Aya Abdelaziz, Yousra M. El-Far, Noha Abdel-Rahman
Ectopic olfactory receptors are expressed in nonolfactory tissues and perform diverse roles including regulation of glucose homeostasis. We explored the effect of citronellal treatment on olfactory receptor 4M1 subtype (OR4M1) signaling in insulin resistance and Type II diabetes in rats. We aimed to validate the anti-diabetic effect of citronellal through Asprosin/OR4M1 modulation. Exploring new antidiabetics and pharmacological targets is important to improve quality of life and limit complications. The model was established in Sprague-Dawley rats by a high-fat diet for 4 weeks followed by a single low-dose streptozotocin (STZ) (35 mg/kg/ip). One week after STZ injection, oral citronellal (100 mg/kg) was administered for 4 weeks. Citronellal lowered serum glucose and triglycerides and ameliorated OGTT and HOMA-IR results. Docking results revealed that citronellal blocked the Asprosin binding site at OR4M1. The hepatic expression of OR4M1 and Asprosin was reduced. Citronellal lowered cAMP levels causing attenuated levels of protein kinase A and downstream gluconeogenic enzymes: glucose-6-phosphatase and phosphoenolpyruvate carboxykinase. Citronellal also inhibited the expression of hepatic TLR-4 and inhibited JNK phosphorylation. Citronellal attenuated hepatic levels of NF-κB, p-NF-κB, and downstream proteins MCP-1 and TNF-α. These results suggest that citronellal alleviates insulin resistance by mitigating Asprosin/OR4M1 and Asprosin/TLR4/JNK signaling.
{"title":"Citronellal Alleviates Insulin Resistance in High-Fat Diet/Streptozocin Model: Role of Asprosin/Olfactory Receptor Axis","authors":"Aya Abdelaziz, Yousra M. El-Far, Noha Abdel-Rahman","doi":"10.1002/mnfr.202400654","DOIUrl":"https://doi.org/10.1002/mnfr.202400654","url":null,"abstract":"Ectopic olfactory receptors are expressed in nonolfactory tissues and perform diverse roles including regulation of glucose homeostasis. We explored the effect of citronellal treatment on olfactory receptor 4M1 subtype (OR4M1) signaling in insulin resistance and Type II diabetes in rats. We aimed to validate the anti-diabetic effect of citronellal through Asprosin/OR4M1 modulation. Exploring new antidiabetics and pharmacological targets is important to improve quality of life and limit complications. The model was established in Sprague-Dawley rats by a high-fat diet for 4 weeks followed by a single low-dose streptozotocin (STZ) (35 mg/kg/ip). One week after STZ injection, oral citronellal (100 mg/kg) was administered for 4 weeks. Citronellal lowered serum glucose and triglycerides and ameliorated OGTT and HOMA-IR results. Docking results revealed that citronellal blocked the Asprosin binding site at OR4M1. The hepatic expression of OR4M1 and Asprosin was reduced. Citronellal lowered cAMP levels causing attenuated levels of protein kinase A and downstream gluconeogenic enzymes: glucose-6-phosphatase and phosphoenolpyruvate carboxykinase. Citronellal also inhibited the expression of hepatic TLR-4 and inhibited JNK phosphorylation. Citronellal attenuated hepatic levels of NF-κB, p-NF-κB, and downstream proteins MCP-1 and TNF-α. These results suggest that citronellal alleviates insulin resistance by mitigating Asprosin/OR4M1 and Asprosin/TLR4/JNK signaling.","PeriodicalId":212,"journal":{"name":"Molecular Nutrition & Food Research","volume":"18 1","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142987176","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
We aimed to explore the association between plant-based dietary (PBD) patterns and obesity trajectories in middle-aged and elderly, as well as obesity trajectories linked to cardiovascular disease (CVD) risk. A total of 7108 middle-aged and elderly UK Biobank participants with at least three physical measurements were included. Dietary information collected at enrolment was used to calculate the healthful plant-based diet index (hPDI). Group-based trajectory modeling identified two trajectories for each adiposity measure: BMI Low-Smooth and High-Growth-Decline; FMI Low-Smooth and High-Growth-Decline; WHR Low-Growth and High-Growth. Logistic regression showed that participants in the medium and high hPDI groups were less likely to follow the BMI High-Growth-Decline (OR = 0.72, 95% CI: 0.60–0.87; OR = 0.49, 95% CI: 0.39–0.61), FMI High-Growth-Decline (OR = 0.71, 95% CI: 0.60–0.84; OR = 0.55, 95% CI: 0.46–0.66), and WHR High-Growth (OR = 0.73, 95% CI: 0.61–0.87; OR = 0.52, 95% CI: 0.43–0.63) trajectories. After a median follow-up time of 3.88 years, Cox regression showed higher CVD risk for participants in these trajectories (HR = 1.70, 95% CI: 1.37–2.11; HR = 1.68, 95% CI: 1.37–2.06; HR = 1.30, 95% CI: 1.04–1.63). A healthy PBD pattern was associated with the maintenance of a healthy BMI classification. Furthermore, the long-term stabilization of a healthy BMI classification may be linked to a reduced risk of CVD.
