Brina Dragar, Simona Kranjc Brezar, Maja Čemažar, Tanja Jesenko, Rok Romih, Mateja Erdani Kreft, Tadeja Kuret, Daša Zupančič
Vitamin A (VitA) is an essential nutrient, affecting many cell functions, such as proliferation, apoptosis, and differentiation, all of which are important for the regeneration of various tissues. In this study, we investigated the effects of a VitA-enriched diet on the regeneration of the urothelium of the urinary bladder in mice after cyclophosphamide (CP)-induced injury. Female mice were fed VitA-enriched and normal diet for 1 week before receiving an intraperitoneal injection of CP (150 mg/kg). Urinary bladders were removed 1 and 3 days after CP. On Day 1, RNA sequencing showed that VitA upregulated two Kyoto Encyclopedia of Genes and Genomes (KEGG) signaling pathways: the cell cycle and the PI3K-Akt pathway. This was confirmed by qPCR, which showed significantly increased expression of the Itga3 and Areg genes. In addition, the effect of VitA on the proliferation of urothelial cells was analyzed by immunohistochemistry of Ki-67, which confirmed an increased proliferation rate. No significant effects of the VitA-enriched diet were observed on the expression of apoptosis-related genes and on differentiation-related markers of superficial urothelial cells. Our results suggest that a VitA-enriched diet improves early urothelial regeneration after CP-induced injury by promoting cell proliferation.
{"title":"Vitamin A-Enriched Diet Increases Urothelial Cell Proliferation by Upregulating Itga3 and Areg After Cyclophosphamide-Induced Injury in Mice","authors":"Brina Dragar, Simona Kranjc Brezar, Maja Čemažar, Tanja Jesenko, Rok Romih, Mateja Erdani Kreft, Tadeja Kuret, Daša Zupančič","doi":"10.1002/mnfr.70045","DOIUrl":"https://doi.org/10.1002/mnfr.70045","url":null,"abstract":"Vitamin A (VitA) is an essential nutrient, affecting many cell functions, such as proliferation, apoptosis, and differentiation, all of which are important for the regeneration of various tissues. In this study, we investigated the effects of a VitA-enriched diet on the regeneration of the urothelium of the urinary bladder in mice after cyclophosphamide (CP)-induced injury. Female mice were fed VitA-enriched and normal diet for 1 week before receiving an intraperitoneal injection of CP (150 mg/kg). Urinary bladders were removed 1 and 3 days after CP. On Day 1, RNA sequencing showed that VitA upregulated two Kyoto Encyclopedia of Genes and Genomes (KEGG) signaling pathways: the cell cycle and the PI3K-Akt pathway. This was confirmed by qPCR, which showed significantly increased expression of the <i>Itga3</i> and <i>Areg</i> genes. In addition, the effect of VitA on the proliferation of urothelial cells was analyzed by immunohistochemistry of Ki-67, which confirmed an increased proliferation rate. No significant effects of the VitA-enriched diet were observed on the expression of apoptosis-related genes and on differentiation-related markers of superficial urothelial cells. Our results suggest that a VitA-enriched diet improves early urothelial regeneration after CP-induced injury by promoting cell proliferation.","PeriodicalId":212,"journal":{"name":"Molecular Nutrition & Food Research","volume":"93 1","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143672764","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}
Lihan Liang, Zepei Zhong, Zezhong Tian, Zhihao Liu, Huiying Kuang, Fang He, Ruijie Wang, Shanshan Hou, Yan Yang
Coenzyme Q10 (CoQ10) is a fat-soluble nutrient, which has antioxidant and anti-inflammatory properties. However, there is insufficient evidence on its daily use and the association with mortality. We aimed to evaluate the trends of CoQ10 supplement use among US noninstitutionalized adults and explore its associations with all-cause and CVD mortality. A prospective cohort study used data from the National Health and Nutrition Examination Survey (1999–2018). The association of CoQ10 supplementation with mortality was assessed with Cox proportional hazard models. The overall reported prevalence of CoQ10 supplement use increased from 1.2% (95% CI 0.7%–1.8%) in 1999–2000 to 4.6% (95% CI 3.4%–6.1%) in 2017–2018 (linear p = 0.002). During an average of 9.8 years of follow-up, 5237 deaths were identified, including 1428 deaths due to CVD. In the multivariable model, CoQ10 supplement use was not associated with all-cause mortality (HR 1.00, 95% CI 0.77–1.30, p = 0.996) and CVD mortality (HR 1.30, 95% CI 0.89–1.90, p = 0.170). Subgroup analyses suggested that the use of CoQ10 supplements was associated with a higher all-cause mortality in obese participants (HR 1.45, 95% CI 1.01–2.08, p for interaction = 0.013). Although the prevalence of CoQ10 supplement use experienced continuous growth from 1999 to 2018 in the general adults of NHANES, CoQ10 supplementation was not associated with all-cause and CVD mortality.
