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All-inorganic CsPbI2Br inverted perovskite solar cells (PSCs) have drawn increasing attention because of their outstanding thermal stability and compatible process with tandem cells. However, relatively low open circuit voltage (Voc) has lagged their progress far behind theoretical limits. Herein, we introduce phenylmethylammonium iodide and 4-trifluoromethyl phenylmethylammonium iodide (CFPMAI) on the surface of a CsPbI2Br perovskite film and investigate their passivation effects. It is found that CFPMAI with a –CF3 substituent significantly decreases the trap density of the perovskite film by forming interactions with the under-coordinated Pb2+ ions and effectively suppresses the non-radiative recombination in the resulting PSC. In addition, CFPMAI surface passivation facilitates the optimization of energy-level alignment at the CsPbI2Br perovskite/[6,6]-phenyl C61 butyric acid methyl ester interface, resulting in improved charge extraction from the perovskite to the charge transport layer. Consequently, the optimized inverted CsPbI2Br device exhibits a markedly improved champion efficiency of 14.43% with a Voc of 1.12 V, a Jsc of 16.31 mA/cm2, and a fill factor of 79.02%, compared to the 10.92% (Voc of 0.95 V) efficiency of the control device. This study confirms the importance of substituent groups on surface passivation molecules for effective passivation of defects and optimization of energy levels, particularly for Voc improvement. [ABSTRACT FROM AUTHOR]

Carbohydrate intolerance, commonly linked to the consumption of lactose, fructose, or sorbitol, affects up to 30% of the population in high-income countries. Although sorbitol intolerance is attributed to malabsorption, the underlying mechanism remains unresolved. Here, we show that a history of antibiotic exposure combined with high fat intake triggered long-lasting sorbitol intolerance in mice by reducing Clostridia abundance, which impaired microbial sorbitol catabolism. The restoration of sorbitol catabolism by inoculation with probiotic Escherichia coli protected mice against sorbitol intolerance but did not restore Clostridia abundance. Inoculation with the butyrate producer Anaerostipes caccae restored a normal Clostridia abundance, which protected mice against sorbitol-induced diarrhea even when the probiotic was cleared. Butyrate restored Clostridia abundance by stimulating epithelial peroxisome proliferator-activated receptor-gamma (PPAR-γ) signaling to restore epithelial hypoxia in the colon. Collectively, these mechanistic insights identify microbial sorbitol catabolism as a potential target for approaches for the diagnosis, treatment, and prevention of sorbitol intolerance.

Recent therapeutic strategies have highlighted the potential of β-hydroxybutyrate (BHB) and α-ketoglutarate (α-KG) as effective anticancer agents, particularly for colon cancer. These metabolites can modulate cellular metabolism and induce epigenetic changes, inhibiting tumor growth. Nonetheless, certain cancer cells may utilize ketone bodies, like BHB as nutrient sources under hypoxic conditions, potentially reducing treatment efficacy. Understanding these mechanisms is crucial for optimizing cancer therapies. This study evaluated the effects of BHB and α-KG on HCT-116 colorectal cancer cell viability under normoxic and low-glucose hypoxic conditions. HCT-116 cell lines were treated with different doses of BHB and α-KG in normoxic and low-glucose hypoxic conditions, and then cell viability was assessed by the MTT assay. Moreover, the mRNA expression levels of SRC, hypoxia-inducible factor 1α (HIF-1α), acetyl-CoA acetyltransferase 1 (ACAT1), and sirtuin 2 (SIRT2) genes were determined using quantitative reverse transcriptase-polymerase chain reaction (q RT-PCR). BHB significantly increased the proliferation of HCT-116 colon cancer cells under low-glucose hypoxic conditions, while α-KG maintained cell viability in normoxic conditions but not in hypoxia. BHB treatment reduced SIRT2 mRNA levels and increased ACAT1, SRC, and HIF-1α expression. Conversely, α-KG decreased ACAT1, SRC, and HIF-1α expression and increased SIRT2 levels in normoxia but could not reverse gene expression during hypoxia. Our study demonstrated that BHB and α-KG exhibited complex interactions with colon cancer cell viability under varying oxygen and glucose conditions. While BHB promoted cell proliferation in hypoxic environments, α-KG showed protective effects in normoxic conditions. This research contributed to the growing body of evidence supporting the role of metabolic modulators in cancer therapy and emphasized the importance of understanding tumor microenvironments to optimize treatment outcomes. However, the need for further research into the metabolic pathways is underscored to enhance therapeutic strategies for cancer treatment. [ABSTRACT FROM AUTHOR]

Background: Metabolic pathways are known to significantly impact the development and advancement of lung cancer. This study sought to establish a signature related to butyrate metabolism that is specifically linked to lung adenocarcinoma (LUAD). Methods: For the purpose of identifying butyrate metabolism-related differentially expressed genes (BMR-DEGs) in the TCGA-LUAD dataset, we introduced transcriptome data. This was followed by the implementation of the univariate Cox and LASSO analyses in order to construct a LUAD gene signature. We performed a comprehensive analysis of gene function enrichment between the two populations at risk, thoroughly examined their immune microenvironment characteristics, and assessed the effectiveness of immunotherapy. Finally, the function of CDKN3 in LUAD was verified by in vitro experiments. Results: Through a comprehensive analysis of the TCGA-LUAD dataset, 51 significant BMR-DEGs were confirmed. Subsequently, five characteristic genes, CPS1, ABCC2, CDKN3, SLC2A1, and IGFBP1 were identified to create prognostic features for butyrate metabolism related outcomes in LUAD. Cox regression analysis determined that the pathological T stage, tumor stage, and RiskScore could serve as independent prognostic indicators. Analysis of the abundance of 22 immune infiltrating cells revealed that 15 immune cell types exhibited substantial differences and were strongly associated with risk ratings and prognosis. An important correlation exists between risk ratings and immunological checkpoints, which can be utilized to forecast the efficacy of treatment. In the high-risk group, there was an upregulation of the expression of PD-L2, PD-L1, and PD-1. Additionally, the risk score showed a positive correlation with TIDE and Exclusion score, while showing a negative correlation with Dysfunction score. Furthermore, the IC50 values for cisplatin, paclitaxel, and docetaxel were notably elevated in the high-risk group, indicating that these medications could potentially provide therapeutic advantages for this particular group. Finally, we determined that knockdown CDKN3 inhibited the proliferation and metastasis of LUAD cells. Conclusion: We identify and validate a novel BMR-related prognostic signature comprising 5 DEGs for LUAD patients. Our data might provide a new molecular target for LUAD treatment. [ABSTRACT FROM AUTHOR]

The gut microbiome and its metabolites may be important role in regulating the pathogenesis of obesity. This study aimed to characterize the gut microbiome and short-chain fatty acid (SCFA) metabolome in obese children. This case–control study recruited children aged 7‒14 years and divided them into a normal group (NG) and an obese group (OG) based on their body mass index. Whole-genome shotgun metagenomic analysis was performed on fecal samples from the OG and NG groups to characterize the signatures and functional potential of the gut microbiota. Serum metabolite profiles were analyzed using high-performance liquid chromatography/mass spectrometry (LC/MS). The Statistical Package for the Social Sciences (SPSS, version 26) and R software were used for data analysis. A total of 99 children were recruited, with 49 in the OG and 50 in the NG. At the phylum level, Proteobacteria were significantly more abundant in children in the OG than those in the NG. At the genus level, Oscillibacter and Alistipes were significantly lower in children in the OG than those in the NG. Caproate levels significantly increased, whereas butyrate and isobutyrate levels decreased in children in the OG than those in the NG. Kyoto encyclopedia of genes and genomes (KEGG) functional analysis revealed 28 enriched KEGG pathways, of which/with the phosphotransferase system (PTS) and enhanced biofilm formation by Escherichia coli were particularly significant in the OG. Spearman's correlation analysis indicated that the genus Oscillibacter and species Clostridium_sp._CAG:302 connect serum metabolites and the gut microbiota in childhood obesity. Childhood obesity is correlated with the symbiotic status of the gut microbiota. The microbiota influences human metabolism via specific pathways, particularly butyrate, caproate, and the genus Oscillibacter, all closely associated with obesity. [ABSTRACT FROM AUTHOR]

Polycystic ovary syndrome (PCOS) is a common endocrine disorder marked by ovarian dysfunction and metabolic abnormality. This study explores the therapeutic potential of leonurine (SCM-198) in PCOS. Our results show that SCM-198 treatment significantly improved ovarian function, hormone disorders and insulin resistance while reducing granulosa cell ferroptosis. This study provides the first evidence that SCM-198 modulates the gut microbiota composition, increases the abundance of Christensenella minuta , and boosts butyrate levels. Transcriptomic and metabolomic analyses revealed that PCOS patients exhibit granulosa cell ferroptosis and decreased butyrate levels in follicular fluid. Butyrate was shown to alleviate ferroptosis in granulosa cells via the SLC7A11/TXNRD1/GPX4 pathway, as confirmed in vitro with KGN cells. The therapeutic mechanism of SCM-198 in the management of PCOS via the gut microbiota-ovary axis involves the enhancement of gut microbiota and its metabolites. This intervention improves ovarian function and alleviates PCOS symptoms by targeting ferroptosis in granulosa cells. [Display omitted] • SCM-198 alleviates ovarian dysfunction and insulin resistance in PCOS-like mice. • Christensenella minuta and butyric acid are key contributors to the treatment of PCOS. • Butyrate inhibits ferroptosis in granulosa cells through the SLC7A11/GPX4 pathway. [ABSTRACT FROM AUTHOR]