{"title":"Association Between Healthful Plant-Based Dietary Pattern and Obesity Trajectories and Future Cardiovascular Diseases in Middle-Aged and Elderly: A Prospective and Longitudinal Cohort Study","authors":"Zhixing Fan, Chaojun Yang, Chenyu Zhao, Hui Wu, Huibo Wang, Ying Yang, Qi Li, Jian Yang","doi":"10.1002/mnfr.202400833","DOIUrl":"https://doi.org/10.1002/mnfr.202400833","url":null,"abstract":"We aimed to explore the association between plant-based dietary (PBD) patterns and obesity trajectories in middle-aged and elderly, as well as obesity trajectories linked to cardiovascular disease (CVD) risk. A total of 7108 middle-aged and elderly UK Biobank participants with at least three physical measurements were included. Dietary information collected at enrolment was used to calculate the healthful plant-based diet index (hPDI). Group-based trajectory modeling identified two trajectories for each adiposity measure: BMI Low-Smooth and High-Growth-Decline; FMI Low-Smooth and High-Growth-Decline; WHR Low-Growth and High-Growth. Logistic regression showed that participants in the medium and high hPDI groups were less likely to follow the BMI High-Growth-Decline (OR = 0.72, 95% CI: 0.60–0.87; OR = 0.49, 95% CI: 0.39–0.61), FMI High-Growth-Decline (OR = 0.71, 95% CI: 0.60–0.84; OR = 0.55, 95% CI: 0.46–0.66), and WHR High-Growth (OR = 0.73, 95% CI: 0.61–0.87; OR = 0.52, 95% CI: 0.43–0.63) trajectories. After a median follow-up time of 3.88 years, Cox regression showed higher CVD risk for participants in these trajectories (HR = 1.70, 95% CI: 1.37–2.11; HR = 1.68, 95% CI: 1.37–2.06; HR = 1.30, 95% CI: 1.04–1.63). A healthy PBD pattern was associated with the maintenance of a healthy BMI classification. Furthermore, the long-term stabilization of a healthy BMI classification may be linked to a reduced risk of CVD.","PeriodicalId":212,"journal":{"name":"Molecular Nutrition & Food Research","volume":"9 1","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142981672","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Yiwei Zhang, Xiaoqin Gan, Hao Xiang, Yanjun Zhang, Sisi Yang, Ziliang Ye, Yu Huang, Yiting Wu, Jinsheng Mai, Jianping Jiang, Xianhui Qin, Yuanyuan Zhang
Scope: The relationship of dietary copper intake with new-onset chronic kidney disease (CKD) remained unclear. We aimed to examine the association of dietary copper intake with new-onset CKD in a 30-year follow-up study from young adulthood to midlife. Methods and results: A total of 4038 U.S. adults aged 18–30 years and without reduced estimated glomerular filtration rate (eGFR) from the Coronary Artery Risk Development in Young Adults (CARDIA) study was included. During a 30-year follow-up, 642 (15.9%) participants developed new-onset CKD. Overall, there was a U-shaped relationship between dietary copper intake and new-onset CKD (p for nonlinearity = 0.034). When copper intake was assessed as quartiles, compared with those in the second quartile (2.03–<2.46 mg/day), the adjusted hazard ratios (HRs) (95% confidence interval [CI]) for new-onset CKD were 1.29 (1.05, 1.66), 1.29 (1.02, 1.64), and 1.49 (1.16, 1.91) for participants in the first (<2.03 mg/day), third (2.46–<3.11 mg/day), and fourth (≥3.11 mg/day) quartiles, respectively. Similar U-shaped associations were observed for new-onset eGFR decline and albuminuria. Conclusions: There was a U-shaped relationship of dietary total copper intake with new-onset CKD, with the lowest risk at a dietary copper intake of 2.03–<2.46 mg/day. Emphasizing the importance of maintaining optimal copper intake levels for the primary prevention of CKD.
