK1/2 by 220% (p = 0.04), and increased L1 triggered changes in tyrosine phosphorylation /dephosphorylation of L1 by 34% (p = 0.026) and 35% (p = 0.02) respectively. Choline ameliorated the redistribution of L1 in lipid rafts by 38% (p = 0.02) and increased L1-mediated mean neurite length by 11% (p = 0.04)., Conclusion: Choline pretreatment of CGN significantly reduced the disruption of L1 function by bilirubin. The supplementation of pregnant women and preterm infants with choline may increase infant resilience to the effects of bilirubin., Impact: This article establishes choline as an intervention for the neurotoxic effects of bilirubin on lipid rafts. This article provides clear evidence toward establishing one intervention for bilirubin neurotoxicity, where little is understood. This article paves the way for future investigation into the mechanism of the ameliorative effect of choline on bilirubin neurotoxicity., (© 2023. The Author(s), under exclusive licence to the International Pediatric Research Foundation, Inc.)

Increases in conversations about race and racial discrimination experiences during adolescence make this a critical developmental period to investigate adolescents' awareness of racism. We examined bidirectional associations between race-based experiences and awareness of systemic racism-operationalized as understanding systemic causes of racial disparities in education. Adolescents who self-identified as African American/Black were surveyed in Grade 6 (n = 317; M age  = 11.12; 48% girls) and Grade 8 (n = 247; M age  = 13.15; 56% girls). Cross-lagged panel analyses revealed that racial barrier messages, but not racial discrimination experiences, in Grade 6 positively predicted awareness of systemic racism in Grade 8. Adolescents' awareness of systemic racism in Grade 6 did not predict racial socialization or racial discrimination experiences in Grade 8., (© 2024 Society for Research on Adolescence.)

Choline is an essential nutrient that the human body needs in vast quantities for cell membrane synthesis, epigenetic modification and neurotransmission. The brain has a particularly high demand for choline, but how it enters the brain remains unknown 1-3 . The major facilitator superfamily transporter FLVCR1 (also known as MFSD7B or SLC49A1) was recently determined to be a choline transporter but is not highly expressed at the blood-brain barrier, whereas the related protein FLVCR2 (also known as MFSD7C or SLC49A2) is expressed in endothelial cells at the blood-brain barrier 4-7 . Previous studies have shown that mutations in human Flvcr2 cause cerebral vascular abnormalities, hydrocephalus and embryonic lethality, but the physiological role of FLVCR2 is unknown 4,5 . Here we demonstrate both in vivo and in vitro that FLVCR2 is a BBB choline transporter and is responsible for the majority of choline uptake into the brain. We also determine the structures of choline-bound FLVCR2 in both inward-facing and outward-facing states using cryo-electron microscopy. These results reveal how the brain obtains choline and provide molecular-level insights into how FLVCR2 binds choline in an aromatic cage and mediates its uptake. Our work could provide a novel framework for the targeted delivery of therapeutic agents into the brain., (© 2024. The Author(s), under exclusive licence to Springer Nature Limited.)

We undertook this review to determine if it is plausible that choline or phosphatidylcholine (PC) deficiency is a factor in necrotizing enterocolitis (NEC) after two clinical trials found a dramatic and unexpected reduction in NEC in an experimental group provided higher PC compared to a control group. Sources and amounts of choline/PC for preterm infants are compared to the choline status of preterm infants at birth and following conventional nutritional management. The roles of choline/PC in intestinal structure, mucus, mesenteric blood flow, and the cholinergic anti-inflammatory system are summarized. Low choline/PC status is linked to prematurity/immaturity, parenteral and enteral feeding, microbial dysbiosis and hypoxia/ischemia, factors long associated with the risk of developing NEC. We conclude that low choline status exists in preterm infants provided conventional parenteral and enteral nutritional management, and that it is plausible low choline/PC status adversely affects intestinal function to set up the vicious cycle of inflammation, loss of intestinal barrier function and worsening tissue hypoxia that occurs with NEC. In conclusion, this review supports the need for randomized clinical trials to test the hypothesis that additional choline or PC provided parenterally or enterally can reduce the incidence of NEC in preterm infants. IMPACT STATEMENT: Low choline status in preterm infants who are managed by conventional nutrition is plausibly linked to the risk of developing necrotizing enterocolitis., (© 2024. The Author(s), under exclusive licence to the International Pediatric Research Foundation, Inc.)

Choline is a vital nutrient and a precursor for the biosynthesis of essential metabolites, including acetylcholine (ACh), that play a central role in fetal development, especially in the brain. In cholinergic neurons, the high-affinity choline transporter (CHT1) provides an extraordinarily efficient reuptake mechanism to reutilize choline derived from intrasynaptical ACh hydrolysis and maintain ACh synthesis in the presynapse. Here, we determined structures of human CHT1 in three discrete states: the outward-facing state bound with the competitive inhibitor hemicholinium-3 (HC-3); the inward-facing occluded state bound with the substrate choline; and the inward-facing apo open state. Our structures and functional characterizations elucidate how the inhibitor and substrate are recognized. Moreover, our findings shed light on conformational changes when transitioning from an outward-facing to an inward-facing state and establish a framework for understanding the transport cycle, which relies on the stabilization of the outward-facing state by a short intracellular helix, IH1., (© 2024. The Author(s), under exclusive licence to Springer Nature America, Inc.)

The mother's thyroid hormone status during gestation and the first few months after delivery can play a crucial role in maturation during the brain development of the child. Transient abnormalities in thyroid function at birth indicate developmental and cognitive disorders in adulthood. Choline supplementation during gestation and the perinatal period in rats causes long-lasting memory improvement in the offspring. However, it remains unclear whether choline is able to restore the deficits in rats with maternal hypothyroidism. The aim of this study was to evaluate the effects of choline supplementation on the alteration of cognitive-behavioral function, long-term potentiation (LTP), and morphological changes as well as apoptosis in pre-pubertal offspring rats. To induce hypothyroidism, 6-propyl-2-thiouracil was added to the drinking water from the 6th day of gestation to the 21st postnatal day (PND). Choline treatment was started twice a day on the first day of the gestation until PND 21 via gavage. LTP recording and Morris water maze (MWM) test were conducted at PND 28. Then, the rats were sacrificed to assess their brains. The results revealed that developmental thyroid hormone deficiency impaired spatial learning and memory and reduced LTP (both: P < 0.001). Choline treatment alleviated LTP (P < 0.001), as well as learning and memory deficits (P < 0.01) in both male and female hypothyroid rats. However, no significant changes were observed in the number of caspase-3 stained cells in choline-receiving hypothyroid groups. The results revealed that developmental thyroid hormone deficiency impaired spatial learning and memory and reduced LTP. Choline treatment alleviated LTP, as well as learning and memory deficits in both male and female hypothyroid rats., (© 2024 International Society for Developmental Neuroscience.)