Butyrate is one of the most abundant short-chain fatty acids (SCFAs), which are important metabolites of dietary fiber by fermentation of gut commensals, and has been shown to be vital in maintaining host health. The present study mainly investigated how sodium butyrate (NaB) supplementation in the diet with high proportion of soybean meal (SBM) affected turbot. Four experimental diets were formulated: (1) fish meal (FM) based diet (control group), (2) SBM protein replacing 45% FM protein in the diet (high SBM group), (3) 0.2% NaB supplementation in the high SBM diet (high SBM + 0.2% NaB group), and (4) 0.5% NaB supplementation in the high SBM diet (high SBM + 0.5% NaB group). The fish were fed four different diets for 8 weeks. The results showed that the high SBM diet significantly suppressed growth performance, induced typical enteritis symptoms and decreased resistance to bacterial infection. However, inclusion of 0.2% and 0.5% NaB in the high SBM diet both effectively increased the growth performance of turbot. Meanwhile, dietary NaB protected the intestinal morphology, and regulated the gene expression of inflammatory cytokines to relieve the inflammation of turbot, such as TNFα, IL-1β, NFκB and IL-10. Moreover, supplementation with NaB in the high SBM diet activated HIF-1α/IL-22/Lysozyme signaling pathway to against Edwardsiella tarda (E. tarda) infection, especially 0.5% NaB supplementation exerted more effectively to defence bacterial infection under inflammatory state. In conclusion, dietary NaB significantly promoted growth and gut health of turbot. Besides, it enhanced the resistance of fish to bacterial infection, especially dietary 0.5% NaB supplementation. [ABSTRACT FROM AUTHOR]

Agaricus bisporus is globally a most extensively consumed species of edible mushrooms. Ethylene secreted by A. bisporus mycelium suppress the initiation of fructification. 1-aminocyclopropane-1-carboxylic acid (ACC) deaminase-producing bacteria decrease the content of ethylene by cleaving ACC produced by the A. bisporus hyphae to α-ketobutyrate and ammonia. This study evaluated the effect of various salts on the population of Bacillus velezensis UTB96 with ACC deaminase activity on button mushroom. The results indicated that CaCl2, MnSO4 and MgSO4 salts increased significantly the bacterial population compared by control, among which the medium supplemented with CaCl2 showed the highest number of living cells in the culture. Evaluation of ACC deaminase gene expression indicated that the highest level belonged to bacteria grown in medium containing CaCl2 in comparison with control as the expression level of ACC deaminase was 20.9-fold upregulated comparing to the control. The assessment of the effect of each salt lonely, UTB96 cultured in LB and LB containing salts of mushroom indicated that yield was increased 23% and 18% in plots treated with UTB96 cultured in media supplemented, respectively, with CaCl2 and MnSO4, in comparison with control. Therefore, UTB96 grown in media supplemented with CaCl2 has a potential use in mushroom production since the induction of ACC deaminase which results in decrease the level of ethylene and promote mushroom growth. [ABSTRACT FROM AUTHOR]

Purpose: To determine the prevalent microbiological profile of biliary atresia (BA) patients at the time of its occurrence by studying their intestinal flora. Methods: A total of 118 gut microbiota samples from three groups of 43 BA patients, 33 disease controls (DC) with other cholestatic diseases and 42 healthy controls (HC), were analyzed by deep mining of public data. Subsequently, a total of 23 fecal samples from three groups of clinically collected patients (11 BA, 6 DC and 6 HC) were sequenced for 16S rRNA gene amplification and analyzed for serum butyrate (BU) level by liquid chromatography. Results: Taxonomic analysis revealed significant differences in the composition of the intestinal microbiota between BA patients and controls, with a reduction in diversity and a higher abundance of Proteobacteria, Streptococcus and Lactobacillus in the BA group. Database and clinical data analyses concluded that Streptococcus/Bacteroides (AUC = 0.9035, 95% CI 0.8347–0.9722, P < 0.0001) or Streptococcus/Eggerthella (AUC = 0.8333, 95% CI 0.6340–1.000, P = 0.027) was the best microbiota to differentiate between BA and DC. Serum butyrate levels were low in the BA and DC groups and differed from the HC group (P = 0.01, P = 0.04). Butyrate levels in BA were negatively correlated with jaundice clearance and cholangitis, but not statistically significant. Conclusions: Our study reveals changes in the composition of the gut microbiota in BA, especially the butyrate-producing microbiota, and suggests the potential for using gut microbiota as a noninvasive diagnostic benefit for BA. Low levels of serum butyrate in BA may indicate a poor prognosis. [ABSTRACT FROM AUTHOR]

Butyrate has been proposed as a drug therapy by acting as a lysine deacetylase (KDAC) inhibitor and elevating protein acetylation, in particular on histones. Nonetheless, recent studies suggest that tissues such as the gut can utilize butyrate as a metabolite. We have previously shown that the addition of butyrate induces a rapid increase of oxygen consumption in whole Drosophila melanogaster heads. Here we show that while head oxygen consumption is increased by the addition of butyrate, no apparent changes are observed on the proteome and acetylome. Instead, we show that butyrate is metabolized and incorporated into the tricarboxylic acid (TCA) cycle. Collectively our data supports the notion that the therapeutic benefits of acute butyrate treatment may be also mediated by improving metabolic rates, rather than solely targeting the epigenome or acetylome. [ABSTRACT FROM AUTHOR]

Objectives: The ketogenic diet (KD) has long been used as an alternative nonpharmacological therapy to manage pharmacoresistant epilepsy. The anticonvulsant mechanisms of KD have yet to be fully elucidated. The present study explored whether a KD could exert antioxidative effects by altering brain Klotho (Kl) gene expression.Methods: Thirty male rats were divided into three groups: the normal diet (ND) group received standard rat chow; the calorie-restricted diet (CRD) group was maintained at 90% of the calculated energy need; and the KD group received a diet composed of 8% protein, 2% carbohydrates, and 90% fat (per calorie macronutrient). The levels of β-hydroxybutyrate (BHB) in the serum, Kl gene expression in the brain, and Kl protein, malondialdehyde (MDA), and protein carbonyl (PC) levels in the serum and brain were evaluated by standard methods.Results: The serum BHB levels in the KD group were significantly greater than those in the ND and CRD groups (p < 0.001). The Kl expression in the brain was significantly greater in the KD group than in the ND group (p = 0.028). The brain MDA levels in the KD group were significantly lower than those in the ND group (p = 0.006). Elevated BHB was positively correlated with brain Kl expression (r = 0.668, p < 0.001). The brain MDA levels were negatively correlated with brain Kl expression (r = −0.531, p = 0.003) and serum BHB levels (r = 0.472, p = 0.020).Discussion: KD might exert antioxidative effects by increasing BHB and upregulating Kl in the brain. This could be considered a possible anticonvulsant mechanism of KD. [ABSTRACT FROM AUTHOR]

Simple Summary: This study addresses the logical deliberation regarding the pathogenesis, behavioral appearances, biochemical characteristics, and reversibility of symptoms of psychiatric disorders through a dietary intervention. A mouse model of neuropsychiatric disorder was originally created with poly I:C, sodium dextran sulfate (DSS), κ-carrageenan (CGN), and Di-(2-ethylhexyl) phthalate (DEHP) usage, in which a noteworthy connection was made between alterations in p62/GLAST protein expression in mouse brains and variations in experimental behavioral test scores. In addition, a potential therapeutic study by means of dietary intervention was performed using low doses of butyrate, trehalose, and piceid. Subsequently, it was shown that these orally available molecules could effectively improve psychiatric behavior as well as the biochemical alterations in p62/GLAST in mouse brains. Neuropsychiatric disorders are a public health concern, in which diagnosis and prognosis may be based on clinical symptoms that might often diverge across individuals. Schizophrenia is a major neuropsychiatric disorder, which may affect millions worldwide. However, the biochemical alterations of this disorder have not been comprehensively distinguished. In addition, there is less confidence in finding specific biomarkers for neuropsychiatric disorders, including schizophrenia, but rather a specific characteristic behavioral pattern. In general, maternal immune activation is considered to be one of the important factors in the development of neuropsychiatric disorders. Here, a mouse model of neuropsychiatric disorders was created, in which poly I:C, sodium dextran sulfate (DSS), and κ-carrageenan (CGN) were utilized for maternal immune activation during the pregnancies of mother mice. Subsequently, we examined the link between biochemical changes in p62 and/or glutamate aspartate transporter (GLAST) in the brains of offspring mice and the alteration in their experimental behavior scores. Furthermore, a therapeutic study was conducted on these neuropsychiatric disorder model mice using butyric acid, piceid, and metformin. It was found that some molecules could effectively improve the behavioral scores of neuropsychiatric model mice. Importantly, significant correlations between certain behavioral scores and p62 protein expression, as well as between the scores and GLAST expression, were recognized. This is the first report of a significant correlation between pathological behaviors and biochemical alterations in neuropsychiatric disorder model animals. This concept could contribute to the development of innovative treatments to at least ameliorate the symptoms of several psychiatric disorders. [ABSTRACT FROM AUTHOR]