{"title":"U-Shaped Association Between Dietary Copper Intake and New-Onset Chronic Kidney Disease: A 30-Year Follow-Up Study From Young Adulthood to Midlife","authors":"Yiwei Zhang, Xiaoqin Gan, Hao Xiang, Yanjun Zhang, Sisi Yang, Ziliang Ye, Yu Huang, Yiting Wu, Jinsheng Mai, Jianping Jiang, Xianhui Qin, Yuanyuan Zhang","doi":"10.1002/mnfr.202400761","DOIUrl":"https://doi.org/10.1002/mnfr.202400761","url":null,"abstract":"Scope: The relationship of dietary copper intake with new-onset chronic kidney disease (CKD) remained unclear. We aimed to examine the association of dietary copper intake with new-onset CKD in a 30-year follow-up study from young adulthood to midlife. Methods and results: A total of 4038 U.S. adults aged 18–30 years and without reduced estimated glomerular filtration rate (eGFR) from the Coronary Artery Risk Development in Young Adults (CARDIA) study was included. During a 30-year follow-up, 642 (15.9%) participants developed new-onset CKD. Overall, there was a U-shaped relationship between dietary copper intake and new-onset CKD (<i>p</i> for nonlinearity = 0.034). When copper intake was assessed as quartiles, compared with those in the second quartile (2.03–<2.46 mg/day), the adjusted hazard ratios (HRs) (95% confidence interval [CI]) for new-onset CKD were 1.29 (1.05, 1.66), 1.29 (1.02, 1.64), and 1.49 (1.16, 1.91) for participants in the first (<2.03 mg/day), third (2.46–<3.11 mg/day), and fourth (≥3.11 mg/day) quartiles, respectively. Similar U-shaped associations were observed for new-onset eGFR decline and albuminuria. Conclusions: There was a U-shaped relationship of dietary total copper intake with new-onset CKD, with the lowest risk at a dietary copper intake of 2.03–<2.46 mg/day. Emphasizing the importance of maintaining optimal copper intake levels for the primary prevention of CKD.","PeriodicalId":212,"journal":{"name":"Molecular Nutrition & Food Research","volume":"74 1","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142987177","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hu Zhao, Xingxing Fu, Yaru Wang, Zhao Shang, BangHua Li, Li Zhou, Yue Liu, Dan Liu, Bo Yi
This study investigated the protective effects of the dietary polyphenol vanillic acid (VA) on dextran sulfate sodium-induced acute ulcerative colitis (UC) in mice, focusing on its impact on the gut microbiota and inflammatory responses. VA was supplemented following dextran sulfate sodium administration, and key indicators, including body weight, disease activity index, colon length, spleen index, and inflammatory markers, were assessed. VA supplementation significantly alleviated UC symptoms, preserved intestinal barrier integrity, and reduced pro-inflammatory cytokine levels. Additionally, VA positively altered the gut microbiota composition, promoting beneficial bacteria such as Akkermansia muciniphila while suppressing the arachidonic acid metabolism pathway. Fecal microbiota transplantation confirmed that the VA-modified gut microbiota contributed to these protective effects. VA also facilitated macrophage polarization from the pro-inflammatory M1 phenotype to the anti-inflammatory M2 phenotype, further mitigating inflammation. These findings highlight the potential of VA as a natural dietary intervention for UC, emphasizing its role in regulating the gut microbiota and inflammatory pathways, which may have significant nutritional relevance in managing inflammatory bowel diseases.