2-Amino-2-methyl-1-propanol (AMP™) is a widely used pH stabilizer in personal care products (PCPs); thus, the safety implications of dermal AMP exposure remain of interest. We have previously reported that exposure to AMP in PCPs when used as intended is not anticipated to result in an increased risk of hepatotoxicity (primarily steatosis and altered phospholipid homeostasis). The current study focuses on AMP in PCP's potential for developmental and reproductive toxicity (DART) in humans, based on data from animal studies. Animal studies suggest that exposure to AMP can result in post-implantation loss. However, such effects occur at maternally toxic doses, posing a challenge for determining appropriate hazard classifications in the context of relevant consumer use scenarios. Our assessment concluded that human exposure to AMP in PCPs is not anticipated to result in DART at non-maternally toxic doses. Further, mode of action (MOA) analysis elucidated the potential biological pathways underlying DART effects observed in high-dose animal studies, such that perturbation of uterine choline synthesis was the most well-supported MOA hypothesis. Downstream uterine effects might reflect choline-dependent changes in epigenetic control of pathways important for implantation maintenance and uterine cell energetics. Since AMP-induced post-implantation loss occurs at doses higher than pathology related to liver toxicity, maintaining AMP exposures from exceeding the onset dose for maternal liver effects will also be protective of DART effects. Furthermore, dermal exposure to AMP expected from the use of PCPs is highly unlikely to result in toxicologically significant systemic AMP concentrations; thus, DART is not anticipated., (© 2023 John Wiley & Sons Ltd.)

The nature and cause of auditory processing deficits in dyslexic individuals have been debated for decades. Auditory processing deficits were argued to be the first step in a causal chain of difficulties, leading to difficulties in speech perception and thereby phonological processing and literacy difficulties. More recently, it has been argued that auditory processing difficulties may not be causally related to language and literacy difficulties. This study compares two groups who have phonological processing impairments for different reasons: dyslexia and a history of otitis media (OM). We compared their discrimination thresholds and response variability to chronological age- and reading age-matched controls, across three auditory processing tasks: frequency discrimination, rise-time discrimination and speech perception. Dyslexic children showed raised frequency discrimination thresholds in comparison with age-matched controls but did not differ from reading age-matched controls or individuals with a history of OM. There were no group differences on speech perception or rise-time tasks. For the dyslexic children, there was an association between phonological awareness and frequency discrimination response variability, but no association with thresholds. These findings are not consistent with a 'causal chain' explanation but could be accounted for within a multiple deficits view of literacy difficulties., (© 2024 The Authors. Dyslexia published by John Wiley & Sons Ltd.)

Purpose: The purpose of this study was to examine the direct and indirect relations between short-term memory (STM), reading, oral language, and writing at the letter, word, and discourse levels in young, developing writers both cross-sectionally and longitudinally. Method: Participants were 449 English-speaking kindergarten students (52% female) from 41 schools in the U.S. Results: The cross-sectional analysis indicated that STM was directly related to oral language (β = 0.62), letter naming fluency (β = 0.43), word reading (β = 0.54), and reading comprehension (β = 0.42), all of which were statistically significant. Results supported a complete mediation model with STM having an indirect effect on writing via reading and oral language. In the cross-sectional analysis, the total effects of STM on handwriting (β = 0.51), spelling (β = 0.57), and written composition (β = 0.47) were substantial and statistically significant. In the longitudinal analysis, the total effects of Fall STM on Spring writing outcomes, handwriting (β = 0.42), spelling (β = 0.70), and written composition (β = 0.44) were also substantial and statistically significant. Conclusion: Findings confirm that STM is a foundational cognitive skill necessary for early writing; however, they provide a more nuanced understanding by showing that the contribution of STM is indirect through reading and oral language. Writing is complex, requiring interaction among higher-order domain-specific and domain-general components. Along with other recent studies, our findings highlight the need to examine the direct and indirect effects for a more precise understanding of skills that support writing development. [ABSTRACT FROM AUTHOR]

Early writing performance strongly predicts long-term literacy performance. It follows that early underachievement in writing is highly correlated with early underachievement in reading. One strategy teachers and students can use to approach writing in the kindergarten classroom is invented spelling. Invented spelling is children's spontaneous or self-directed attempts to represent words in print by matching sounds to known letters or phonics patterns. A quasi-experimental study was used to evaluate the impact of invented spelling on foundational literacy skills and writing motivation in 63 kindergarten students at a rural school in the Mid-South. The research questions focused on the impact of invented spelling instruction on a variety of literacy outcomes, including foundational skills, spelling, and motivation. The results indicate the significant main effects of invented spelling instruction on students' invented spelling (p < 0.001), conventional spelling (p < 0.001), complex vocabulary use (p < 0.001, writing motivation (p = 0.040), and writing achievement (p < 0.001). Other outcomes as well as implications and future directions are reported. The invented spelling intervention encouraged low-stake risk taking when writing and removed barriers to writing entry. Allowing time and space for invented spellings means students can focus on communicating their ideas in print without being hindered by the expectation to conform to conventional spellings. [ABSTRACT FROM AUTHOR]