Cisplatin is a particularly potent antineoplastic drug. However, its usefulness is restricted due to the induction of nephrotoxicity. More recent research has indicated that β-hydroxybutyrate (β-HB) protects against acute or chronic organ damage as an efficient healing agent. Nonetheless, the therapeutic mechanisms of β-HB in acute kidney damage caused by chemotherapeutic drugs remain unclear. Our study developed a model of cisplatin-induced acute kidney injury (AKI), which involved the administration of a ketogenic diet or β-HB. We analyzed blood urea nitrogen (BUN) and creatinine (Cr) levels in serum, and used western blotting and immunohistochemical staining to assess ferroptosis and the calcium/calmodulin-dependent kinase kinase 2 (Camkk2)/AMPK pathway. The mitochondrial morphology and function were examined. Additionally, we conducted in vivo and in vitro experiments using selective Camkk2 inhibitor or activator to investigate the protective mechanism of β-HB on cisplatin-induced AKI. Exogenous or endogenous β-HB effectively alleviated cisplatin-induced abnormally elevated levels of BUN and Cr and renal tubular necrosis in vivo. Additionally, β-HB reduced ferroptosis biomarkers and increased the levels of anti-ferroptosis biomarkers in the kidney. β-HB also improved mitochondrial morphology and function. Moreover, β-HB significantly attenuated cisplatin-induced cell ferroptosis and damage in vitro. Furthermore, western blotting and immunohistochemical staining indicated that β-HB may prevent kidney injury by regulating the Camkk2-AMPK pathway. The use of the Camkk2 inhibitor or activator verified the involvement of Camkk2 in the renal protection by β-HB. This study provided evidence of the protective effects of β-HB against cisplatin-induced nephrotoxicity and identified inhibited ferroptosis and Camkk2 as potential molecular mechanisms. Cisplatin induces disruptions in mitochondrial energy metabolism and lipid peroxidation. Both endogenous and exogenous β-hydroxybutyrate can protected against cisplatin-induced renal damage by repairing mitochondrial energy homeostasis and preventing ferroptosis, and this protective effect might be attributed to Camkk2 regulation. β-HB protects against cisplatin-induced renal damage both in vivo and in vitro. Moreover, β-HB is effective in attenuating cisplatin-induced lipid peroxidation and ferroptosis. The regulation of energy metabolism, as well as the treatment involving β-HB, is associated with Camkk2. [ABSTRACT FROM AUTHOR]

Simple Summary: Including gluconeogenic precursors such as calcium propionate and sodium propionate in ruminant diets has been shown to positively impact animal growth. However, information on the effects of calcium or sodium propionate on dietary energetics, ruminal fermentation, and meat quality of lambs is scarce. This study aimed to evaluate the effects of dietary supplementation with calcium propionate and sodium propionate on growth performance, dietary energetics, ruminal fermentation, and meat quality of finishing lambs. Calcium propionate and sodium propionate do not affect growth performance, dietary energy utilization efficiency, ruminal fermentation, or meat quality of finishing lambs. This study aimed to evaluate the effect of dietary supplementation with calcium propionate (CaPr) or sodium propionate (NaPr) on growth performance, ruminal fermentation, and meat quality of finishing lambs. Twenty-seven non-castrated Creole male lambs (24.95 ± 2.15 kg body weight (BW); 4.5 ± 0.5 months old) were randomly assigned to three treatments: (a) CON: basal diet without the addition of CaPr or Na Pr; (b) basal diet + CaPr (10 g/kg DM); and (c) basal diet + NaPr (10 g/kg DM). The data were analyzed using a completely randomized experimental design, with each lamb considered an experimental unit (nine replicates/treatment). Dietary supplementation with CaPr or NaPr did not affect (p > 0.05) growth performance or dietary energetics. However, greater (p = 0.05) apparent dry matter digestibility was observed in the lambs that consumed the diet with NaPr10. Dietary supplementation with CaPr or NaPr did not affect (p > 0.05) ruminal pH or ruminal concentrations of ammonia nitrogen, acetate, propionate, butyrate, and total volatile fatty acids. However, ruminal lactate concentration increased (p = 0.01) in lambs consuming the NaPr diet. Hot carcass weight and yield, backfat thickness, meat pH, meat color (L*, a*, and b*), cooking loss, and water holding capacity were not affected by dietary supplementation with CaPr or NaPr. In conclusion, dietary supplementation with 10 g/kg DM of calcium propionate or sodium propionate does not affect growth performance, dietary energetics, ruminal fermentation, and the meat quality of finishing lambs. [ABSTRACT FROM AUTHOR]

The common practice of using toxic chemicals as a preservative for rubberwood is much of a concern regarding environmental issues, its effect on human health, and compromising the wood's strength. This study focuses on the alternative strategy to preserve rubberwood using sodium acetate and sodium butyrate. These two salts were obtained from the reaction between sodium hydroxide and the fermentation products of landfill leachate, namely acetic acid and butyric acid. The effect of these salt concentrations and treatment duration on the rubberwood were studied and assessed from the biological decay, mechanical and chemical aspects. Almost all treated rubberwood subjected to decay by Phanerochaete chrysosporium, Trametes menziesii, species fungi A (white-rot), and species fungi B (brown-rot) have lower mass loss than untreated rubberwood. Treatment with 0.5M sodium butyrate was the best concentration in protecting the wood from degradation caused by fungal attacks. For the mechanical test, most of the salt concentrations positively impacted the bending strength and modulus of the treated rubberwood. Lastly, a chemical test conducted on rubberwood treated with 0.75M sodium butyrate for 21 days gave the highest retention and penetration of the salt into the rubberwood. [ABSTRACT FROM AUTHOR]

Calcium aluminum layered double hydroxide (CaAl‐LDH) has gained significance for drug delivery applications due to its multiple advantages, including high drug‐loading capacity, pH sensitivity, biocompatibility, high acceptable intake values of metal ions, and its ability to provide sustained release of the intercalated drug. In this study, pristine CaAl‐LDH was synthesized by co‐precipitation method at different pH values (9 and 10) and aging times (16 and 24 h) to obtain LDH with higher d‐spacing, which is beneficial for achieving a high drug loading efficiency. Ofloxacin (OFX), an antibiotic drug, was loaded into CaAl‐LDH via regeneration (CaAl‐LDH‐OFX(RG)) and co‐precipitation (CaAl‐LDH‐OFX(CPT)) methods, and achieved drug loading of 28.3% and 36.5%, respectively. The release behavior of OFX from CaAl‐LDH‐OFX(RG) and CaAl‐LDH‐OFX(CPT) formulations was examined in simulated conditions representing the gastrointestinal tract. CaAl‐LDH‐OFX(RG) showed less initial burst release of OFX compared to CaAl‐LDH‐OFX(CPT) in acidic as well as neutral pH conditions. In order to overcome the degradation of the drug before reaching the target site, CaAl‐LDH‐OFX(RG) was reinforced at 1, 3, and 5 wt% in poly (3‐hydroxybutyrate) (PHB) matrix by sonication‐assisted solution casting method. The PHB‐based nanocomposites were characterized by XRD, FESEM, TGA, and FTIR analyses. FESEM characterization of PHB‐based films loaded with 3 wt% of CaAl‐LDH‐OFX(RG) revealed compact morphology without any aggregate formation. Moreover, PHB/3CaAl‐LDH‐OFX(RG) films demonstrated sustained release of OFX at pH 1.2 (95.60% in 96 h), pH 6.8 (78% in 113 h), and pH 7.4 (40.90% in 107 h). The promising potential of PHB‐based formulations for antibacterial drug delivery systems was confirmed by their significant antibacterial activity against Escherichia coli and Staphylococcus aureus. Highlights: pH and aging time influence the structural characteristics of pristine CaAl‐LDH.Ofloxacin loaded CaAl‐LDH prepared by co‐precipitation and regeneration methods.Sustained release of ofloxacin from poly (3‐hydroxybutyrate)‐based formulation.Poly (3‐hydroxybutyrate)‐based formulations exhibit excellent antibacterial activity. [ABSTRACT FROM AUTHOR]

