Journal of Nutritional Biochemistry最新文献

{"title":"Anti-obesity effect of butyrate links to modulation of gut microbiome and epigenetic regulation of muscular circadian clock","authors":"Jinyoung Shon ,&nbsp;Yerim Han ,&nbsp;Seungmin Song ,&nbsp;So Young Kwon ,&nbsp;Khuhee Na ,&nbsp;Anders M. Lindroth ,&nbsp;Yoon Jung Park","doi":"10.1016/j.jnutbio.2024.109590","DOIUrl":"10.1016/j.jnutbio.2024.109590","url":null,"abstract":"<div><p>The role of the muscle circadian clock in regulating oxidative metabolism exerts a significant influence on whole-body energy metabolism; however, research on the connection between the muscle circadian clock and obesity is limited. Moreover, there is a lack of studies demonstrating the regulatory effects of dietary butyrate on muscle circadian clock and the resulting antiobesity effects. This study aimed to investigate the impacts of dietary butyrate on metabolic and microbiome alterations and muscle circadian clock in a diet-induced obesity model. Male Sprague–Dawley rats were fed a high-fat diet with or without butyrate. Gut microbiota and serum metabolome were analyzed, and molecular changes were examined using tissues and a cell line. Further correlation analysis was performed on butyrate-induced results. Butyrate supplementation reduced weight gain, even with increased food intake. Gut microbiome analysis revealed an increased abundance of <em>Firmicutes</em> in butyrate group. Serum metabolite profile in butyrate group exhibited reduced amino acid and increased fatty acid content. Muscle circadian clock genes were upregulated, resulting in increased transcription of fatty acid oxidation-related genes. In myoblast cells, butyrate also enhanced pan-histone acetylation via histone deacetylase inhibition, particularly modulating acetylation at the promoter of circadian clock genes. Correlation analysis revealed potential links between <em>Firmicutes</em> phylum, including certain genera within it, and butyrate-induced molecular changes in muscle as well as phenotypic alterations. The butyrate-driven effects on diet-induced obesity were associated with alterations in gut microbiota and a muscle-specific increase in histone acetylation, leading to the transcriptional activation of circadian clock genes and their controlled genes.</p></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":null,"pages":null},"PeriodicalIF":5.6,"publicationDate":"2024-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0955286324000238/pdfft?md5=c60d1dea4ec9a54106c3c38d9d6dcca9&pid=1-s2.0-S0955286324000238-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139662666","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sex-specific effects of ketogenic diet on anxiety-like behavior and neuroimmune response in C57Bl/6J mice","authors":"Mohit Kumar ,&nbsp;Babita Bhatt ,&nbsp;Chitralekha Gusain ,&nbsp;Nayan Mahajan ,&nbsp;Mahendra Bishnoi","doi":"10.1016/j.jnutbio.2024.109591","DOIUrl":"10.1016/j.jnutbio.2024.109591","url":null,"abstract":"<div><p>The ketogenic diet (KD) has been shown to reduce anxiety and enhance cognitive functions in neurological diseases. However, the sex-specific effects of KD on anxiety-like behavior in healthy individuals and the underlying molecular mechanisms contributing to these effects, including neuroinflammation, are unelucidated. This study investigated the sex-specific effects of KD on anxiety-like behavior and the neuroimmune response in the prefrontal cortex (PFC) and hippocampus of healthy C57BL/6J male and female mice. Animals were fed either a control diet (CD- 17% fat, 65% carb, 18% protein) or a KD (80% fat, 5% carb, 15% protein) for 4 weeks. KD increased the levels of circulating β-hydroxybutyrate (BHB) both in males and females. However, PFC BHB levels were found to be elevated only in KD males. Moreover, KD did not affect the behavior of females but improved motor abilities and reduced anxiety levels in males. KD suppressed the mRNA expression of the pan microglial markers (<em>Cd68, P2ry12</em>) and induced morphological changes in the male PFC microglia. A sex-specific decrease in IL1β and an increase in IL-10 levels was found in the PFC of KD males. A similar trend was observed in the hippocampus of males where KD reduced the mRNA expression of <em>P2ry12, Il1β,</em> and <em>cFos</em>. Additionally, BHB increased the production of IL-10 whereas it decreased the production of IL1β from human microglia in <em>in-vitro</em> conditions. In summary, these results demonstrate that the anxiolytic and motor function enhancement abilities of KD are male-specific. Reduced pro-inflammatory and improved anti-inflammatory factors in the male PFC and hippocampus may underlie these effects.