{"title":"Trends in Coenzyme Q10 Supplement Use and Associations With All-Cause and Cardiovascular Mortality: A Population-Based Cohort Study","authors":"Lihan Liang, Zepei Zhong, Zezhong Tian, Zhihao Liu, Huiying Kuang, Fang He, Ruijie Wang, Shanshan Hou, Yan Yang","doi":"10.1002/mnfr.70019","DOIUrl":"https://doi.org/10.1002/mnfr.70019","url":null,"abstract":"Coenzyme Q10 (CoQ10) is a fat-soluble nutrient, which has antioxidant and anti-inflammatory properties. However, there is insufficient evidence on its daily use and the association with mortality. We aimed to evaluate the trends of CoQ10 supplement use among US noninstitutionalized adults and explore its associations with all-cause and CVD mortality. A prospective cohort study used data from the National Health and Nutrition Examination Survey (1999–2018). The association of CoQ10 supplementation with mortality was assessed with Cox proportional hazard models. The overall reported prevalence of CoQ10 supplement use increased from 1.2% (95% CI 0.7%–1.8%) in 1999–2000 to 4.6% (95% CI 3.4%–6.1%) in 2017–2018 (linear <i>p</i> = 0.002). During an average of 9.8 years of follow-up, 5237 deaths were identified, including 1428 deaths due to CVD. In the multivariable model, CoQ10 supplement use was not associated with all-cause mortality (HR 1.00, 95% CI 0.77–1.30, <i>p</i> = 0.996) and CVD mortality (HR 1.30, 95% CI 0.89–1.90, <i>p</i> = 0.170). Subgroup analyses suggested that the use of CoQ10 supplements was associated with a higher all-cause mortality in obese participants (HR 1.45, 95% CI 1.01–2.08, <i>p</i> for interaction = 0.013). Although the prevalence of CoQ10 supplement use experienced continuous growth from 1999 to 2018 in the general adults of NHANES, CoQ10 supplementation was not associated with all-cause and CVD mortality.","PeriodicalId":212,"journal":{"name":"Molecular Nutrition & Food Research","volume":"70 1","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143666481","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}
Jia Li, Peiran Li, Xue Wu, Zibin Li, Yunlong Li, Chao Liu, Ji Bian, Lin Han, Min Wang
Metabolic dysfunction-associated steatotic liver disease (MASLD) is highly prevalent and has emerged as a pressing issue for human health. A highly palmitoylated cluster of differentiation 36 (CD36) promotes free fatty acid (FFA) uptake, which contributes to the development of MASLD. Protocatechuic acid (PCA), the main metabolite of anthocyanins, was reported to inhibit MASLD by regulating the expression of CD36. However, the impact of PCA on CD36 palmitoylation has not been extensively studied. In the present study, we found that PCA could significantly reduce lipid uptake and accumulation in hepatocytes by decreasing CD36 palmitoylation. Inhibitors were used to prove that PCA suppressed CD36 palmitoylation by lowering zinc finger DHHC-type palmitoyltransferase 5 (DHHC5) palmitoylation, but not in an acyl protein thioesterase 1 (APT1)-dependent manner. Further experiments showed that PCA-mediated inhibition of DHHC5 palmitoylation and acyltransferase activity was closely related to the reduction of the CD36/Fyn/Lyn complex. PCA diminished the palmitoylation of CD36 and DHHC5 and ultimately lessened lipid uptake and accumulation in hepatocytes.