Abstract\nHIGHLIGHTSFlavonoids, a class of polyphenolic compounds, are widely distributed in plant-based foods and have been recognized for their potential to promote overall health and well-being. Flavonoids in fruits and vegetables offer various beneficial effects such as anti-aging, anticancer, and anti-inflammatory properties. Flavonoids have been extensively studied for their neuroprotective properties, which are attributed to their ability to cross the blood-brain barrier and interact with neural cells. Factors like gut microbiota composition, age, genetics, and diet can impact how well flavonoids are absorbed in the gut. The gut microbiota can enhance the absorption of flavonoids through enzymatic processes, making microbiota composition a key factor influenced by age, genetics, and diet. Flavonoids can modulate the gut microbiota through prebiotic and antimicrobial effects, affecting the production of beneficial microbial metabolites like short-chain fatty acids (SCFAs) such as butyrate, which play a role in brain function and health. The gut microbiome also modulates the immune system, which is critical for preventing neuroinflammation. Additionally, flavonoids can benefit mental and psychological health by influencing anti-inflammatory signaling pathways in brain cells and increasing the absorption of tyrosine and tryptophan, precursors to neurotransmitters like serotonin, dopamine, norepinephrine, adrenaline, and gamma-aminobutyric acid (GABA). The flavonoid-gut microbiome axis is a complex and multifaceted relationship that has significant implications for neurological health. This review will explore how genetic and environmental factors can impact flavonoid absorption and the positive effects of flavonoids on brain health and the gut microbiota network.Flavonoids alter gut microbiota by replacing pathogens with beneficial bacteria and enhancing SCFA production.Gut microbiota metabolizes flavonoids into bioactive metabolites that influence brain health.Gut microbiota metabolizes flavonoids, turning them to more bioactive metabolitesFlavonoids are potential neuroprotective agents that affect neurological health through their interactions with the gut microbiome.Diet, age, genetics, and epigenetics influence brain health through flavonoid modification and gut microbiome.Flavonoids alter gut microbiota by replacing pathogens with beneficial bacteria and enhancing SCFA production.Gut microbiota metabolizes flavonoids into bioactive metabolites that influence brain health.Gut microbiota metabolizes flavonoids, turning them to more bioactive metabolitesFlavonoids are potential neuroprotective agents that affect neurological health through their interactions with the gut microbiome.Diet, age, genetics, and epigenetics influence brain health through flavonoid modification and gut microbiome. [ABSTRACT FROM AUTHOR]

Arthropathy is a common complication in haemophilia and decreases quality of life. It has been known that concentrations of β-hydroxybutyrate (BHB) in blood are increased by a ketogenic diet, and elevated levels of circulating BHB restricts the progression of inflammation-mediated joint pathological changes. We hypothesized that elevation of blood BHB concentrations could be effective for reducing the progression of bleeding-induced arthropathy by moderating the inflammatory responses of macrophages. In this study, we investigated whether BHB alleviates the arthropathy caused by repeated intra-articular blood injection in rats. To increase blood BHB levels, rats were fed with ketogenic diet. Repeated intra-articular blood injection induced significant joint swelling, whereas ketogenic diet intake significantly increased blood BHB concentrations and ameliorated the joint swelling. The periarticular tissue-fibrosis observed in the control diet intake group appeared to be significantly alleviated in the ketogenic diet intake group. In addition, the IL-1β, which is involved in the progression of arthropathy, levels in the supernatants of blood-exposed macrophages derived from THP-1 cell line were significantly suppressed by BHB supplementation. In summary, BHB moderated the pathological joint changes caused by intra-articular blood exposure. [ABSTRACT FROM AUTHOR]

Alcohol use disorder (AUD) represents a public health crisis with few FDA-approved medications for its treatment. Growing evidence supports the key role of the bidirectional communication between the gut microbiota and the central nervous system (CNS) during the initiation and progression of alcohol use disorder. Among the different protective molecules that could mediate this communication, short chain fatty acids (SCFAs) have emerged as attractive candidates, since these gut microbiota-derived molecules have multi-target effects that could normalize several of the functional and structural parameters altered by chronic alcohol abuse. The present study, conducted in male alcohol-preferring UChB rats, shows that the initiation of voluntary ethanol intake was inhibited in 85% by the intragastric administration of a combination of SCFAs (acetate, propionate and butyrate) given before ethanol exposure, while SCFAs administration after two months of ethanol intake induced a 90% reduction in its consumption. These SCFAs therapeutic effects were associated with (1) a significant reduction of ethanol-induced intestinal inflammation and damage; (2) reduction of plasma lipopolysaccharide levels and hepatic inflammation; (3) reduction of ethanol-induced astrocyte and microglia activation; and (4) attenuation of the ethanol-induced gene expression changes within the nucleus accumbens. Finally, we determined that among the different SCFAs evaluated, butyrate was the most potent, reducing chronic ethanol intake in a dose–response manner. These findings support a key role of SCFAs, and especially butyrate, in regulating AUD, providing a simple, inexpensive, and safe approach as a preventive and intervention-based strategy to address this devastating disease. [ABSTRACT FROM AUTHOR]

This study explores the development of whole-grain sourdough bread with reduced FODMAP (fermentable oligosaccharides, disaccharides, monosaccharides, and polyols) content to offer dietary solutions for individuals with irritable bowel syndrome (IBS). Three sourdough breads were prepared using different lactic acid bacteria (LAB) strains including Lactiplantibacillus plantarum FST1.7 (SD-FST1.7), Lacticaseibacillus paracasei R3 (SD-R3), and Pediococcus pentosaceus RYE106 (SD-RYE106). A control sourdough bread was prepared using baker's yeast (SD-control). In vitro digestion and in vitro colonic fermentation were employed on bread samples with cellulose (negative control) and inulin (positive control), followed by 16S rRNA sequencing and short-chain fatty acid (SCFA) analysis to evaluate the impact on gut microbiota and SCFA levels. Alpha and beta diversity did not reveal any significant differences within the groups following in vitro colonic fermentation (FDR > 0.05). Taxonomic analysis displayed Firmicutes as the predominant phylum across all fecal samples at the end of colonic fermentation. Actinobacteriota was significantly lower in cellulose fermented fecal samples compared to samples fermented with SD-Control (ANCOMBC, FDR = 0.02) and inulin (ANCOMBC, FDR = 0.0001). Fecal samples fermented with inulin had significantly higher Bacteroidota levels compared to those fermented with cellulose (ANCOMBC, FDR =0.002). Acetate levels were higher in fecal samples fermented with SD-FST1.7 compared to those fermented with SD-R3 and SD-RYE106 (p = 0.03 for both). Positive correlations between butyrate and Lachnospira , Agathobacter , and Bifidobacterium were observed, demonstrating the potential of sourdough fermentation to influence gut health and support IBS management. [ABSTRACT FROM AUTHOR]

Background: Specific sources of dietary fibres in sow gestation and lactation diets, such as inulin or wheat bran, have been shown to affect both the sow and its litter health by modulating the piglet's intestinal microbial population and composition. However, only a few studies have reported the effects of some specific fractions of the cell wall of the plants in the sow's lactation diet. Therefore, this study investigates the effect of increasing the level of HCs in a sow's lactation diet on the nutrient apparent total tract digestibility (ATTD), the faecal volatile fatty acid (VFA) profile, the microbiota of the sow and the microbiota and the performances of slow-growing (SG) and fast-growing (FG) piglets. Results: Increasing HCs level increased (P < 0.05) the proportions of butyrate and valerate on day 3, and the ATTD of acid detergent fibres (ADF), neutral detergent fibres (NDF), and gross energy and decreased (P < 0.05) the proportion of propionate on day 17, and the ATTD of crude protein. The beta diversity was affected (r2 = 0.11; P = 0.02) by the maternal dietary treatments with 11 common genera differing (P < 0.05) in the sow's faecal microbiota, and five in the piglet's microbiota. Regardless of the maternal dietary treatment, SG piglets had a lower (P < 0.05) proportion of isobutyrate and isovalerate, a lower (P < 0.05) abundance of Lachnospiraceae_XPB1014_group, Enterococcus, and Succinovibrio genera, and a greater (P < 0.05) abundance of Olsenella than FG piglets. Conclusions: Increased HCs level in a sow's lactation diet affects the ATTD of nutrients, the faecal VFA and microbiota profiles of the sows with limited effects on SG and FG piglets' faecal microbiota and no effects on the performance or VFA profile of these piglets. [ABSTRACT FROM AUTHOR]

Simple Summary: Short-chain fatty acids have been shown to play a role both in the maintenance of a healthy mucosal barrier and the recovery following injury. The objective of this study is to determine whether there are differences in butyrate concentrations between horses with surgical large colon obstructive lesions and healthy horses both during and after surgery. Three key short-chain fatty acids were assessed: butyrate; propionate; and acetate. We did not find any significant differences between butyrate content in the colon of horses undergoing surgical intervention for large colonic obstructive lesions and healthy controls; additionally, there was no difference in fecal butyrate content and controls within the initial post-operative period. Despite this, we noted an alteration in the proportions of the three short-chain fatty acids in relation to one another. While these differences were not statistically significant, they represented an area requiring further research to fully investigate the roles of short-chain fatty acids in equine large colon obstructive lesions. A major cause of morbidity and mortality in horses with large colon obstructive lesions is injury to the colonic mucosal barrier from ischemic injury. Since butyrate has been shown to play a critical role in the maintenance of a healthy mucosal barrier, it may play a role in the recovery process. This study's objective was to determine whether the differences in butyrate concentrations existed between horses with surgical large colon obstructive lesions and healthy horses both during and after surgery. Eleven horses presenting with surgical colic lesions were enrolled; colonic samples were acquired during surgery, and fecal samples were obtained 36 h later. Colonic and fecal samples were also obtained from control groups. Samples were analyzed for butyrate, acetate, and propionate concentrations. There was no significant difference in butyrate content between surgical colonic or fecal samples and controls; however, an alteration in the proportion of SCFAs in relation to one another was noted. These changes in the individual SCFA levels were not statistically significant. The study findings demonstrated that there were no significant differences in butyrate proportions when comparing samples from horses with surgical colic lesions to healthy control horses. [ABSTRACT FROM AUTHOR]

Accumulated data indicate that epigenetic regulations, including histone modifications and DNA methylation, are important means for adjusting the expression of genes in response to various stimuli. In contrast to the success in studying the role of DNA methylation in laboratory rodents, the role of DNA methylation in the terrestrial snail Helix lucorum has been studied only in behavioral experiments. This prompted us to further investigate the role of DNA methylation and the interaction between DNA methylation and histone acetylation in the mechanisms of neuroplasticity in terrestrial snails using in vitro experiments. Dysregulation of DNA methylation by the DNMT inhibitor RG108 significantly suppressed the long-term potentiation (LTP) of synaptic inputs in identified neurons. We then tested whether the RG108-induced weakening of potentiation can be reversed under co-application of histone deacetylase inhibitors sodium butyrate or trichostatin A. It was found that increased histone acetylation significantly compensated for RG108-induced LTP deficiency. These data bring important insights into the functional role of DNA methylation as an important regulatory mechanism and a necessary condition for the development and maintenance of long-term synaptic changes in withdrawal interneurons of terrestrial snails. Moreover, these results support the idea of the interaction of DNA methylation and histone acetylation in the epigenetic regulation of synaptic plasticity. [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.)