{"title":"Therapeutic Potential of Vanillic Acid in Ulcerative Colitis Through Microbiota and Macrophage Modulation","authors":"Hu Zhao, Xingxing Fu, Yaru Wang, Zhao Shang, BangHua Li, Li Zhou, Yue Liu, Dan Liu, Bo Yi","doi":"10.1002/mnfr.202400785","DOIUrl":"https://doi.org/10.1002/mnfr.202400785","url":null,"abstract":"This study investigated the protective effects of the dietary polyphenol vanillic acid (VA) on dextran sulfate sodium-induced acute ulcerative colitis (UC) in mice, focusing on its impact on the gut microbiota and inflammatory responses. VA was supplemented following dextran sulfate sodium administration, and key indicators, including body weight, disease activity index, colon length, spleen index, and inflammatory markers, were assessed. VA supplementation significantly alleviated UC symptoms, preserved intestinal barrier integrity, and reduced pro-inflammatory cytokine levels. Additionally, VA positively altered the gut microbiota composition, promoting beneficial bacteria such as <i>Akkermansia muciniphila</i> while suppressing the arachidonic acid metabolism pathway. Fecal microbiota transplantation confirmed that the VA-modified gut microbiota contributed to these protective effects. VA also facilitated macrophage polarization from the pro-inflammatory M1 phenotype to the anti-inflammatory M2 phenotype, further mitigating inflammation. These findings highlight the potential of VA as a natural dietary intervention for UC, emphasizing its role in regulating the gut microbiota and inflammatory pathways, which may have significant nutritional relevance in managing inflammatory bowel diseases.","PeriodicalId":212,"journal":{"name":"Molecular Nutrition & Food Research","volume":"92 1","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142981673","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Maria Pierdomenico, Paola Giardullo, Giuliana Bruno, Loretta Bacchetta, Oliviero Maccioni, Olivia C. Demurtas, Maria Sulli, Gianfranco Diretto, Caterina Arcangeli, Flavio Colini, Salvatore Chiavarini, Barbara Benassi
The effect of a mucilage extracted from Opuntia ficus-indica (L.) Mill (OFI) cladodes was tested in lipopolysaccharide (LPS)-challenged HepG2 hepatocarcinoma cells, through a combined in vitro–in silico approach. The OFI mucilage was characterized by gas chromatography-mass spectrometry and liquid chromatography-high resolution mass spectrometry. In cells treated with OFI (5–10 µg/mL) prior to LPS (1 µg/mL, 24 h), the gene expression profile of pro-inflammatory mediators, namely tumor necrosis factor alpha, interleukin-1 beta, interleukin-8, and cyclo-oxygenase-2, was significantly (p < 0.01) reduced if compared to single LPS-challenged cells. The OFI-mediated cytokines reduction was also validated in polystyrene scaffold-grown 3D HepG2 cultures, undergoing treatment with the OFI mucilage (50 µg/mL, 24 h) and LPS stimulation (50 µg/mL, 24 h). We further demonstrated that OFI suppresses the LPS-triggered inflammatory response via impairment of the Toll-like receptor 4 (TLR4)/Myeloid differentiation protein-88/Nuclear factor-kappa B (NF-kB) pathway, by interfering with NF-kB phosphorylation at Serine 536. By molecular docking approach, we provided in silico demonstration of the direct molecular interaction between the mucilage monosaccharides and the TLR4 that interferes with the LPS receptor binding and down-stream inflammatory cascade activation. We also demonstrated that OFI cladodes mucilage downregulates the TLR4 pathway, showing an anti-inflammatory potential in HepG2 cells.