Globally, millets are small-seeded grasses cultivated for human consumption and livestock feed. They thrive in low rainfall regions, poor soil quality, and challenging terrains. Millets are a healthy food choice due to their high nutrient content, including proteins, soluble fiber, vitamins, and minerals such as copper, magnesium, phosphorus, and manganese. Compared to major cereals, millets are packed with antioxidants and essential amino acids. They have a low glycemic index (GI) due to their high complex carbohydrate content, which provides a healthier option than conventional wheat flour. Millets support a healthy gut microbiome, reduce constipation, and decrease excessive gas. Their soluble fiber helps lower "bad" cholesterol levels, reducing the risk of atherosclerosis, and produces a gel in the stomach that alleviates ulcer conditions. Millets serve as nutrient-dense foods and are nutritionally assessed across six attributes: carbohydrates, protein, fat, fiber, vitamins, and minerals. In this review and comparative statistical evaluation of eight millets with Rice and Wheat, the overall ranking for all six nutritional attributes was derived using the Smith Selection Index. The top five ranked grains were Finger millet (first rank), Pearl millet (second rank), Wheat (third rank), Foxtail millet (fourth rank), and Kodo millet (fifth rank). First ranked Finger millet: Finger millet is superior to Rice and Wheat for protein quality, fiber quality, and mineral profile; superior to Rice for vitamin profile; and superior to Wheat for carbohydrate quality parameters. Additionally, Finger millet surpasses Foxtail millet, Sorghum, Little millet, Kodo millet, and Pearl millet in carbohydrate quality; Sorghum in protein quality; Kodo millet, Proso millet, Pearl millet, and Sorghum in fiber quality; and Sorghum in mineral profile. Second ranked Pearl millet: Pearl millet is superior to Rice and Wheat for protein and fiber quality, as well as for vitamin and mineral profiles. It also surpasses Wheat in carbohydrate quality parameters. Pearl millet is superior to all millets except Proso millet in protein quality; Sorghum in fiber quality; Kodo millet and Finger millet in fat quality; all millets in vitamin profile; and all except Finger millet in mineral profile. Third ranked Wheat: Wheat is superior to Finger millet, Sorghum, and Rice in protein quality; Sorghum and Rice in fiber quality; Rice, Pearl millet, Kodo millet, and Finger millet in fat quality; all millets except Pearl millet and Rice in vitamin profile; and all except Finger millet and Pearl millet in mineral profile. Fourth ranked Foxtail millet: Foxtail millet is superior to Sorghum, Proso millet, Kodo millet, Pearl millet, and Rice in carbohydrate quality parameters; Finger millet, Sorghum, Wheat, and Rice in protein quality; all millets, Rice, and Wheat in fiber quality; all except Barnyard millet in fat quality; Sorghum, Kodo millet, Little millet, and Rice in vitamin profile; and Little millet, Kodo millet, Sorghum, Proso millet, Barnyard millet, and Rice in mineral profile. Fifth ranked Kodo millet: Kodo millet is superior to Pearl millet and Rice in carbohydrate quality; all millets except Proso millet and Pearl millet, Rice, and Wheat in protein quality; Proso millet, Pearl millet, Sorghum, Rice, and Wheat in fiber quality; Finger millet in fat quality; Little millet, Proso millet, Barnyard millet, and Rice in vitamin profile; and Sorghum, Proso millet, Barnyard millet, and Rice in mineral profile. Tenth ranked Rice: Rice holds the lowest rank, indicating its inferiority to all millets and Wheat in overall nutritional attributes. However, Rice is superior to all millets and Wheat in carbohydrate quality parameters but inferior to all millets except Sorghum in protein quality; inferior to all millets and Wheat in fiber quality; inferior to all except Pearl millet, Kodo millet, and Finger millet in fat quality; all except Proso millet and Barnyard millet in vitamin profile; and inferior to all millets and Wheat in mineral profile. [ABSTRACT FROM AUTHOR]

Cardiac metabolism ensures a continuous ATP supply, primarily using fatty acids in a healthy state and favoring glucose in pathological conditions. Pyruvate kinase muscle (PKM) controls the final step of glycolysis, with PKM1 being the main isoform in the heart. PKM2, elevated in various heart diseases, has been suggested to play a protective role in cardiac stress, but its function in basal cardiac metabolism remains unclear. We examined hearts from global PKM2 knockout (PKM2−/−) mice and found reduced intracellular glucose. Isotopic tracing of U‐13C glucose revealed a shift to biosynthetic pathways in PKM2−/− cardiomyocytes. Total ATP content was two‐thirds lower in PKM2−/− hearts, and functional analysis indicated reduced mitochondrial oxygen consumption. Total reactive oxygen species (ROS) and mitochondrial superoxide were also increased in PKM2−/− cardiomyocytes. Intriguingly, PKM2−/− hearts had preserved ejection fraction compared to controls. Mechanistically, increased calcium/calmodulin‐dependent kinase II activity and phospholamban phosphorylation may contribute to higher sarcoendoplasmic reticulum calcium ATPase 2 pump activity in PKM2−/− hearts. Loss of PKM2 led to altered glucose metabolism, diminished mitochondrial function, and increased ROS in cardiomyocytes. These data suggest that cardiac PKM2 acts as an important rheostat to maintain ATP levels while limiting oxidative stress. Although loss of PKM2 did not impair baseline contractility, its absence may make hearts more sensitive to environmental stress or injury. [ABSTRACT FROM AUTHOR]

Choline is recognized as an essential nutrient for Atlantic salmon at all developmental stages. However, its dietary requirement is not well defined. Choline plays a critical role in lipid transport, and the clearest deficiency sign is intestinal steatosis. The present work, aiming to find whether lipid source and fish size may affect steatosis symptoms, was one of a series of studies conducted to identify which production-related conditions may influence choline requirement. Six choline-deficient diets were formulated varying in ratios of rapeseed oil to fish oil and fed to Atlantic salmon of 1.5 and 4.5 kg. After eight weeks, somatic characteristics were observed, and the severity of intestinal steatosis was assessed by histological, biochemical, and molecular analyses. Fatty acid composition in pyloric intestine, mesenteric tissue, and liver samples was also quantified. The increasing rapeseed oil level increased lipid digestibility markedly, enhancing lipid supply to the fish. Moreover, small fish consumed more feed, and consequently had a higher lipid intake. In conclusion, the results showed that choline requirement depends on dietary lipid load, which depends on the fatty acid profile as well as the fish size. [ABSTRACT FROM AUTHOR]

Cardiovascular diseases (CVDs) remain a leading global cause of morbidity and mortality. These diseases have a multifaceted nature being influenced by a multitude of biochemical, genetic, environmental, and behavioral factors. Epigenetic modifications have a crucial role in the onset and progression of CVD. Epigenetics, which regulates gene activity without altering the DNA's primary structure, can modulate cardiovascular homeostasis through DNA methylation, histone modification, and non-coding RNA regulation. The effects of environmental stimuli on CVD are mediated by epigenetic changes, which can be reversible and, hence, are susceptible to pharmacological interventions. This represents an opportunity to prevent diseases by targeting harmful epigenetic modifications. Factors such as high-fat diets or nutrient deficiencies can influence epigenetic enzymes, affecting fetal growth, metabolism, oxidative stress, inflammation, and atherosclerosis. Recent studies have shown that plant-derived bioactive compounds can modulate epigenetic regulators and inflammatory responses, contributing to the cardioprotective effects of diets. Understanding these nutriepigenetic effects and their reversibility is crucial for developing effective interventions to combat CVD. This review delves into the general mechanisms of epigenetics, its regulatory roles in CVD, and the potential of epigenetics as a CVD therapeutic strategy. It also examines the role of epigenetic natural compounds (ENCs) in CVD and their potential as intervention tools for prevention and therapy. [ABSTRACT FROM AUTHOR]