</p></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":null,"pages":null},"PeriodicalIF":5.6,"publicationDate":"2024-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139677449","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"All-trans retinoic acid induces lipophagy through the activation of the AMPK-Beclin1 signaling pathway and reduces Rubicon expression in adipocytes","authors":"Yuki Mori ,&nbsp;Masashi Masuda ,&nbsp;Risa Yoshida-Shimizu,&nbsp;Saki Aoyagi,&nbsp;Yuichiro Adachi,&nbsp;Anh The Nguyen,&nbsp;Yusuke Maruyama,&nbsp;Yosuke Okumura,&nbsp;Yuki Kamei,&nbsp;Maiko Sakai,&nbsp;Kohta Ohnishi,&nbsp;Hirokazu Ohminami,&nbsp;Yutaka Taketani","doi":"10.1016/j.jnutbio.2024.109589","DOIUrl":"10.1016/j.jnutbio.2024.109589","url":null,"abstract":"<div><p>Lipophagy is defined as a lipolysis pathway that degrades lipid droplet (LD) <em>via</em> autophagy. All-<em>trans</em> retinoic acid (atRA), a metabolite of vitamin A, stimulates lipolysis through hormone-sensitive lipase and β-oxidation. However, the regulation of lipolysis by atRA-induced autophagy in adipocytes remains unclear. In this study, we investigated the effect of atRA on autophagy in epididymal fat of mice and the molecular mechanisms of autophagy in 3T3-L1 adipocytes. Western blotting showed that atRA decreased the expression of p62, a cargo receptor for autophagic degradation, and increased the expression of the lipidated LC3B (LC3B-II), an autophagy marker, in epididymal fat. Next, we confirmed that atRA increased autophagic flux in differentiated 3T3-L1 cells using the GFP-LC3-RFP-LC3ΔG probe. Immunofluorescent staining revealed that the colocalization of LC3B with perilipin increased in differentiated 3T3-L1 cells treated with atRA. The knockdown of <em>Atg5</em>, an essential gene in autophagy induction, partly suppressed the atRA-induced release of non-esterified fatty acid (NEFA) from LDs in differentiated 3T3-L1 cells. atRA time-dependently elicited the phosphorylation of AMPK and Beclin1, autophagy-inducing factors, in mature 3T3-L1 adipocytes. Inversely, atRA decreased the protein expression of Rubicon, an autophagy repressor, in differentiated 3T3-L1 cells and epididymal fat. Interestingly, the expression of ALDH1A1, atRA-synthesizing enzymes, increased in epididymal fat with decreased protein expression of Rubicon in aged mice. These results suggest that atRA may partially induce lipolysis through lipophagy by activating the AMPK-Beclin1 signaling pathway in the adipocytes and increased atRA levels may contribute to decreased Rubicon expression in the epididymal fat of aged mice. (248/250 words)</p></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":null,"pages":null},"PeriodicalIF":5.6,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0955286324000226/pdfft?md5=194ce7b6ced76568208efb8bff25755c&pid=1-s2.0-S0955286324000226-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139677384","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lipids and lipid signaling molecules in human milk and infant formula, a chemical characterization of relevant biochemical components","authors":"Roberta Ottria ,&nbsp;Matteo Della Porta ,&nbsp;Ornella Xynomilakis ,&nbsp;Sara Casati ,&nbsp;Roberta Cazzola ,&nbsp;Pierangela Ciuffreda","doi":"10.1016/j.jnutbio.2024.109580","DOIUrl":"10.1016/j.jnutbio.2024.109580","url":null,"abstract":"<div><p>Breastfeeding is the gold standard in infant nutrition and continuous researches aim to optimize infant formula composition as the best alternative available. Human milk lipid content provides more than 50% of energy requirements for infants together with essential vitamins, polyunsaturated fatty acids, and other bioactive components. While fatty acids and vitamins human milk content has been extensively studied and, when needed those have been added to infant formulas, less is known about polyunsaturated fatty acids functional derivatives and other bioactive components. Here we describe the comparison of lipid compositions in breast milk from 22 healthy volunteers breastfeeding mothers and the six most common infant formula devoting particular attention to two families of signaling lipids, endocannabinoids, and eicosanoids. The main differences between breast milk and formulas lie in a variety of saturated fatty and unsaturated fatty acids, in the total amount (45–95% less in infant formula) and a variety of endocannabinoids and eicosanoids (2-AG, 5(s)HETE, 15(S)-HETE and 14,15-EET).