{"title":"The Mucilage From the Opuntia ficus-indica (L.) Mill. Cladodes Plays an Anti-Inflammatory Role in the LPS-Stimulated HepG2 Cells: A Combined In Vitro and In Silico Approach","authors":"Maria Pierdomenico, Paola Giardullo, Giuliana Bruno, Loretta Bacchetta, Oliviero Maccioni, Olivia C. Demurtas, Maria Sulli, Gianfranco Diretto, Caterina Arcangeli, Flavio Colini, Salvatore Chiavarini, Barbara Benassi","doi":"10.1002/mnfr.202400479","DOIUrl":"https://doi.org/10.1002/mnfr.202400479","url":null,"abstract":"The effect of a mucilage extracted from <i>Opuntia ficus-indica</i> (L.) Mill (OFI) cladodes was tested in lipopolysaccharide (LPS)-challenged HepG2 hepatocarcinoma cells, through a combined in vitro–in silico approach. The OFI mucilage was characterized by gas chromatography-mass spectrometry and liquid chromatography-high resolution mass spectrometry. In cells treated with OFI (5–10 µg/mL) prior to LPS (1 µg/mL, 24 h), the gene expression profile of pro-inflammatory mediators, namely tumor necrosis factor alpha, interleukin-1 beta, interleukin-8, and cyclo-oxygenase-2, was significantly (<i>p</i> < 0.01) reduced if compared to single LPS-challenged cells. The OFI-mediated cytokines reduction was also validated in polystyrene scaffold-grown 3D HepG2 cultures, undergoing treatment with the OFI mucilage (50 µg/mL, 24 h) and LPS stimulation (50 µg/mL, 24 h). We further demonstrated that OFI suppresses the LPS-triggered inflammatory response via impairment of the Toll-like receptor 4 (TLR4)/Myeloid differentiation protein-88/Nuclear factor-kappa B (NF-kB) pathway, by interfering with NF-kB phosphorylation at Serine 536. By molecular docking approach, we provided in silico demonstration of the direct molecular interaction between the mucilage monosaccharides and the TLR4 that interferes with the LPS receptor binding and down-stream inflammatory cascade activation. We also demonstrated that OFI cladodes mucilage downregulates the TLR4 pathway, showing an anti-inflammatory potential in HepG2 cells.","PeriodicalId":212,"journal":{"name":"Molecular Nutrition & Food Research","volume":"82 1","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142968042","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Fecal microbiota transplantation (FMT) could significantly alter the recipient's gut bacteria composition and attenuate obesity and obesity-related metabolic syndromes. DL-norvaline is a nonproteinogenic amino acid and possesses anti-obesity potential. However, the specific mechanisms by which gut microbiota might mediate beneficial effects of DL-norvaline have not been completely elucidated. In this study, DL-norvaline-mediated FMT upregulated the beneficial bacteria (Clostridia_UCG_014, Christensenellales, Bacilli, Ileibacterium, Dubosiella, Lactobacillus, Muribaculaceae, and Bacteroidaceae) and downregulated the harmful bacteria (Tuzzerella and Marinifilaceae), further intestinal inflammation, oxidative stress, and intestinal barrier were alleviated as well as short chain fatty acids levels were increased, thus alleviating glucose and insulin metabolism, improving biochemical indexes and energy metabolism and decreasing body weight gain and tissue weight. However, heat-inactivated FMT did not demonstrate any of those improvements in obese mice. Notably, both DL-norvaline-mediated FMT and heat-inactivated FMT increased Bacteroidaceae and Muribaculaceae, this being a signature of alterations to the gut microbiota marker caused by DL-norvaline. Therefore, the beneficial effects of DL-norvaline were transmissible via FMT. This study highlighted the pivotal involvement of the gut microbiota in the development of obesity and provided a novel insight into the underlying mechanisms of FMT, thereby potentially enhancing the efficacy and refinement of FMT utilization.