Recent research suggests that microbial molecules translocated from the intestinal lumen into the host's internal environment may play a role in various physiological functions, including sleep. Previously, we identified that butyrate, a short-chain fatty acid produced by intestinal bacteria, and lipoteichoic acid, a cell wall component of gram-positive bacteria, induce sleep when their naturally occurring translocation is mimicked by direct delivery into the portal vein. Building upon these findings, we aimed to explore the sleep signaling potential of intraportally administered lipopolysaccharide (LPS), a primary component of gram-negative bacterial cell walls, in rats. Low dose of LPS (1 μg/kg) increased sleep duration and prolonged fever, without affecting systemic LPS levels. Interestingly, administering LPS systemically outside the portal region at a dose 20 times higher did not affect sleep, indicating a localized sensitivity within the hepatoportal region for the sleep and febrile effects of LPS. Furthermore, both the sleep- and fever-inducing effects of LPS were inhibited by indomethacin, a prostaglandin synthesis inhibitor, and replicated by intraportal administration of prostaglandin E2 or arachidonic acid, suggesting the involvement of the prostaglandin system in mediating these actions. [ABSTRACT FROM AUTHOR]

The butyrate biosynthetic pathway not only contributes to electron management and energy generation in butyrate forming bacteria, but also confers evolutionary advantages to the host by inhibiting the growth of surrounding butyrate-sensitive microbes. While high butyrate levels induce toxic stress, effects of non-toxic levels on cell growth, health, metabolism, and sporulation remain unclear. Here, we show that butyrate stimulates cellular processes of Clostridium acetobutylicum , a model butyrate forming Firmicute. First, we deleted the 3-hydroxybutyryl-CoA dehydrogenase gene (hbd) from the C. acetobutylicum chromosome to eliminate the butyrate synthetic pathway and thus butyrate formation. A xylose inducible Cas9 cassette was chromosomally integrated and utilized for the one-step markerless gene deletions. Non-toxic butyrate levels significantly affected growth, health, and sporulation of C. acetobutylicum. After deleting spo0A , the gene encoding the master regulator of sporulation, Spo0A, and conducting butyrate addition experiments, we conclude that butyrate affects cellular metabolism through both Spo0A-dependent and independent mechanisms. We also deleted the hbd gene from the chromosome of the asporogenous C. acetobutylicum M5 strain lacking the pSOL1 plasmid to examine the potential involvement of pSOL1 genes on the observed butyrate effects. Addition of crotonate, the precursor of butyrate biosynthesis, to the hbd deficient M5 strain was used to probe the role of butyrate biosynthesis pathway in electron and metabolic fluxes. Finally, we found that butyrate addition can enhance the growth of the non-butyrate forming Clostridium saccharolyticum. Our data suggest that butyrate functions as a stimulator of cellular processes, like a growth factor, in C. acetobutylicum and potentially evolutionarily related Clostridium organisms. • Deployed chromosomally integrated spCas9 for markerless one-step Clostridium acetobutylicum genome engineering. • Deleted 3-hydroxybutyryl-CoA dehydrogenase gene (hbd) from Clostridium acetobutylicum chromosome. • Elucidated the roles of butyrate in cellular processes of Clostridium acetobutylicum. • Demonstrated butyrate as a growth factor stimulating cellular processes in Clostridium acetobutylicum. • Demonstrated butyrate as a potentially growth factor for other Clostridium species. • Suggested butyrate as a potential modulator of microbial population. [ABSTRACT FROM AUTHOR]

T‐2 toxin is a member of class A aspergilloides toxins, one of the most prevalent mycotoxins that contaminate feed and food. Direct ingestion of animals or feed contaminated by T‐2 toxin can cause various animal diseases. Butyrate is an organic fatty acid featuring a four‐carbon chain, which is commonly found in the form of sodium butyrate (NaB). NaB has several biological functions and pharmacological effects. However, the role of sodium butyrate in alleviating T‐2 toxin–induced hepatorenal toxicity has not been explored. In this study, 240 juvenile quails were evenly assigned into 4 groups. The experimental setup comprised four groups: The control group received a standard diet; the toxin group received a diet containing 0.9 mg/kg T‐2 toxin; the butyrate group received a diet containing 0.5 g/kg NaB; and the T‐2 treatment group received a diet containing both 0.9 mg/kg T‐2 toxin and 0.5 g/kg NaB. We evaluated the histopathological changes in the kidney and liver on Days 14 and 28 and explored the molecular mechanisms involving oxidative stress, inflammation, and expression of nuclear xenobiotic receptors (NXRs). Our results showed that T‐2 toxin exposure–induced inflammation in the liver and kidney by activating the oxidative stress pathway and modulating expression of NXRs to regulate related CYP450 isoforms, ultimately leading to histopathological injury in the liver and kidney, whereas sodium butyrate ameliorated this injury. These results offer novel insights into the molecular mechanisms underlying the protective effects of sodium butyrate in mitigating T‐2 toxin–induced hepatorenal injury in juvenile quails. Practical Application: The mechanisms of T‐2 toxin toxicity have been well described in experimental animals, but studies in birds are limited. With the development of society, the market scale of quails farming has been expanding, and the value of quails meat and eggs is increasing; there is an urgent need to clarify the harm of T‐2 toxin to quails and its mechanism. [ABSTRACT FROM AUTHOR]

The article explores the use of probiotic bacteria and butyrate in preventing allergic airway and gut inflammation in humanized mice. The study found that a specific probiotic formulation, BactoFlor® 10/20, and butyrate effectively prevented inflammation in the gut and lungs of mice with allergen-induced inflammation. The protective effect was linked to the modulation of regulatory T cells and the mucosal epithelium. The research highlights the potential of probiotics in managing allergic diseases in the gastrointestinal and respiratory tracts. [Extracted from the article]

Organic solar cells (OSCs) have emerged as a promising technology for renewable energy generation due to their low cost, lightweight, flexibility, and compatibility with roll-to-roll manufacturing. However, OSCs still face challenges in achieving high power conversion efficiency (PCE) due to various factors, including recombination loss. In this study, we investigated the effect of introducing a layer of eight atomic percent gadolinium-doped zinc oxide (Zn0.92Gd0.08O) between the poly(3-hexylthiophene) (P3HT): [6,6]-phenyl butyric acid methyl ester (PCBM) active layer and the fluorine-doped tin oxide (FTO) electrode of the OSC. The reference cell, which has an Au/P3HT:PCBM/ZnO/FTO structure, exhibits a PCE of 0.52%. Remarkably, when the Zn0.92Gd0.08O layer was inserted (Au/P3HT:PCBM/Zn0.92Gd0.08O/FTO), the PCE increased significantly to 3.42%, which is more than six times the increase. Through further analysis, we present that the insertion of the Zn0.92Gd0.08O layer induces spin polarization in the P3HT:PCBM layer, leading to enhanced charge transport and reducing the recombination rate. Based on the findings, it can be concluded that the Zn0.92Gd0.08O film can potentially improve OSC performance. [ABSTRACT FROM AUTHOR]