</p></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":null,"pages":null},"PeriodicalIF":5.6,"publicationDate":"2024-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S0955286324000147/pdfft?md5=1fd9a66f9de93245966f2626fade1de6&pid=1-s2.0-S0955286324000147-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139564374","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Thinned young apple powder prevents obesity-induced neuronal apoptosis via improving mitochondrial function of cerebral cortex in mice","authors":"Jiacheng Fang ,&nbsp;Peng Jiang ,&nbsp;Xincen Wang ,&nbsp;Zhongshi Qi ,&nbsp;Xin He ,&nbsp;Lei Chen ,&nbsp;Yurong Guo ,&nbsp;Xiaoyun Xu ,&nbsp;Run Liu ,&nbsp;Duo Li","doi":"10.1016/j.jnutbio.2024.109588","DOIUrl":"10.1016/j.jnutbio.2024.109588","url":null,"abstract":"<div><p>Mitochondrial dysfunction is one of the triggers for obesity-induced neuron apoptosis. Thinned young apple is getting more attention on account of the extensive biological activities because of rich polyphenols and polysaccharides. However, the neuroprotective effect of thinned young apple powder (YAP) is still unclear. The aim of the present study was to investigate the preventive effect of YAP on obesity-induced neuronal apoptosis. C57BL/6J male mice were divided into 5 groups, control (CON), high fat diet (HFD), HFD + orlistat (ORL), HFD + low-dose young apple powder (LYAP) and HFD + high-dose young apple powder (HYAP) groups and intervened for 12 weeks. It was found that the YAP effectively reduced body weight gain. Importantly, the levels of pro-apoptosis protein were lower in LYAP and HYAP groups than the HFD group, such as Bak/Bcl2 and cleaved caspase3/caspase3. Pathway analysis based on untargeted metabolomics suggested that YAP alleviated obesity-induced neuronal apoptosis by three main metabolic pathway including arginine metabolism, citrate cycle (TCA cycle) and glutathione metabolism. Meanwhile, YAP improved the protein expression of mitochondrial respiratory chain complex, maintained the homeostasis of TCA cycle intermediates, protected the balance of mitochondrial dynamics and alleviated lipid accumulation. In addition, the levels of several antioxidants in cerebral cortex were higher in HYAP group than the HFD group like superoxide dismutase (SOD) and catalase (CAT). In summary, YAP supplementation suppressed neuronal apoptosis in the cerebral cortex of HFD-induced obesity mice by improving mitochondrial function and inhibiting oxidative stress.</p></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":null,"pages":null},"PeriodicalIF":5.6,"publicationDate":"2024-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139546667","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Calorie restriction mimetic, resveratrol, attenuates hepatic ischemia and reperfusion injury through enhancing efferocytosis of macrophages via AMPK/STAT3/S1PR1 pathway","authors":"Xueya Yao ,&nbsp;Yingxiang Liu ,&nbsp;Menghan Mao ,&nbsp;Liqun Yang ,&nbsp;Qionghui Zhan ,&nbsp;Jie Xiao","doi":"10.1016/j.jnutbio.2024.109587","DOIUrl":"10.1016/j.jnutbio.2024.109587","url":null,"abstract":"<div><p><span><span>Calorie restriction<span> (CR) mimetic, resveratrol (RSV), has the capacity of promoting </span></span>phagocytosis<span><span>. However, its role in hepatic ischemia<span> and reperfusion<span> injury (HIRI) remains poorly understood. This study aimed to investigate the effect of RSV on alleviating HIRI and explore the underlying mechanisms. RSV was intraperitoneally injected in mice HIRI model, while RSV was co-incubated with culture medium for 24 h in RAW 264.7 cells and kupffer cells. Macrophage </span></span></span>efferocytosis<span> was assessed by immunostaining<span> of PI and F4/80. The clearance of apoptotic neutrophils<span> in the liver was determined by immunostaining of Ly6-G and cleaved-caspase-3. HE staining, Suzuki's score, serum levels of ALT, AST, TNF-α and IL-1β were analyzed to evaluate HIRI. The efferocytosis inhibitor, </span></span></span></span></span>Cytochalasin D<span>, was utilized to investigate the effect of RSV on HIRI. Western blot<span><span> was employed to measure the levels of AMPKα, phospho-AMPKα, STAT3, phospho-STAT3 and </span>S1PR1<span>. SiSTAT3 and inhibitors targeting AMPK, STAT3 and S1PR1, respectively, were used to confirm the involvement of AMPK/STAT3/S1PR1 pathway in RSV-mediated efferocytosis and HIRI. RSV facilitated the clearance of apoptotic neutrophils and attenuated HIRI, which was impeded by Cytochalasin D. RSV boosted macrophage efferocytosis by up-regulating the levels of phospho-AMPKα, phospho-STAT3 and S1PR1, which was reversed by AMPK, STAT3 and S1PR1 inhibitors, respectively. Inhibition of STAT3 suppressed RSV-induced clearance of apoptotic neutrophils and exacerbated HIRI. CR mimetic, RSV, alleviates HIRI by promoting macrophages efferocytosis through AMPK/STAT3/S1PR1 pathway, providing valuable insights into the mechanisms underlying the protective effects of CR on attenuating HIRI.