{"title":"Amelioration of Obesity-Related Disorders in High-Fat Diet-Fed C57BL/6 Mice Following Fecal Microbiota Transplantation From DL-Norvaline-Dosed Mice","authors":"Xin Li, Bohan Sun, Yanting Qin, Fangfang Yue, Xin Lü","doi":"10.1002/mnfr.202400577","DOIUrl":"https://doi.org/10.1002/mnfr.202400577","url":null,"abstract":"Fecal microbiota transplantation (FMT) could significantly alter the recipient's gut bacteria composition and attenuate obesity and obesity-related metabolic syndromes. DL-norvaline is a nonproteinogenic amino acid and possesses anti-obesity potential. However, the specific mechanisms by which gut microbiota might mediate beneficial effects of DL-norvaline have not been completely elucidated. In this study, DL-norvaline-mediated FMT upregulated the beneficial bacteria (<i>Clostridia_UCG_014</i>, <i>Christensenellales</i>, <i>Bacilli</i>, <i>Ileibacterium</i>, <i>Dubosiella</i>, <i>Lactobacillus</i>, <i>Muribaculaceae</i>, and <i>Bacteroidaceae</i>) and downregulated the harmful bacteria (<i>Tuzzerella</i> and <i>Marinifilaceae</i>), further intestinal inflammation, oxidative stress, and intestinal barrier were alleviated as well as short chain fatty acids levels were increased, thus alleviating glucose and insulin metabolism, improving biochemical indexes and energy metabolism and decreasing body weight gain and tissue weight. However, heat-inactivated FMT did not demonstrate any of those improvements in obese mice. Notably, both DL-norvaline-mediated FMT and heat-inactivated FMT increased <i>Bacteroidaceae</i> and <i>Muribaculaceae</i>, this being a signature of alterations to the gut microbiota marker caused by DL-norvaline. Therefore, the beneficial effects of DL-norvaline were transmissible via FMT. This study highlighted the pivotal involvement of the gut microbiota in the development of obesity and provided a novel insight into the underlying mechanisms of FMT, thereby potentially enhancing the efficacy and refinement of FMT utilization.","PeriodicalId":212,"journal":{"name":"Molecular Nutrition & Food Research","volume":"16 1","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-01-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142940189","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Issue Information: Mol. Nutr. Food Res. 1'25","authors":"","doi":"10.1002/mnfr.202570001","DOIUrl":"https://doi.org/10.1002/mnfr.202570001","url":null,"abstract":"Click on the article title to read more.","PeriodicalId":212,"journal":{"name":"Molecular Nutrition & Food Research","volume":"22 1","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142935249","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Shuai Han, Yi Luo, Zuomin Hu, Xinhua Li, Yaping Zhou, Feijun Luo
Since the development of immune checkpoint inhibitors (ICIs), immunotherapy has been widely used as a novel cancer treatment. However, the efficacy of tumor immunotherapy is largely dependent on the tumor microenvironment (TME). The high degree of heterogeneity within TME remains a major obstacle to acquire satisfactory therapeutic. Emerging studies suggest that gut microbiota is becoming an important regulator of TME. Polysaccharides as tumor immunotherapeutic agents or immune adjuvants not only exhibit antitumor activity by targeting gut microbiota, but also expand their role in the tumor immunotherapy by remodeling TME. To date, the mechanism by which polysaccharides targeting TME for tumor prevention via gut microbiota has not been deeply investigated. In this review, recent advances in the regulation of TME by polysaccharides through gut microbiota were systematically outlined, and the challenges and possible solutions in the clinical application of TME‐targeted polysaccharides were discussed. Exploring the relationship between polysaccharides and TME from the perspective of gut microbiota may provide new ideas for the application of polysaccharides in tumor immunotherapy. This is a new area with major challenges that deserve further exploration.