[Display omitted] The photocatalytic degradation of polychlorinated biphenyls (PCBs) is advancing, yet the efficiency of degradation within the visible spectral range continues to encounter significant challenges. In this study, two biochar-based organic semiconductor photocatalysts, Active Carbon@PTQ10 (5,8-Dibromo-6,7-difluoro-2-(2-hexyldecoxy)quinoxaline; trimethyl-(5-trimethylstannylthiophen-2-yl)stannane): ITIC-Th (Propanedinitrile,2,2′-[[6,6,12,12-tetrakis(5-hexyl-2-thienyl)-6,12-dihydrodithieno[2,3-d: 2′,3′-d'] −s-indaceno[1,2-b:5,6-b'] dithiophene-2,8-diyl] bis[methylidyne(3-oxo-1H-indene-2,1(3H)-diylidene)]] bis-) (AC@PI) and Active Carbon@PTQ10: PC 71 BM (6,6)-phenyl C 71 butyric acid methyl ester), were synthesized using a wide bandgap material, PTQ10, as the electron donor, along with a non-fullerene material, ITIC-Th, and a fullerene material, PC 71 BM, as the acceptors, respectively. Under optimized conditions, AC@PI degraded 93.4 % of 2,2 ',4,4 '-tetrachlorobiphenyl (PCB 47) within 60 min. By incorporating a non-fullerene acceptor (ITIC-Th), AC@PI exhibits a larger surface photopressure, a lower hole-electron transfer ratio, a broader absorption spectrum (400 – 1000 nm), and enhanced structural stability. AC@PI can generate photogenerated electrons and holes, as well as superoxide anions (O 2 −) and hydroxyl radicals (OH), through type II heterojunctions, which contributes to its exceptional properties. This study synthesized novel organic semiconductor catalysts that offer a green, efficient, and non-toxic method for the degradation of aromatic pollutants, such as polychlorinated biphenyls. [ABSTRACT FROM AUTHOR]

Background Methods Results Conclusion Accumulating evidence has suggested that neuropeptides such as orexin, ghrelin, or oxytocin act centrally in the brain to regulate intestinal barrier function through the vagus nerve. It has been reported that the vagal cholinergic anti‐inflammatory pathway was blocked by splenectomy. In the present study, we therefore examined the effect of splenectomy on neuropeptides‐induced improvement of increased intestinal permeability.Colonic permeability was determined in vivo by quantifying the absorbed Evans blue in colonic tissue for 15 min spectrophotometrically in rats.Splenectomy increased colonic permeability. The increased permeability by splenectomy was significantly blocked by vagal activation induced by carbachol or 2‐deoxy‐d‐glucose which was prevented by atropine, suggesting vagal activation could prevent colonic hyperpermeability in splenectomized rats. In the splenectomized rats, intracisternal injection of orexin, ghrelin, oxytocin, or butyrate failed to inhibit increased colonic permeability while intracisternal glucagon‐like peptide‐1 (GLP‐1) analogue, liraglutide, potently blocked the increased colonic permeability in a dose‐dependent manner. The liraglutide‐induced improvement of increased colonic permeability was blocked by atropine in splenectomized rats. Intracisternal injection of GLP‐1 receptor antagonist attenuated 2‐deoxy‐d‐glucose‐induced improvement of colonic hyperpermeability in splenectomized rats.The present results suggested that the spleen is important in the improvement of intestinal barrier function by brain orexin, ghrelin or oxytocin, and butyrate. On the other hand, GLP‐1 acts centrally in the brain to improve colonic hyperpermeability in a spleen‐independent manner. All these results suggest that dual mechanisms (spleen dependent or independent) may exist for the brain‐gut regulation in intestinal barrier function. [ABSTRACT FROM AUTHOR]

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A finely tuned balance between excitation and inhibition (E/I) is essential for proper brain function. Disruptions in the GABAergic system, which alter this equilibrium, are a common feature in various types of neurological disorders, including autism spectrum disorders (ASDs). Mutations in Phosphatase and Tensin Homolog (PTEN), the main negative regulator of the phosphatidylinositol 3-phosphate kinase/Akt pathway, are strongly associated with ASD. However, it is unclear whether PTEN deficiencies can differentially affect inhibitory and excitatory signaling. Using the Caenorhabditis elegans neuromuscular system, where both excitatory (cholinergic) and inhibitory (GABAergic) inputs regulate muscle activity, we found that daf-18/PTEN mutations impact GABAergic (but not cholinergic) neurodevelopment and function. This selective impact results in a deficiency in inhibitory signaling. The defects observed in the GABAergic system in daf-18/PTEN mutants are due to reduced activity of DAF-16/FOXO during development. Ketogenic diets (KGDs) have proven effective for disorders associated with E/I imbalances. However, the mechanisms underlying their action remain largely elusive. We found that a diet enriched with the ketone body β-hydroxybutyrate during early development induces DAF-16/FOXO activity, therefore improving GABAergic neurodevelopment and function in daf-18/PTEN mutants. Our study provides valuable insights into the link between PTEN mutations and neurodevelopmental defects and delves into the mechanisms underlying the potential therapeutic effects of KGDs. [ABSTRACT FROM AUTHOR]

Recent studies underscore the role of gut and oral microbiota in influencing neuroinflammation through the microbiota–gut–brain axis, including in Alzheimer's disease (AD). This review aims to provide a comprehensive synthesis of recent findings on the involvement of gut and oral microbiota in the neuroinflammatory processes associated with AD, emphasizing novel insights and therapeutic implications. This review reveals that dysbiosis in AD patients' gut and oral microbiota is linked to heightened peripheral and central inflammatory responses. Specific bacterial taxa, such as Bacteroides and Firmicutes in the gut, as well as Porphyromonas gingivalis in the oral cavity, are notably altered in AD, leading to significant changes in microglial activation and cytokine production. Gut microbiota alterations are associated with increased intestinal permeability, facilitating the translocation of endotoxins like lipopolysaccharides (LPS) into the bloodstream and exacerbating neuroinflammation by activating the brain's toll-like receptor 4 (TLR4) pathways. Furthermore, microbiota-derived metabolites, including short-chain fatty acids (SCFAs) and amyloid peptides, can cross the blood-brain barrier and modulate neuroinflammatory responses. While microbial amyloids may contribute to amyloid-beta aggregation in the brain, certain SCFAs like butyrate exhibit anti-inflammatory properties, suggesting a potential therapeutic avenue to mitigate neuroinflammation. This review not only highlights the critical role of microbiota in AD pathology but also offers a ray of hope by suggesting that modulating gut and oral microbiota could represent a novel therapeutic strategy for reducing neuroinflammation and slowing disease progression. [ABSTRACT FROM AUTHOR]

Inflammatory bowel disease is a chronic condition characterized by recurrent intestinal inflammation. Its etiopathogenesis is driven by a series of events that disrupt the mucosal barrier, alter the healthy balance of intestinal microbiota, and abnormally stimulate intestinal immune responses. Therefore, numerous studies suggest the use of short-chain fatty acids and their immunomodulatory effects as a therapeutic approach in this disease. The objective of this systematic review was to synthesize previous evidence on the relevance and therapeutic use of short-chain fatty acids, particularly butyrate, in the immune regulation of inflammatory bowel disease. This systematic review of articles linking inflammatory bowel disease with short-chain fatty acids was conducted according to the PRISMA-2020 guidelines. The Medline and the Web of Science databases were searched in August 2024. The risk of bias was assessed using the Joanna Briggs Institute checklists. A total of 1460 articles were reviewed, of which, 29 met the inclusion criteria. Short-chain fatty acids, particularly butyrate, play a critical role in the regulation of intestinal inflammation and can be used as a strategy to increase the levels of short-chain fatty acid-producing bacteria for use in therapeutic approaches. [ABSTRACT FROM AUTHOR]

This study explores the application of pillar nanostructures in organic solar cells (OSCs). The aluminum pillar nanostructures (AlPNSs) are fabricated on an active layer surface comprising of a blend poly(3‐hexylthiophene‐2,5‐diyl) and [6,6]‐phenyl C61 butyric acid methyl ester using nanoimprinting. Aluminum back electrodes are formed, resulting in AlPNSs with an imprinted pattern height of 60 ± 6 nm and a pitch of 212 ± 49 nm. Atomic force microscope images and current density versus voltage curves are obtained for the fabricated devices, both with and without AlPNSs. The results indicate a solar cell efficiency increase of 15.16% in the AlPNS OSCs compared to the reference cells. To investigate the role of AlPNSs in the enhancement, impedance spectroscopy, incident photon‐to‐current efficiency, UV–Vis reflection spectroscopy, and finite‐difference time‐domain simulations are performed for the both devices. The results demonstrate that the combination of propagating surface plasmon resonance and light‐trapping properties due to AlPNSs significantly enhances the overall optical performance. This research provides new insights into the potential of imprinted nanostructures for enhancing OSC performance, including their plasmonic and optical characteristics. [ABSTRACT FROM AUTHOR]

Copyright of Science & Technology of Food Industry is the property of Science & Technology of Food Industry Editorial Office 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.)