</span></span></span></p></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":null,"pages":null},"PeriodicalIF":5.6,"publicationDate":"2024-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139510071","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Creatine supplementation with exercise reduces α-synuclein oligomerization and necroptosis in Parkinson's disease mouse model","authors":"Yea-Hyun Leem ,&nbsp;Jin-Sun Park ,&nbsp;Jung-Eun Park ,&nbsp;Do-Yeon Kim ,&nbsp;Hee-Sun Kim","doi":"10.1016/j.jnutbio.2024.109586","DOIUrl":"10.1016/j.jnutbio.2024.109586","url":null,"abstract":"<div><p>Parkinson's disease (PD) is an incurable neurological disorder that causes typical motor deficits. In this study, we investigated the effects of creatine supplementation and exercise in the subacute 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD. We found that 2% creatine supplementation and/or exercise intervention for 4 weeks elicited neurobehavioral recovery and neuroprotective effects regarding dopaminergic cell loss in MPTP-treated mice; this effect implies functional preservation of dopaminergic cells in the substantia nigra, as reflected by tyrosine hydroxylase expression recovery. Creatine and exercise reduced necroptotic activity in dopaminergic cells by lowering mixed lineage kinase domain-like protein (MLKL) modification to active phenotypes (phosphorylation at Ser345 and oligomerization) and phosphorylated receptor-interacting protein kinase 1 (RIPK1) (Ser166-p) and RIPK3 (Ser232-p) levels. In addition, creatine and exercise reduced the MPTP-induced increase in pathogenic α-synuclein forms, such as Ser129 phosphorylation and oligomerization. Furthermore, creatine and exercise had anti-inflammatory and antioxidative effects in MPTP mice, as evidenced by a decrease in microglia activation, NF-κB-dependent pro-inflammatory molecule expression, and increase in antioxidant enzyme expression. These phenotypic changes were associated with the exercise/creatine-induced AMP-activated protein kinase (AMPK)/nuclear factor erythroid 2-related factor 2 (Nrf2) and sirtuin 3 (SIRT3)/forkhead box O3 (FoxO3a) signaling pathways. In all experiments, combining creatine with exercise resulted in considerable improvement over either treatment alone. Consequently, these findings suggest that creatine supplementation with exercise has anti-inflammatory, antioxidative, and anti-α-synucleinopathy effects, thereby reducing necroptotic cell death in a PD mouse model.</p></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":null,"pages":null},"PeriodicalIF":5.6,"publicationDate":"2024-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139515461","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dietary purple potato supplement attenuates DSS-induced colitis in mice: impact on mitochondrial function","authors":"Qi Sun ,&nbsp;Shima Bibi ,&nbsp;Yansong Xue ,&nbsp;Min Du ,&nbsp;Boon Chew ,&nbsp;Mei-Jun Zhu","doi":"10.1016/j.jnutbio.2024.109585","DOIUrl":"10.1016/j.jnutbio.2024.109585","url":null,"abstract":"<div><p>Inflammatory bowel disease (IBD) is a condition characterized by disrupted intestinal barrier function, abnormal immune response, and mucosal structure loss. This study evaluated the beneficial role of purple potato (PP) supplementation against IBD symptoms using a murine model of dextran sulfate sodium (DSS)-induced colitis, and further explored the underlying mechanisms. Six-week-old C57BL/6J male mice were randomized into two groups and fed a standard rodent diet with or without 10% PP powder for 7 weeks. At the 5th week of dietary supplements, mice in each group were further divided into two subgroups and were either induced with or without 2.5% DSS induction for 7 days, followed by 7 days of recovery. Data showed that PP supplementation ameliorated the disease activity index in DSS-treated mice and reversed the colonic structure loss, mucosal damage, macrophage infiltration, and pro-inflammatory cytokine secretion induced by DSS in the colonic tissue. PP supplementation also restored the levels of tight junction proteins and caudal type homeobox 2 in DSS-treated mice. Furthermore, dietary PP enhanced peroxisome proliferator-activated receptor-γ coactivator-1α signaling pathway, mitochondrial biogenesis, mitochondrial proteostasis, and protein-folding capacity. In summary, dietary PP ameliorated DSS-induced colitis and improved gut structures and barrier function, which was associated with improved mitochondrial function. These results support further investigation of PP as a potential dietary intervention for IBD.