{"title":"Tumor Microenvironment Targeted by Polysaccharides in Cancer Prevention: Expanding Roles of Gut Microbiota and Metabolites","authors":"Shuai Han, Yi Luo, Zuomin Hu, Xinhua Li, Yaping Zhou, Feijun Luo","doi":"10.1002/mnfr.202400750","DOIUrl":"https://doi.org/10.1002/mnfr.202400750","url":null,"abstract":"Since the development of immune checkpoint inhibitors (ICIs), immunotherapy has been widely used as a novel cancer treatment. However, the efficacy of tumor immunotherapy is largely dependent on the tumor microenvironment (TME). The high degree of heterogeneity within TME remains a major obstacle to acquire satisfactory therapeutic. Emerging studies suggest that gut microbiota is becoming an important regulator of TME. Polysaccharides as tumor immunotherapeutic agents or immune adjuvants not only exhibit antitumor activity by targeting gut microbiota, but also expand their role in the tumor immunotherapy by remodeling TME. To date, the mechanism by which polysaccharides targeting TME for tumor prevention via gut microbiota has not been deeply investigated. In this review, recent advances in the regulation of TME by polysaccharides through gut microbiota were systematically outlined, and the challenges and possible solutions in the clinical application of TME‐targeted polysaccharides were discussed. Exploring the relationship between polysaccharides and TME from the perspective of gut microbiota may provide new ideas for the application of polysaccharides in tumor immunotherapy. This is a new area with major challenges that deserve further exploration.","PeriodicalId":212,"journal":{"name":"Molecular Nutrition & Food Research","volume":"203 1","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142929012","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cisplatin (CIS) is a broad-spectrum anticancer drug widely used in the clinic; however, one of its side effects is that it can cause intestinal damage such as loss of appetite, vomiting, and diarrhea in patients. Epigallocatechin gallate (EGCG) is one of the main active substances in green tea, which has the effects of antitumor multiple drug resistance, antioxidation, and antiinflammatory properties. The aim of this study was to explore the protective effect of EGCG on CIS-induced intestinal injury in rats. First, physiological indices and HE staining indicated that compared with the control group, the physiological state of rats in the CIS group was worse, and the intestinal tissue was damaged, especially the ileum. In contrast, pretreatment with EGCG (20, 40, and 80 mg/kg) effectively alleviated the intestinal damage induced by CIS, with the 40 mg/kg dose demonstrating the most substantial protective effect. Additionally, 40 mg/kg EGCG pretreatment mitigated CIS-induced morphological and ultrastructural damage to intestinal tissues, reduced bacterial translocation, and preserved the integrity of the intestinal barrier. This treatment also altered the abundance of 19 bacterial species, including Lactobacillus and Shigella, and influenced amino acid metabolism and 15 metabolic pathways, including vitamin B6 metabolism by 16S RNA and metabolome sequencing. Furthermore, the expression of proteins associated with autophagy and the NRF2/Keap1 signaling pathway was inhibited. Lastly, ML385 (NRF2 signaling pathway inhibitor) reversed the protective effects of EGCG. Taken together, our findings indicate that EGCG ameliorates CIS induced hepatoenteric toxicity in rats by regulating the intestinal flora and targeting the Nrf2/Keap1 signal axis.