The role of estrogens in prostate cancer (PCa) is shrouded in mystery, with its actions going from angelic to devilish. The findings by Huggins and Hodges establishing PCa as a hormone-sensitive cancer have provided the basis for using estrogens in therapy. However, despite the clinical efficacy in suppressing tumor growth and the panoply of experimental evidence describing its anticarcinogenic effects, estrogens were abolished from PCa treatment because of the adverse secondary effects. Notwithstanding, research work over the years has continued investigating the effects of estrogens, reporting their pros and cons in prostate carcinogenesis. In contrast with the beneficial therapeutic effects, many reports have implicated estrogens in the disruption of prostate cell fate and tissue homeostasis. On the other hand, epidemiological data demonstrating the lower incidence of PCa in Eastern countries associated with a higher consumption of phytoestrogens support the beneficial role of estrogens in counteracting cancer development. Many studies have investigated the effects of phytoestrogens and the underlying mechanisms of action, which may contribute to developing safe estrogen-based anti-PCa therapies. This review compiles the existing data on the anti- and protumorigenic actions of estrogens and summarizes the anticancer effects of several phytoestrogens, highlighting their promising features in PCa treatment. [ABSTRACT FROM AUTHOR]

Sphingolipids (SLs) constitute a discrete subdomain of metabolism, and they display both structural and signaling functions. Accumulating evidence also points to intimate connections between intermediary metabolism and SL metabolism. Given that many SLs exhibit bioactive properties (i.e. transduce signals), these raise the possibility that an important function of SLs is to relay information on metabolic changes into specific cell responses. This could occur at various levels. Some metabolites are incorporated into SLs, whereas others may initiate regulatory or signaling events that, in turn, modulate SL metabolism. In this review, we elaborate on the former as it represents a poorly appreciated aspect of SL metabolism, and we develop the hypothesis that the SL network is highly sensitive to several specific metabolic changes, focusing on amino acids (serine and alanine), various fatty acids, choline (and ethanolamine), and glucose. [ABSTRACT FROM AUTHOR]

Monosodium glutamate (MSG) is used as a common food additive in some foods. However, based on our search and knowledge, no comprehensive study discussed the effect of MSG on the human gut microbiome. In this study, the effects of MSG on the gut microbiome, liver, and kidney were performed. Data were collected from databases including PubMed, Scopus, Web of Science, and ScienceDirect using the search strategy and keywords. Finally, 14 eligible studies were selected for systematic review. This study provides a new perspective on the effects of MSG on the gut flora, shedding light on the potential relationship between MSG intake and human health. [ABSTRACT FROM AUTHOR]

Polyphenols, natural micronutrients derived from plants, are valued for their anti‐inflammatory and antioxidant properties. The escalating global prevalence of non‐alcoholic fatty liver disease (NAFLD) underscores its status as a chronic progressive liver condition. Furthermore, the dysregulation of gut microbiota (GM) is implicated in the onset and progression of NAFLD through the actions of metabolites such as bile acids (BAs), lipopolysaccharide (LPS), choline, and short‐chain fatty acids (SCFAs). Additionally, GM may influence the integrity of the intestinal barrier. This review aims to evaluate the potential effects of polyphenols on GM and intestinal barrier function, and their subsequent impact on NAFLD. We searched through a wide range of databases, such as Web of Science, PubMed, EMBASE, and Scopus to gather information for our non‐systematic review of English literature. GM functions and composition can be regulated by polyphenols such as chlorogenic acid, curcumin, green tea catechins, naringenin, quercetin, resveratrol, and sulforaphane. Regulating GM composition improves NAFLD by alleviating inflammation, liver fat accumulation, and liver enzymes. Furthermore, it improves serum lipid profile and gut barrier integrity. All of these components affect NAFLD through the metabolites of GM, including SCFAs, choline, LPS, and BAs. Current evidence indicates that chlorogenic acid, resveratrol, quercetin, and curcumin can modulate GM, improving intestinal barrier integrity and positively impacting NAFLD. More studies are necessary to evaluate the safety and efficacy of naringenin, sulforaphane, and catechin. [ABSTRACT FROM AUTHOR]

Copyright of China Condiment is the property of China Condiment and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of China Condiment is the property of China Condiment and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: Aberrant activation of the classic renin-angiotensin system (RAS) and intestinal micro dysbiosis adversely affect insulin resistance (IR), dyslipidemia, and other metabolic syndrome markers. However, the action of angiotensinconverting enzyme 2 (ACE2) and gut health in systemic homeostasis vary, and their interaction is not completely understood. Methods: We adopted a combinatory approach of metabolomics and fecal 16S rRNA analysis to investigate gut microbiota and metabolite in two different mouse models, ACE2 knockout (ACE2 KO) mice and the ACE2-overexpressing obese mice. Results: 16S rRNA gene sequencing revealed that ACE2 influences microbial community composition and function, and ACE2 KO mice had increased Deferribacteres, Alcaligenaceae, Parasutterella, Catenibacterium, and Anaerotruncus, with decreased short-chain fatty acid (SCFA)-producing bacteria (Marvinbryantia and Alistipes). In contrast, ACE2-overexpressed mice exhibited increased anti-inflammatory probiotic (Oscillospiraceae, Marinifilaceae, and Bifidobacteriaceae) and SCFA-producing microbes (Rikenellaceae, Muribaculaceae, Ruminococcaceae, Odoribacter, and Alistipes) and decreased Firmicutes/Bacteroidetes, Lactobacillaceae, Erysipelotrichaceae, and Lachnospiraceae. Metabolome analysis indicated differential metabolites in ACE2 KO and ACE2-overexpression mice, especially the glucolipid metabolismrelated compounds. Furthermore, correlation analysis between gut microbiota and metabolites showed a dynamic mutual influence affecting host health. Conclusion: Our study confirms for the first time a significant association between ACE2 status and gut microbiome and metabolome profiles, providing a novel mechanism for the positive effect of ACE2 on energy homeostasis. [ABSTRACT FROM AUTHOR]