</p></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":null,"pages":null},"PeriodicalIF":5.6,"publicationDate":"2024-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139510322","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Very low-carbohydrate diet with higher protein ratio improves lipid metabolism and inflammation in rats with diet-induced nonalcoholic fatty liver disease","authors":"I-Ting Wu ,&nbsp;Wan-Ju Yeh ,&nbsp;Wen-Chih Huang ,&nbsp;Hsin-Yi Yang","doi":"10.1016/j.jnutbio.2024.109583","DOIUrl":"10.1016/j.jnutbio.2024.109583","url":null,"abstract":"<div><p><span>Non-alcoholic fatty liver disease (NAFLD) is commonly associated with obesity, and it is mainly treated through lifestyle modifications. The very low-carbohydrate diet (VLCD) can help lose weight rapidly but the possible effects of extreme dietary patterns on lipid metabolism<span><span><span> and inflammatory responses in individuals with NAFLD remain debatable. Moreover, VLCD protein content may affect its effectiveness in weight loss, steatosis, and inflammatory responses. Therefore, we investigated the effects of VLCDs with different protein contents in NAFLD rats and the mechanisms underlying these effects. After a 16-week inducing period, the rats received an isocaloric normal diet (NC group) or a VLCD with high or low protein content (NVLH vs. NVLL group, energy ratio:protein/carbohydrate/lipid=20/1/79 vs. 6/1/93) for the next 8 weeks experimental period. We noted that the body weight decreased in both the NVLH and NVLL groups; nevertheless, the NVLH group demonstrated improvements in </span>ketosis. The NVLL group led to hepatic </span>lipid accumulation, possibly by increasing very-low-density lipoprotein receptor (VLDLR) expression and elevating liver </span></span>oxidative stress<span>, subsequently activating the expression of Nrf2, and inflammation through the TLR4/TRIF/NLRP3 and TLR4/MyD88/NF-κB pathway. The NVLH was noted to prevent the changes in VLDLR and the TLR4-inflammasome pathway partially. The VLCD also reduced the diversity of gut microbiota<span> and changed their composition. In conclusion, although low-protein VLCD consumption reduces BW, it may also lead to metabolic disorders<span> and changes in microbiota composition; nevertheless, a VLCD with high protein content may partially alleviate these limitations.</span></span></span></p></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":null,"pages":null},"PeriodicalIF":5.6,"publicationDate":"2024-01-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139498193","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fructose dose-dependently influences colon barrier function by regulation of some main physical, immune, and biological factors in rats","authors":"Qianyun Gan ,&nbsp;Ge Song ,&nbsp;Wei Fang ,&nbsp;Yong Wang ,&nbsp;Wentao Qi","doi":"10.1016/j.jnutbio.2024.109582","DOIUrl":"10.1016/j.jnutbio.2024.109582","url":null,"abstract":"<div><p><span><span><span>Little is known about the effects of fructose on colonic function. Here, forty-eight 7-week-old male SD rats were randomly divided into four groups and given 0, 7.5%, 12.75%, and 35% fructose in diet for 8 weeks respectively to investigate the regulatory influence of fructose on colonic barrier function. The exact amount of fructose intake was tracked and recorded. We showed that fructose affects colonic barrier function in a dose-dependent manner. High-fructose at a dose of 1.69±0.23 g/kg/day could damage the physical barrier function of the colon by down-regulating expression of </span>tight junction proteins (ZO-1 and occludin) and </span>mucus<span> layer biomarkers (MUC2 and TFF3). High fructose reduced sIgA<span><span> and the anti-inflammatory cytokine (IL-10), induced abdominal fat accumulation and pro-inflammatory cytokines (IL-6 and IL-8), leading to </span>colon inflammation and immune barrier dysfunction. In addition, high-fructose altered the biological barrier of the colon by decreasing the abundance of </span></span></span><span><em>Blautia</em><span><em>, </em><em>Ruminococcus</em><em>,</em></span></span> and <em>Lactobacillius</em>, and increasing the abundance of <em>Allobaculum</em><span> at the genus level, leading to a reduction in short-chain fatty acids (SCFAs), amino acids<span>, and carbohydrates, etc. Low fructose at a dose of 0.31±0.05 g/kg/day showed no adverse effects on the colonic barrier. The ability of fructose to affect the colonic barrier through physical, immune, and biological pathways provides additional insight into the intestinal disorders caused by high-fructose diets.</span></span></p></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":null,"pages":null},"PeriodicalIF":5.6,"publicationDate":"2024-01-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139498195","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}