Flat black tea (FBT) has been innovatively developed to alleviate homogenisation competition, but the dynamic changes in aroma components during the process remain unclear. This study employed HS-SPME-GC-MS to analyse the aroma components of tea samples from various processing stages of FBT, and to make a comparative assessment with conventional strip-like Congou black tea (SBT). Additionally, a proteomic analysis was conducted on fresh leaves, withered leaves, and frozen–thawed leaves. Significant changes were observed in the aroma components and proteins during the processing. The results of the multivariate and odour activity value analysis demonstrated that the principal aroma components present during the processing of FBT were linalool, (E)-2-hexen-1-al, methyl salicylate, geraniol, hexanal, benzeneacetaldehyde, (Z)-3-hexenyl butyrate, dimethyl sulphide, 2-methylbutanal, 2-ethylfuran, nonanal, nonanol, 3-methylbutanal, (Z)-3-hexen-1-ol, 2-pentylfuran, linalool oxide I, and β-myrcene. Freezing–thawing and final roasting are the key processing steps for forming the aroma quality of FBT. The final roasting yielded a considerable quantity of pyrazines and pyrroles, resulting in a high-fried aroma, but caused a significant reduction in linalool, geraniol, β-myrcene, and esters, which led to a loss of floral and fruity aromas. The freezing–thawing treatment resulted in an accelerated loss of aroma substances, accompanied by a decrease in the expression level of lipoxygenase and 2-C-methyl-D-erythritol 2,4-cyclodiphosphate synthase. The formation of aroma substances in the linoleic acid metabolic pathway and terpenoid metabolic process was hindered, which had a negative impact on tea aroma. This study elucidates the causes of unsatisfactory aroma quality in tea products made from frozen tea leaves, providing theoretical support for the utilisation of frostbitten tea leaves, and helps us to understand the mechanism of aroma formation in black tea. [ABSTRACT FROM AUTHOR]

Highlights The present research investigates the influence of chemical modifications on the surface of Diss fibers (Ampelodesmos mauritanicus) as an effective reinforcing agent for biocomposites based on poly (3‐hydroxybutyrate‐co‐3‐hydroxyvalerate) (PHBV). The Diss fiber surface underwent three different chemical treatments: alkaline, alkaline/peroxide, and alkaline/silane. Changes in morphology, mechanical properties, thermomechanical behavior, and contact angle measurements of the biocomposite materials were studied according to the following weight ratio PHBV/Diss fibers 80/20. Scanning electron microscopy (SEM) analysis of the fractured surface of the biocomposite samples revealed improved adhesion between Diss fibers and the PHBV matrix after surface modification, compared with the unmodified sample. The study demonstrated that the incorporation of Diss fibers leads to an enhancement in the mechanical performances of PHBV‐based biocomposites. The tensile properties of the modified biocomposites showed a significant increase in Young's modulus compared with the biocomposites with untreated fiber. Similar trends were observed in the data obtained from dynamic mechanical analysis (DMA) and contact angle measurement. Overall, the study highlights the beneficial effects of Diss fibers modification, particularly with the alkali–silane combination, in enhancing the properties of PHBV biocomposites, there by broadening their potential application fields. The study explores the potential of Diss fibers as an effective reinforcement for PHBV‐based biocomposites. Fully biodegradable biocomposites based on PHBV/Diss fibers are melt‐compounded. Diss fibers are chemically modified by alkaline, alkaline/peroxide, and alkaline/silane. The chemical treatment has considerably enhanced the properties and morphology of the biocomposites, being however much higher for alkaline/silane treatment. The method can be used for specific applications and large‐scale production. [ABSTRACT FROM AUTHOR]

Astragalus polysaccharide is one of the most extensively studied traditional Chinese medicinal polysaccharides because of its immunomodulatory activity and has attracted considerable attention. Existing evidence suggests that its potential immunomodulatory mechanism is related to the modulation of intestinal microbiota. However, current research methods on the gut microbiota mainly focus on 16S rRNA sequencing, providing limited evidence of specific changes in functional bacterial groups in the intestine. Butyrate is a class of short‐chain fatty acids among the microbial metabolites in the gut and is most closely associated with immunomodulatory activity. Thus, in this study, we extracted and purified a polysaccharide from astragalus composed of a main chain of →4)‐α‐D‐Glcp‐(1 → and →4,6)‐α‐D‐Glcp‐(1→, with side chains of →6)‐α‐D‐Glcp‐(1→ and aggregated arabinose, and investigated the changes in butyrate‐producing bacterial groups in mice during the immunomodulation process of astragalus polysaccharide, using two butyrate‐producing bacterial‐specific primers. The results showed that oral administration of astragalus polysaccharide significantly increased butyrate production in the mouse intestine, restoring the disrupted butyrate‐producing bacterial abundance and diversity caused by immunosuppression. In conclusion, our study provides the first evidence of the targeted modulation of the butyrate‐producing gut microbiota by astragalus polysaccharide, offering insights into its pharmacological activity. [ABSTRACT FROM AUTHOR]

Atopic dermatitis (AD) is characterized by a T-helper cell type 2 (Th2) inflammatory response leading to skin damage with erythema and edema. Comparative fecal sample analysis has uncovered a strong correlation between AD and Faecalibacterium prausnitzii strain A2-165, specifically associated with butyrate production. Therefore, understanding the functional mechanisms of crucial enzymes in the butyrate pathway, such as 3-hydroxybutyryl-CoA dehydrogenase of A2-165 (A2HBD), is imperative. Here, we have successfully elucidated the three-dimensional structure of A2HBD in complex with acetoacetyl-CoA and NAD+ at a resolution of 2.2Å using the PAL-11C beamline (third generation). Additionally, X-ray data of A2HBD in complex with acetoacetyl-CoA at a resolution of 1.9 Å were collected at PAL-XFEL (fourth generation) utilizing Serial Femtosecond Crystallography (SFX). The monomeric structure of A2HBD consists of two domains, N-terminal and C-terminal, with cofactor binding occurring at the N-terminal domain, while the C-terminal domain facilitates dimerization. Our findings elucidate the binding mode of NAD+ to A2HBD. Upon acetoacetyl-CoA binding, the crystal structure revealed a significant conformational change in the Clamp-roof domain (root-mean-square deviation of 2.202 Å). Notably, residue R143 plays a critical role in capturing the adenine phosphate ring, underlining its significance in substrate recognition and catalytic activity. The binding mode of acetoacetyl-CoA was also clarified, indicating its lower stability compared to NAD+. Furthermore, the conformational change of hydrophobic residues near the catalytic cavity upon substrate binding resulted in cavity shrinkage from an open to closed conformation. This study confirms the conformational changes of catalytic triads involved in the catalytic reaction and presents a proposed mechanism for substrate reduction based on structural observations. [ABSTRACT FROM AUTHOR]

Colorectal carcinoma (CRC) is one of the most common malignant tumors in the digestive tract. It was found that butyric acid could inhibit the expression of miR-183 to slow down malignant progression of CRC in the early stage. However, its regulatory mechanism remains unclear. This study screened the IC50 value of butyrate on inhibition of CRC cells malignant progression. Its inhibitory effects were detected by MTT assay, colony formation experiment, Transwell migration experiment, and apoptosis evaluation by flow cytometry. Next, the expressions of miR-183 and DNAJB4 were, respectively, determined in butyrate treated and miR-183 analog or si-DNAJB4-transfected CRC cells to further detect the role of upregulated miR-183 or silencing DNAJB4 in CRC cells malignant progression. Subsequently, the targeted regulatory relationship between miR-183 and si-DNAJB4 was confirmed by bioinformatic prediction tools and double luciferase report genes analysis method. The regulatory mechanism of butyrate on miR-183/DNAJB4 axis signal pathway was evaluated in molecular level, and verified in nude mouse xerograft tumor model and immunohistochemical analysis tests of Ki67 positive rates. The results displayed that butyrate with increased concentration can hinder the proliferation and improve apoptosis of CRC cells by decreasing the expression of miR-183. Thus, butyrate reduces miR-183 expression and increases DNAJB4 expression via the miR-183/DNAJB4 axis, ultimately inhibiting the malignant progression and increasing apoptosis of CRC. While over expression of miR-183 downregulate the expression of DNAJB4, which can reverse the inhibitory effect of butyrate. [ABSTRACT FROM AUTHOR]

A maternal diet rich in dietary fiber, such as β-glucan, plays a crucial role in the offspring's acquisition of gut microbiota and the subsequent shaping of its microbiome profile and metabolome. This in turn has been shown to aid in neurodevelopmental processes, including early microglial maturation and immunomodulation via metabolites like short chain fatty acids (SCFAs). This study aimed to investigate the effects of oat β-glucan supplementation, solubilized by citric acid hydrolysis, from gestation to adulthood. Female C57BL/6J mice were orally supplemented with soluble oat β-glucan (ObG) or carboxymethyl cellulose (CMC) via drinking water at 200 mg/kg body weight during breeding while the control group received 50 mg/kg body weight of carboxymethyl cellulose. ObG supplementation increased butyrate production in the guts of both dams and 4-week-old pups, attributing to alterations in the gut microbiota profile. One-week-old pups from the ObG group showed increased neurodevelopmental markers similar to four-week-old pups that also exhibited alterations in serum markers of metabolism and anti-inflammatory cytokines. Notably, at 8 weeks, ObG-supplemented pups exhibited the highest levels of spatial memory and cognition compared to the control and CMC groups. These findings suggest a potential enhancement of neonatal neurodevelopment via shaping of early-life gut microbiome profile, and the subsequent increased later-life cognitive function. [ABSTRACT FROM AUTHOR]