Copyright of Shipin Kexue/ Food Science is the property of Food Science Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Multiple organs and tissues coordinate to respond to dietary and environmental challenges. It is interorgan crosstalk that contributes to systemic metabolic homeostasis. The liver and brain, as key metabolic organs, have their unique dialogue to transmit metabolic messages. The interconnected pathogenesis of liver and brain is implicated in numerous metabolic and neurodegenerative disorders. Recent insights have positioned the liver not only as a central metabolic hub but also as an endocrine organ, capable of secreting hepatokines that transmit metabolic signals throughout the body via the bloodstream. Metabolites from the liver or gut microbiota also facilitate a complex dialogue between liver and brain. In parallel to humoral factors, the neural pathways, particularly the hypothalamic nuclei and autonomic nervous system, are pivotal in modulating the bilateral metabolic interplay between the cerebral and hepatic compartments. The term "liver–brain axis" vividly portrays this interaction. At the end of this review, we summarize cutting-edge technical advancements that have enabled the observation and manipulation of these signals, including genetic engineering, molecular tracing, and delivery technologies. These innovations are paving the way for a deeper understanding of the liver–brain axis and its role in metabolic homeostasis. [ABSTRACT FROM AUTHOR]

Neurodegenerative diseases, such as Alzheimer's disease (AD) and Parkinson's disease (PD), are severe age-related disorders with complex and multifactorial causes. Recent research suggests a critical link between neurodegeneration and the gut microbiome, via the gut–brain communication pathway. This review examines the role of trimethylamine N-oxide (TMAO), a gut microbiota-derived metabolite, in the development of AD and PD, and investigates its interaction with microRNAs (miRNAs) along this bidirectional pathway. TMAO, which is produced from dietary metabolites like choline and carnitine, has been linked to increased neuroinflammation, protein misfolding, and cognitive decline. In AD, elevated TMAO levels are associated with amyloid-beta and tau pathologies, blood–brain barrier disruption, and neuronal death. TMAO can cross the blood–brain barrier and promote the aggregation of amyloid and tau proteins. Similarly, TMAO affects alpha-synuclein conformation and aggregation, a hallmark of PD. TMAO also activates pro-inflammatory pathways such as NF-kB signaling, exacerbating neuroinflammation further. Moreover, TMAO modulates the expression of various miRNAs that are involved in neurodegenerative processes. Thus, the gut microbiome–miRNA–brain axis represents a newly discovered mechanistic link between gut dysbiosis and neurodegeneration. MiRNAs regulate the key pathways involved in neuroinflammation, oxidative stress, and neuronal death, contributing to disease progression. As a direct consequence, specific miRNA signatures may serve as potential biomarkers for the early detection and monitoring of AD and PD progression. This review aims to elucidate the complex interrelationships between the gut microbiota, trimethylamine-N-oxide (TMAO), microRNAs (miRNAs), and the central nervous system, and the implications of these connections in neurodegenerative diseases. In this context, an overview of the current neuroradiology techniques available for studying neuroinflammation and of the animal models used to investigate these intricate pathologies will also be provided. In summary, a bulk of evidence supports the concept that modulating the gut–brain communication pathway through dietary changes, the manipulation of the microbiome, and/or miRNA-based therapies may offer novel approaches for implementing the treatment of debilitating neurological disorders. [ABSTRACT FROM AUTHOR]

Background: One-carbon metabolism coenzymes may influence brain aging in cognitively unimpaired adults. Methods: Baseline data were used from the UK Biobank cohort. Estimated intake of vitamin B6, B12, and folate was regressed onto neural network functional connectivity in five resting-state neural networks. Linear mixed models tested coenzyme main effects and interactions with Alzheimer’s disease (AD) risk factors. Results: Increased B6 and B12 estimated intake were linked with less functional connectivity in most networks, including the posterior portion of the Default Mode Network. Conversely, higher folate was related to more connectivity in similar networks. AD family history modulated these associations: Increased estimated intake was positively associated with stronger connectivity in the Primary Visual Network and Posterior Default Mode Network in participants with an AD family history. In contrast, increased vitamin B12 estimated intake was associated with less connectivity in the Primary Visual Network and the Cerebello– Thalamo–Cortical Network in those without an AD family history. Conclusions: The differential patterns of association between B vitamins and resting-state brain activity may be important in understanding AD-related changes in the brain. Notably, AD family history appears to play a key role in modulating these relationships. [ABSTRACT FROM AUTHOR]

Poor birth outcomes in low- and middle income countries are associated with maternal vitamin D deficiency and chronic helminth infections. Here, we investigated whether maternal Schistosoma haematobium affects maternal or cord vitamin D status as well as birth outcomes. In a prospective cross-sectional study of pregnant women conducted in Lambaréné, Gabon, we diagnosed maternal parasitic infections in blood, urine and stool. At delivery we measured vitamin D in maternal and cord blood. S. haematobium, soil-transmitted helminths, and microfilariae were found at prevalences of 30.2%, 13.0%, and 8.8%, respectively. Insufficient vitamin D and calcium levels were found in 28% and 15% of mothers, and in 11.5% and 1.5% of newborns. Mothers with adequate vitamin D had lower risk of low birthweight babies (aOR = 0.11, 95% CI 0.02–0.52, p = 0.01), whilst offspring of primipars had low cord vitamin D levels, and low vitamin D levels increased the risk of maternal inflammation. Maternal filariasis was associated with low calcium levels, but other helminth infections affected neither vitamin D nor calcium levels in either mothers or newborns. Healthy birth outcomes require maintenance of adequate vitamin D and calcium levels. Chronic maternal helminth infections do not disrupt those levels in a semi-rural setting in sub-Saharan Africa. [ABSTRACT FROM AUTHOR]