{"title":"Epigallocatechin Gallate Alleviates Cisplatin Induced Intestinal Injury in Rats via Inhibiting NRF2/Keap1 Signaling Pathway and Regulating Gut Microbiota and Metabolites","authors":"Enshuang Xu, Yue Sun, Zhiying Yu, Jiasan Zheng","doi":"10.1002/mnfr.202400784","DOIUrl":"https://doi.org/10.1002/mnfr.202400784","url":null,"abstract":"Cisplatin (CIS) is a broad-spectrum anticancer drug widely used in the clinic; however, one of its side effects is that it can cause intestinal damage such as loss of appetite, vomiting, and diarrhea in patients. Epigallocatechin gallate (EGCG) is one of the main active substances in green tea, which has the effects of antitumor multiple drug resistance, antioxidation, and antiinflammatory properties. The aim of this study was to explore the protective effect of EGCG on CIS-induced intestinal injury in rats. First, physiological indices and HE staining indicated that compared with the control group, the physiological state of rats in the CIS group was worse, and the intestinal tissue was damaged, especially the ileum. In contrast, pretreatment with EGCG (20, 40, and 80 mg/kg) effectively alleviated the intestinal damage induced by CIS, with the 40 mg/kg dose demonstrating the most substantial protective effect. Additionally, 40 mg/kg EGCG pretreatment mitigated CIS-induced morphological and ultrastructural damage to intestinal tissues, reduced bacterial translocation, and preserved the integrity of the intestinal barrier. This treatment also altered the abundance of 19 bacterial species, including <i>Lactobacillus</i> and <i>Shigella</i>, and influenced amino acid metabolism and 15 metabolic pathways, including vitamin B6 metabolism by 16S RNA and metabolome sequencing. Furthermore, the expression of proteins associated with autophagy and the NRF2/Keap1 signaling pathway was inhibited. Lastly, ML385 (NRF2 signaling pathway inhibitor) reversed the protective effects of EGCG. Taken together, our findings indicate that EGCG ameliorates CIS induced hepatoenteric toxicity in rats by regulating the intestinal flora and targeting the Nrf2/Keap1 signal axis.","PeriodicalId":212,"journal":{"name":"Molecular Nutrition & Food Research","volume":"14 1","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-01-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142929540","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Systemic lupus erythematosus (SLE) is a complex autoimmune disease with a number of immunological aberrations in the mechanisms of innate and adaptive immune responses. Spontaneous and induced mouse models of the disease have contributed significantly to the advancement in lupus treatments. The involvement of humanized models, engrafted with lupus patients’ immune cells, represented the possibility to study the development of SLE. In the current research, we engrafted NSG/Rag2-γc- mice with PBMCs from lupus patients and put the mice on specific diet composed of extra amounts of methyl-containing micronutrients and cofactors which are key participants in the DNA methylation processes. The results showed a decrease in anti-dsDNA IgG antibody and in proteinuria levels, less glomerular proliferation and protected renal structures in all mice put on the supplemented diet compared to humanized mice fed with the control diet. The observed therapeutic effect may be related to possible alterations in the methylation level and to targeted suppression of gene expression in the immune cells, which correlate negatively with the development of the clinical SLE characteristics. These findings point to the significant immunomodulating role of methyl donors in human models of SLE and represent new therapeutic opportunities with clinical potential.
{"title":"Targeting the Progression of Lupus-Like Disease in Humanized Mouse Model by Specific Dietary Components","authors":"Nikola Ralchev, Lidiya Kechidzhieva, Blagovesta Boneva, Kalina Tumangelova-Yuzeir, Dobroslav Kyurkchiev, Desislava Kalinova, Simeon Monov, Andrey Tchorbanov, Kalina Nikolova-Ganeva","doi":"10.1002/mnfr.202400473","DOIUrl":"https://doi.org/10.1002/mnfr.202400473","url":null,"abstract":"Systemic lupus erythematosus (SLE) is a complex autoimmune disease with a number of immunological aberrations in the mechanisms of innate and adaptive immune responses. Spontaneous and induced mouse models of the disease have contributed significantly to the advancement in lupus treatments. The involvement of humanized models, engrafted with lupus patients’ immune cells, represented the possibility to study the development of SLE. In the current research, we engrafted NSG/Rag2-γc- mice with PBMCs from lupus patients and put the mice on specific diet composed of extra amounts of methyl-containing micronutrients and cofactors which are key participants in the DNA methylation processes. The results showed a decrease in anti-dsDNA IgG antibody and in proteinuria levels, less glomerular proliferation and protected renal structures in all mice put on the supplemented diet compared to humanized mice fed with the control diet. The observed therapeutic effect may be related to possible alterations in the methylation level and to targeted suppression of gene expression in the immune cells, which correlate negatively with the development of the clinical SLE characteristics. These findings point to the significant immunomodulating role of methyl donors in human models of SLE and represent new therapeutic opportunities with clinical potential.","PeriodicalId":212,"journal":{"name":"Molecular Nutrition & Food Research","volume":"27 1","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142917364","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
京公网安备 11010802042870号
京ICP备2023020795号-1
扫码关注我们
求助内容：
应助结果提醒方式：