Butyrate, a short-chain fatty acid (SCFA) produced by the fermentation of dietary fibers in the colon, plays a pivotal role in regulating metabolic health, particularly by enhancing insulin sensitivity. Given the rising incidence of metabolic disorders, understanding the factors that influence butyrate production is of significant interest. This study explores the link between salivary amylase activity and butyrate levels in overweight women of reproductive age. Participants were categorized into low (LSA) and high (HSA) salivary amylase activity groups and further divided into two subgroups: one followed a low-starch diet (LS), and the other underwent caloric restriction (CR). We assessed salivary amylase activity and measured serum butyrate concentrations to examine their associations. Our findings showed a significant, though weak, positive correlation (ρ = 0.0486, p < 0.05), suggesting a link between salivary amylase activity and butyrate levels. The statistical significance, despite the weak correlation, implies that this relationship is not random. Moreover, higher baseline butyrate levels were observed in women with elevated salivary amylase activity. Also, women with low salivary amylase activity on a low-starch diet experienced a more pronounced increase in butyrate levels compared to those on caloric restriction. These results suggest that salivary amylase activity and dietary intake interact to influence butyrate production, with potential implications for improving insulin sensitivity and metabolic health. The study underscores the potential of butyrate in enhancing insulin sensitivity and promoting overall metabolic well-being. Further research is necessary to clarify the mechanisms involved and to understand the long-term effects of butyrate on metabolic health across different populations. [ABSTRACT FROM AUTHOR]

Bacterial therapy for colorectal cancer (CRC) represents a burgeoning frontier. The probiotic Limosilactobacillus fermentum GR-3, derived from traditional food "Jiangshui", exhibited superior antioxidant capacity by producing indole derivatives ICA and IPA. In an AOM/DSS-induced CRC mouse model, GR-3 treatment alleviated weight loss, colon shortening, rectal bleeding and intestinal barrier disruption by reducing oxidative stress and inflammation. GR-3 colonization in distant colon induced apoptosis and reduced tumor incidence by 51.2%, outperforming the control strain and vitamin C. The beneficial effect of GR-3 on CRC was associated with gut microbiome modulation, increasing SCFA producer Lachnospiraceae NK4A136 group and suppressing pro-inflammatory strain Bacteroides. Metagenomic and metabolic analyses revealed that GR-3 intervention upregulated antioxidant genes (xseA, ALDH) and butyrate synthesis gene (bcd), while increasing beneficial metabolites (SCFAs, ICA, IPA, VB12 and VD3) and reducing harmful secondary bile acids. Overall, GR-3 emerges as a promising candidate in CRC therapy, offering effective gut microbiome remediation. [ABSTRACT FROM AUTHOR]

The experiment aimed to investigate the effects of different levels of Chinese herbal additives on the growth performance, serum biochemical indicators, and diarrhea condition of lactating lambs, in order to screen for the appropriate addition level. A total of 48 healthy male lactating lambs with an aged 23 days and a body weight of (6.59±0.03) kg were selected and divided into four groups using a single-factor randomized block design, with three replicates per group and four lambs per replicate. The control group was fed with a basic concentrate, while the experimental groups were fed with concentrate feed containing 0.1% (group 1), 0.3% (group 2), and 0.5% (group 3) Chinese herbal additives, respectively. The trial period was 37 days, with a preliminary trial period of 7 days and a formal trial period of 30 days. The results indicated that compared to the control group, group 1, and group 2, the weight of lambs in the group 3 was extremely increased at 45 and 60 days of age (P<0.01), and the average daily weight gain was extremely increased from 30 to 60 days of age (P<0.01). Compared to the control group, the weight of lambs in the group 2 was extremely increased at 60 days of age (P<0.01), and the feed-to-gain ratio was extremely decreased for the groups 2 and 3 from 30 to 60 days of age (P<0.01). Compared to the control group, the levels of serum glucose (GLU), insulin (INS), total cholesterol (TC), triglycerides (TG), and total protein (TP) in lambs from the group 3 were extremely increased (P<0.01), the albumin (ALB) content was significantly increased (P<0.05), glucagon (PG) content was extremely decreased (P<0.01), and non-esterified fatty acids (NEFA) content was significantly decreased (P<0.05). The TP content in lambs from the group 2 was significantly increased (P<0.05). The levels of β-hydroxybutyrate (β-HB) and blood urea nitrogen (BUN) in lambs from the groups 2 and 3 were significantly decreased (P<0.05), and uric acid (UA) content was extremely decreased (P<0.01). Compared to the control group, the diarrhea rate was extremely decreased (P<0.01), and the recovery rate was extremely increased (P<0.01), with a significant decrease in recovery time (P<0.01) for lambs in the groups 2 and 3. Studies show that the addition of Chinese herbal additives to lactating lamb concentrate can improve the growth performance of lambs, enhance the metabolism synthesis of nutrients, prevent and control the occurrence of diarrhea and accelerate the recovery of diarrhea in lambs, and the addition amount of 0.5% is the best effect. [ABSTRACT FROM AUTHOR]

Alcoholic liver disease (ALD) is a globally prevalent form of liver disease for which there is no effective treatment. Recent studies have found that a significant decrease in butyrate was closely associated with ALD development. Given the low compliance and delivery efficiency associated with oral-route butyrate administration, a highly effective butyrate-yielding dietary supplement, butyrylated high-amylose maize starch (HAMSB), is a good alternative approach. Here, we synthesized HAMSB, evaluated the effect of HAMSB on acute ALD in mice, compared its effect with that of oral administration of butyrate, and further studied the potential mechanism of action. The results showed HAMSB alleviated acute ALD in mice, as evidenced by the inhibition of hepatic-function impairment and the improvement in liver steatosis and lipid metabolism; in these respects, HAMSB supplementation was superior to oral sodium butyrate administration. These improvements can be attributed to the reduction of oxidative stress though the regulation of Nrf2-mediated antioxidant signaling in the liver and the improvement in the composition and function of microbiota in the intestine. In conclusion, HAMSB is a safe and effective dietary supplement for preventing acute ALD that could be useful as a disease-modifying functional food or candidate medicine. [ABSTRACT FROM AUTHOR]

Maternal high-fat diet intake has profound effects on the long-term health of offspring, predisposing them to a higher susceptibility to obesity and metabolic dysfunction-associated steatotic liver disease. However, the detailed mechanisms underlying the role of a maternal high-fat diet in hepatic lipid accumulation in offspring, especially at the weaning age, remain largely unclear. In this study, female C57BL/6J mice were randomly assigned to either a high-fat diet or a control diet, and lipid metabolism parameters were assessed in male offspring at weaning. Gut microbiota analysis and targeted metabolomics of short-chain fatty acids (SCFAs) in these offspring were further performed. Both in vivo and in vitro studies were conducted to explore the role of butyrate in hepatic cholesterol excretion in the liver and HepG2 cells. Our results showed that maternal high-fat feeding led to obesity and dyslipidemia, and exacerbated hepatic lipid accumulation in the livers of offspring at weaning. We observed significant decreases in the abundance of the Firmicutes phylum and the Allobaculum genus, known as producers of SCFAs, particularly butyrate, in the offspring of dams fed a high-fat diet. Additionally, maternal high-fat diet feeding markedly decreased serum butyrate levels and down-regulated ATP-binding cassette transporters G5 (ABCG5) in the liver, accompanied by decreased phosphorylated AMP-activated protein kinase (AMPK) and histone deacetylase 5 (HADC5) expressions. Subsequent in vitro studies revealed that butyrate could induce ABCG5 activation and alleviate lipid accumulation via the AMPK-pHDAC5 pathway in HepG2 cells. Moreover, knockdown of HDAC5 up-regulated ABCG5 expression and promoted cholesterol excretion in HepG2 cells. In conclusion, our study provides novel insights into how maternal high-fat diet feeding inhibits hepatic cholesterol excretion and down-regulates ABCG5 through the butyrate-AMPK-pHDAC5 pathway in offspring at weaning. [ABSTRACT FROM AUTHOR]

3-Nitrooxypropanol (3-NOP) is a nitrooxy compound that specifically targets methyl-coenzyme M reductase (MCR), ultimately resulting in a reduction in methane production. In this study, we undertook an in vitro investigation of the effects of different dosages of 3-NOP on ruminal fermentation parameters, methane production, and the microbial community. A single-factor completely randomized design was adopted, comprising a control treatment (C), where no 3-NOP was added to the fermentation substrate, and three 3-NOP treatments, where 0.025 mg (low-dose treatment, LD), 0.05 mg (medium-dose treatment, MD), or 0.1 mg (high-dose treatment, HD) was added to 1 g of fermentation substrate (DM basis), followed by incubation for 24 h in vitro. The results showed that, compared with the control treatment, the three dosages of 3-NOP reduced total gas production, methane production, and acetate production (all p < 0.01). In contrast, 3-NOP treatment increased H2 production and the molar proportions of propionate and butyrate (all p ≤ 0.02), resulting in a decrease in the acetate-propionate ratio (p < 0.01). Meanwhile, the microbial profiles were not altered by the treatments, but the relative abundances of Prevotella, Methanobrevibacter, and Ophryoscolex were increased by the MD and HD treatments (all p < 0.01), whereas those of Methanosarcina, Methanosaeta, Sphaerochaeta, RFN20, Entodinium, and Diplodinium were decreased by the HD treatment (all p ≤ 0.03). Moreover, the results of a correlation analysis showed that there was a certain correlation between these microorganisms and total gas production, methane production, H2 production, acetate, propionate, and butyrate. In summary, under in vitro conditions, the addition of 3-NOP to the diet affected the microbial community structure, thereby altering the ruminal fermentation pattern and reducing methane production. Our results indicated that 0.05 mg per g of dietary DM is the recommended inclusion ratio for 3-NOP in the diet of lambs. [ABSTRACT FROM AUTHOR]