Choline is an essential nutrient, with high requirements during fetal and postnatal growth. Tissue concentrations of total choline are tightly regulated, requiring an increase in its pool size proportional to growth. Phosphatidylcholine and sphingomyelin, containing a choline headgroup, are constitutive membrane phospholipids, accounting for >85% of total choline, indicating that choline requirements are particularly high during growth. Daily phosphatidylcholine secretion via bile for lipid digestion and very low-density lipoproteins for plasma transport of arachidonic and docosahexaenoic acid to other organs exceed 50% of its hepatic pool. Moreover, phosphatidylcholine is required for converting pro-apoptotic ceramides to sphingomyelin, while choline is the source of betaine as a methyl donor for creatine synthesis, DNA methylation/repair and kidney function. Interrupted choline supply, as during current total parenteral nutrition (TPN), causes a rapid drop in plasma choline concentration and accumulating deficit. The American Society for Parenteral and Enteral Nutrition (A.S.P.E.N.) defined choline as critical to all infants requiring TPN, claiming its inclusion in parenteral feeding regimes. We performed a systematic literature search in Pubmed with the terms "choline" and "parenteral nutrition", resulting in 47 relevant publications. Their results, together with cross-references, are discussed. While studies on parenteral choline administration in neonates and older children are lacking, preclinical and observational studies, as well as small randomized controlled trials in adults, suggest choline deficiency as a major contributor to acute and chronic TPN-associated liver disease, and the safety and efficacy of parenteral choline administration for its prevention. Hence, we call for choline formulations suitable to be added to TPN solutions and clinical trials to study their efficacy, particularly in growing children including preterm infants. [ABSTRACT FROM AUTHOR]

Sodium nitrite (NaNO2) is a widely used food ingredient, although excessive concentrations can pose potential health risks. In the present study, we evaluated the deterioration effects of NaNO2 additives on hematology, metabolic profile, liver function, and kidney function of male Wistar rats. We further explored the therapeutic potential of supplementation with S. costus root ethanolic extract (SCREE) to improve NaNO2-induced hepatorenal toxicity. In this regard, 65 adult male rats were divided into eight groups; Group 1: control, Groups 2, 3, and 4 received SCREE in 200, 400, and 600 mg/kg body weight, respectively, Group 5: NaNO2 (6.5 mg/kg body weight), Groups 6, 7 and 8 received NaNO2 (6.5 mg/kg body weight) in combination with SCREE (200, 400, and 600 mg/kg body weight), respectively. Our results revealed that the NaNO2-treated group shows a significant change in deterioration in body and organ weights, hematological parameters, lipid profile, and hepatorenal dysfunction, as well as immunohistochemical and histopathological alterations. Furthermore, the NaNO2-treated group demonstrated a considerable increase in the expression of TNF-α cytokine and tumor suppressor gene P53 in the kidney and liver, while a significant reduction was detected in the anti-inflammatory cytokine IL-4 and the apoptosis suppressor gene BCL-2, compared to the control group. Interestingly, SCREE administration demonstrated the ability to significantly alleviate the toxic effects of NaNO2 and improve liver function in a dose-dependent manner, including hematological parameters, lipid profile, and modulation of histopathological architecture. Additionally, SCREE exhibited the ability to modulate the expression levels of inflammatory cytokines and apoptotic genes in the liver and kidney. The phytochemical analysis revealed a wide set of primary metabolites in SCREE, including phenolics, flavonoids, vitamins, alkaloids, saponins and tannins, while the untargeted UPLC/T-TOF-MS/MS analysis identified 183 metabolites in both positive and negative ionization modes. Together, our findings establish the potential of SCREE in mitigating the toxic effects of NaNO2 by modulating metabolic, inflammatory, and apoptosis. Together, this study underscores the promise of SCREE as a potential natural food detoxifying additive to counteract the harmful impacts of sodium nitrite. [ABSTRACT FROM AUTHOR]

Background: Trimethylamine-N-oxide (TMAO) is produced by hepatic flavin-containing monooxygenase 3 (FMO3) from trimethylamine (TMA). High TMAO level is a biomarker of cardiovascular diseases and metabolic disorders, and it also affects periodontitis through interactions with the gastrointestinal microbiome. While recent findings indicate that periodontitis may alter systemic TMAO levels, the specific mechanisms linking these changes and particular oral pathogens require further clarification. Methods: In this study, we established a C57BL/6J male mouse model by orally administering Porphyromonas gingivalis (P. gingivalis, Pg), Fusobacterium nucleatum (F. nucleatum, Fn), Streptococcus mutans (S. mutans, Sm) and PBS was used as a control. We conducted LC-MS/MS analysis to quantify the concentrations of TMAO and its precursors in the plasma and cecal contents of mice. The diversity and composition of the gut microbiome were analyzed using 16S rRNA sequencing. TMAO-related lipid metabolism and enzymes in the intestines and liver were assessed by qPCR and ELISA methods. We further explored the effect of Pg on FMO3 expression and lipid molecules in HepG2 cells by stimulating the cells with Pg-LPS in vitro. Results: The three oral pathogenic bacteria were orally administered to the mice for 5 weeks. The Pg group showed a marked increase in plasma TMAO, betaine, and creatinine levels, whereas no significant differences were observed in the gut TMAO level among the four groups. Further analysis showed similar diversity and composition in the gut microbiomes of both the Pg and Fn groups, which were different from the Sm and control groups. The profiles of TMA-TMAO pathway- related genera and gut enzymes were not significantly different among all groups. The Pg group showed significantly higher liver FMO3 levels and elevated lipid factors (IL-6, TG, TC, and NEFA) in contrast to the other groups. In vitro experiments confirmed that stimulation of HepG2 cells with Pg-LPS upregulated the expression of FMO3 and increased the lipid factors TC, TG, and IL-6. Conclusion: This study conclusively demonstrates that Pg, compared to Fn and Sm, plays a critical role in elevating plasma TMAO levels and significantly influences the TMA-TMAO pathway, primarily by modulating the expression of hepatic FMO3 and directly impacting hepatic lipid metabolism. [ABSTRACT FROM AUTHOR]

The nutritional status of the mother-to-be has a key impact on the proper development of the fetus. Although all nutrients are important for the developing baby, recent research indicates the importance of adequate choline intake during the periconceptional period, pregnancy, and lactation. Choline plays a key role in the biosynthesis of cell membranes, supporting liver function, neurotransmission, brain development, and DNA and histone methylation. Choline participates in the formation of a child's nervous system, supports its cognitive development, and reduces the risk of neural tube defects. The human body is incapable of producing sufficient choline to meet its needs; therefore, it must be obtained from the diet. Current data indicate that most women in their reproductive years do not achieve the recommended daily intake of choline. The presented narrative review indicates the importance of educating mothers-to-be and thereby increasing their awareness of the effects of choline on maternal and child health, which can lead to a more aware and healthy pregnancy and proper child development. [ABSTRACT FROM AUTHOR]

Copyright of Educational Academic Research is the property of Ataturk University Coordinatorship of Scientific Journals and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Epigenetics plays a crucial role in various clinical diseases, such as autism, by mediating the impact of environmental variables on genomic regulation. Autism spectrum disorder (ASD) is a neurological disorder influenced by both genetic and environmental factors that affect the developing brain. DNA methylation, histone tail modifications, and noncoding RNA activity can change the function of genes without altering nucleotide sequences. Genes and environment combine to produce the etiology of ASD. One of the main areas of ASD research now being studied is the effects of epigenetic factors on gene expression, such as DNA methylation. Autistic patients exhibit evidence of oxidative stress and impaired methylation, which may reflect the effects of toxic exposure on sulfur metabolism that may lead to cellular damage in the brain and altered expression of epigenetic genes. This review paper summarizes the findings of the supplementary therapy studies of ASD, showing that supplements, including B9, B12, B6, D, E, C, glutathione, omega-3, and choline, are highly effective in modifying methylation in autism, improving many nutrient and metabolic problems, and resulting in significant improvements in symptoms. [ABSTRACT FROM AUTHOR]

Introduction: Pectobacterium betavasculorum is a member of the Pectobacerium genus that inhabits a variety of niches and is found in all climates. Bacteria from the Pectobacterium genus can cause soft rot disease on various plants due to the secretion of plant cell wall degrading enzymes (PCWDEs). The species P. betavasculorum is responsible for the vascular necrosis of sugar beet and soft rot of many vegetables. It also infects sunflowers and artichokes. The main sugar present in sugar beet is sucrose while xylose is one of the main sugars in artichoke and sunflower. Methods: In our work, we applied metabolomic studies coupled with genomics to investigate the metabolism of P. betavasculorum in the presence of xylose and sucrose as the only carbon source. The ability of the strains to use various sugars as the only carbon source were confirmed by the polypyridyl complex of Ru(II) method in 96-well plates. Results: Our studies provided information on the metabolic pathways active during the degradation of those substrates. It was observed that different metabolic pathways are upregulated in the presence of xylose in comparison to sucrose. Discussion: The presence of xylose enhances extracellular metabolism of sugars and glycerol as well as stimulates EPS and IPS synthesis. In contrast, in the presence of sucrose the intensive extracellular metabolism of amines and amino acids is promoted. [ABSTRACT FROM AUTHOR]

Early-life adversities, whether prenatal or postnatal exposure, have been linked to adverse mental health outcomes later in life increasing the risk of several psychiatric disorders. Research on its neurobiological consequences demonstrated an association between exposure to adversities and persistent alterations in the structure, function, and connectivity of the brain. Consistent evidence supports the idea that regulation of gene expression through epigenetic mechanisms are involved in embedding the impact of early-life experiences in the genome and mediate between social environments and later behavioral phenotypes. In addition, studies from rodent models and humans suggest that these experiences and the acquired risk factors can be transmitted through epigenetic mechanisms to offspring and the following generations potentially contributing to a cycle of disease or disease risk. However, one of the important aspects of epigenetic mechanisms, unlike genetic sequences that are fixed and unchangeable, is that although the epigenetic markings are long-lasting, they are nevertheless potentially reversible. In this review, we summarize our current understanding of the epigenetic mechanisms involved in the mental health consequences derived from early-life exposure to malnutrition, maltreatment and poverty, adversities with huge and pervasive impact on mental health. We also discuss the evidence about transgenerational epigenetic inheritance in mammals and experimental data suggesting that suitable social and pharmacological interventions could reverse adverse epigenetic modifications induced by early-life negative social experiences. In this regard, these studies must be accompanied by efforts to determine the causes that promote these adversities and that result in health inequity in the population. [ABSTRACT FROM AUTHOR]

Purpose: The prevalence of non-alcoholic fatty liver disease (NAFLD) and its related mortality is increasing at an unprecedented rate. Traditional Chinese medicine (TCM) has been shown to offer potential for early prevention and treatment of NAFLD. The new mechanism of "Shenling Baizhu San" (SLBZS) is examined in this study for the prevention and treatment of NAFLD at the preclinical level. Methods: Male C57BL/6J mice were randomly divided into three groups: normal diet (ND), western diet + CCl4 injection (WDC), and SLBZS intervention (WDC + SLBZS). Body weights, energy intake, liver enzymes, pro-inflammatory factors, and steatosis were recorded in detail. Meanwhile, TPH1, 5-HT, HTR2A, and HTR2B were tested using qRT-PCR or ELISA. Dynamic changes in the gut microbiota and metabolites were further detected through the 16S rRNA gene and untargeted metabolomics. Results: SLBZS intervention for 6 weeks could reduce the serum and liver lipid profiles, glucose, and pro-inflammatory factors while improving insulin resistance and liver function indexes in the mice, thus alleviating NAFLD in mice. More importantly, significant changes were found in the intestinal TPH-1, 5-HT, liver 5- HT, and related receptors HTR2A and HTR2B. The 16S rRNA gene analysis suggested that SLBZS was able to modulate the disturbance of gut microbiota, remarkably increasing the relative abundance of probiotics (Bifidobacterium and Parvibacter) and inhibiting the growth of proinflammatory bacteria (Erysipelatoclostridium and Lachnoclostridium) in mice with NAFLD. Combined with metabolomics in positive- and negative-ion-mode analyses, approximately 50 common differential metabolites were selected via non-targeted metabolomics detection, which indicated that the targeting effect of SLBZS included lipid metabolites, bile acids (BAs), amino acids (AAs), and tryptophan metabolites. In particular, the lipid metabolites 15-OxEDE, vitamin D3, desoxycortone, and oleoyl ethanol amide were restored by SLBZS. Conclusion: Integrating the above results of multiple omics suggests that SLBZS ameliorates NAFLD via specific gut microbiota, gut-derived 5-HT, and related metabolites to decrease fat accumulation in the liver and inflammatory responses. [ABSTRACT FROM AUTHOR]

Adequate maternal nutrient intake of vitamin B12 is critical to fetal brain development and subsequent neurodevelopmental outcomes. We conducted a scoping review to map the current state of knowledge from human epidemiological studies on the associations between maternal vitamin B12 during pregnancy and children's brain, cognitive, language, and motor development to identify gaps in the literature and suggest directions for future research. PubMed and OVID MEDLINE were searched. Search terms were vitamin B12, prenatal or maternal, neurodevelopment or cognitive development or brain. Animal studies were excluded. In total, 148 publications were identified, of which 19 met our inclusion criteria: (1) maternal vitamin B12 assessed via a measure of status, dietary intake, supplementation, or deficiency; and (2) an outcome related to brain development or cognitive, language, or motor development in children less than 18 years of age was assessed. This scoping review suggests that evidence supporting a relationship between maternal vitamin B12 during pregnancy and children's neurodevelopmental outcomes is inconclusive. Further longitudinal research is needed to clarify the effects of maternal vitamin B12 supplementation, status, and intake on children's brain development and neurodevelopmental outcomes. [ABSTRACT FROM AUTHOR]

The safety of vegetable food is compromised by various factors, including the inefficient or excessive use of sanitizers. Instances of individuals falling ill after consuming raw vegetables have been reported, with outbreaks of diseases caused by pathogens on fresh vegetables becoming increasingly prevalent globally, attracting significant media coverage and impacting the economic viability of vegetable cultivation. Measures to enhance food safety in postharvest horticultural produce involve controlling microbial proliferation and minimizing cross-contamination. Sanitizers were utilized in the food safety arsenal for a variety of purposes, including pathogen elimination and microbe reduction, hand, tool, and vegetable contact surface cleaning, and produce shelf-life extension. Choosing an appropriate sanitizer for all vegetables is difficult due to a lack of knowledge on which sanitizers are ideal for the many types of vegetables grown on farms under different environmental circumstances. Although chlorine-based sanitizers, such as sodium or calcium hypochlorite, have been widely used for the past 50 years, recent research has revealed that chlorine reacts with an organic compound in fresh vegetables to produce trihalomethane, a carcinogen precursor, and as a result, many countries have prohibited the use of chlorine in all foods. As a result, horticulture research groups worldwide are exploring non-chlorine, ecologically friendly sanitizers for the vegetable industry. They also want to understand more about the present procedures in the vegetable business for employing alternative sanitizers, as well as the efficacy and potential dangers to the food safety of fresh salad vegetables. This review paper presents detailed information on non-chlorine sanitizers, such as their efficacy, benefits, drawbacks, regulatory requirements, and the need for additional research to lower the risk of marketed salad vegetable food safety. [ABSTRACT FROM AUTHOR]

Copyright of Shipin Kexue/ Food Science is the property of Food Science Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The fur color of mammals is mainly determined by melanin synthesized by melanocytes. Cell staining includes melanocyte development, melanin synthesis and metabolism, and signal pathways regulating melanin synthesis. Melanocytes can be classified into many types, and these types can be identified by a variety of melanocyte markers. Fur color can judge the physical condition and nutritional status of animals, and different fur colors may have certain influence on animal production. This paper reviews the structural basis and development cycle of mammalian fur color formation, describes the cytochrome process from neural crest to mature melanocytes residing in several tissues, summarizes the types of melanocytes and the markers of each type of melanocytes, and discusses the application of animal coat color in animal production, providing help for analyzing the genetic mechanism of mammalian fur color formation and providing effective suggestions for animal production affected by fur color. [ABSTRACT FROM AUTHOR]

Copyright of Food & Fermentation Industries is the property of Food & Fermentation Industries and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The present lifestyle, dietary patterns, psychological pressure, environmental factors, and the widespread exploitation of processed substances in food production and farming have collectively contributed to a substantial expediting in the development of various health problems. Globally, researchers have been seeking natural pharmaceutical substances with the potential to be employed in treating lifestyle‐related diseases or delaying their onset. Fenugreek seeds have gained significant attention in various fields, including health, nutrition, and cutting‐edge nanotechnology applications, due to their versatile qualities. The current investigation offers a comprehensive discussion of the nutritional composition and therapeutic potential of fenugreek seeds, with an emphasis on their plentiful reservoir of bioactive compounds. This seed demonstrates promising medicinal potential in addressing a wide range of health issues. Significantly, these findings indicate noteworthy properties, such as antidiabetic, antioxidant, anti‐obesity, hypocholesterolemic, anticancer, and cardioprotective effects. Moreover, the components of fenugreek seeds are important in the development of a multitude of foods, which is the reason why they are used extensively in the area of food research. In addition to their nutritional value, their exploration of nanotechnology reveals a promising domain, utilizing the distinctive characteristics of seeds for many purposes, such as nanoparticle synthesis and oil for edible films and nanoemulsions. This review article focuses on a comprehensive analysis of fenugreek seeds, examining their wide‐ranging applications in the fields of health, nutrition, food, and nanotechnology. [ABSTRACT FROM AUTHOR]

Introduction: Type C hepatic encephalopathy (HE) is a decompensating event of chronic liver disease leading to severe motor and cognitive impairment. The progression of type C HE is associated with changes in brain metabolite concentrations measured by 1H magnetic resonance spectroscopy (MRS), most noticeably a strong increase in glutamine to detoxify brain ammonia. In addition, alterations of brain cellular architecture have been measured ex vivo by histology in a rat model of type C HE. The aim of this study was to assess the potential of diffusion-weighted MRS (dMRS) for probing these cellular shape alterations in vivo by monitoring the diffusion properties of the major brain metabolites. Methods: The bile duct-ligated (BDL) rat model of type C HE was used. Five animals were scanned before surgery and 6- to 7-week post-BDL surgery, with each animal being used as its own control. 1H-MRS was performed in the hippocampus (SPECIAL, TE = 2.8 ms) and dMRS in a voxel encompassing the entire brain (DWSTEAM, TE = 15 ms, diffusion time = 120 ms, maximum b-value = 25 ms/µm2) on a 9.4 T scanner. The in vivo MRS acquisitions were further validated with histological measures (immunohistochemistry, Golgi-Cox, electron microscopy). Results: The characteristic 1H-MRS pattern of type C HE, i.e., a gradual increase of brain glutamine and a decrease of the main organic osmolytes, was observed in the hippocampus of BDL rats. Overall increased metabolite diffusivities (apparent diffusion coefficient and intra-stick diffusivity--Callaghan's model, significant for glutamine, myo-inositol, and taurine) and decreased kurtosis coefficients were observed in BDL rats compared to control, highlighting the presence of osmotic stress and possibly of astrocytic and neuronal alterations. These results were consistent with the microstructure depicted by histology and represented by a decline in dendritic spines density in neurons, a shortening and decreased number of astrocytic processes, and extracellular edema. Discussion: dMRS enables non-invasive and longitudinal monitoring of the diffusion behavior of brain metabolites, reflecting in the present study the globally altered brain microstructure in BDL rats, as confirmed ex vivo by histology. These findings give new insights into metabolic and microstructural abnormalities associated with high brain glutamine and its consequences in type C HE. [ABSTRACT FROM AUTHOR]