{"title":"Protocatechuic Acid Reduces Liver Fatty Acid Uptake in HFD-Fed Mice Associated With the Inhibition of DHHC5-Mediated CD36 Palmitoylation","authors":"Jia Li, Peiran Li, Xue Wu, Zibin Li, Yunlong Li, Chao Liu, Ji Bian, Lin Han, Min Wang","doi":"10.1002/mnfr.70012","DOIUrl":"https://doi.org/10.1002/mnfr.70012","url":null,"abstract":"Metabolic dysfunction-associated steatotic liver disease (MASLD) is highly prevalent and has emerged as a pressing issue for human health. A highly palmitoylated cluster of differentiation 36 (CD36) promotes free fatty acid (FFA) uptake, which contributes to the development of MASLD. Protocatechuic acid (PCA), the main metabolite of anthocyanins, was reported to inhibit MASLD by regulating the expression of CD36. However, the impact of PCA on CD36 palmitoylation has not been extensively studied. In the present study, we found that PCA could significantly reduce lipid uptake and accumulation in hepatocytes by decreasing CD36 palmitoylation. Inhibitors were used to prove that PCA suppressed CD36 palmitoylation by lowering zinc finger DHHC-type palmitoyltransferase 5 (DHHC5) palmitoylation, but not in an acyl protein thioesterase 1 (APT1)-dependent manner. Further experiments showed that PCA-mediated inhibition of DHHC5 palmitoylation and acyltransferase activity was closely related to the reduction of the CD36/Fyn/Lyn complex. PCA diminished the palmitoylation of CD36 and DHHC5 and ultimately lessened lipid uptake and accumulation in hepatocytes.","PeriodicalId":212,"journal":{"name":"Molecular Nutrition & Food Research","volume":"124 1","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143660388","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}
Colorectal cancer (CRC) is the third leading cause of cancer-related mortality globally and presents significant challenges in treatment and patient care. Capecitabine, a widely used prodrug of 5-fluorouracil (5-FU), offers targeted delivery with reduced systemic toxicity compared to traditional chemotherapies. However, capacitabine is associated with adverse effects, such as hand-foot syndrome, gastrointestinal issues, and mucositis. Emerging evidence suggests that probiotics, particularly Bifidobacterium, play a pivotal role in gut microbiota modulation, promoting anti-inflammatory cytokines and short-chain fatty acids, such as butyrate, which possess both intestinal protective and anti-cancer properties. In this review, we explored the potential of Bifidobacterium to improve chemotherapy outcomes by mitigating inflammation and enhancing mucosal immunity in CRC patients. Furthermore, we demonstrated in silico approaches, including molecular docking and protein–protein interaction analysis, for Bifidobacterium and Toll-like receptor 2 (TLR-2), a key mediator of intestinal immunity. Docking results revealed strong binding affinity, suggesting the activation of anti-inflammatory pathways. Notably, this interaction enhanced IL-10 production while reducing pro-inflammatory cytokines, such as IL-6 and TNF-α, fostering gut homeostasis and mitigating chronic inflammation, a key driver of CRC progression. Therefore, future research should focus on personalized probiotics and validating their synergy with chemotherapy and immunotherapy to improve CRC treatment outcomes.
{"title":"Enhancing Colorectal Cancer Treatment: The Role of Bifidobacterium in Modulating Gut Immunity and Mitigating Capecitabine-Induced Toxicity","authors":"Aswathi Ramesh, Dhasarathdev Srinivasan, Rajasekaran Subbarayan, Ankush Chauhan, Loganathan Krishnamoorthy, Jeevan Kumar, Madhan Krishnan, Rupendra Shrestha","doi":"10.1002/mnfr.70023","DOIUrl":"https://doi.org/10.1002/mnfr.70023","url":null,"abstract":"Colorectal cancer (CRC) is the third leading cause of cancer-related mortality globally and presents significant challenges in treatment and patient care. Capecitabine, a widely used prodrug of 5-fluorouracil (5-FU), offers targeted delivery with reduced systemic toxicity compared to traditional chemotherapies. However, capacitabine is associated with adverse effects, such as hand-foot syndrome, gastrointestinal issues, and mucositis. Emerging evidence suggests that probiotics, particularly Bifidobacterium, play a pivotal role in gut microbiota modulation, promoting anti-inflammatory cytokines and short-chain fatty acids, such as butyrate, which possess both intestinal protective and anti-cancer properties. In this review, we explored the potential of Bifidobacterium to improve chemotherapy outcomes by mitigating inflammation and enhancing mucosal immunity in CRC patients. Furthermore, we demonstrated in silico approaches, including molecular docking and protein–protein interaction analysis, for Bifidobacterium and Toll-like receptor 2 (TLR-2), a key mediator of intestinal immunity. Docking results revealed strong binding affinity, suggesting the activation of anti-inflammatory pathways. Notably, this interaction enhanced IL-10 production while reducing pro-inflammatory cytokines, such as IL-6 and TNF-α, fostering gut homeostasis and mitigating chronic inflammation, a key driver of CRC progression. Therefore, future research should focus on personalized probiotics and validating their synergy with chemotherapy and immunotherapy to improve CRC treatment outcomes.","PeriodicalId":212,"journal":{"name":"Molecular Nutrition & Food Research","volume":"49 1","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143660389","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. 6'25","authors":"","doi":"10.1002/mnfr.70032","DOIUrl":"https://doi.org/10.1002/mnfr.70032","url":null,"abstract":"Click on the article title to read more.","PeriodicalId":212,"journal":{"name":"Molecular Nutrition & Food Research","volume":"38 1","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143660648","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}
Scope: Insulin resistance (IR), which causes chronic hyperglycemia, has been one of the most prevalent components of metabolic syndrome over the centuries. Pennogenin 3-O-β-chacotrioside (P3C), the main steroid glycoside derived from Paris polyphylla, has been found to exert various biological activities. However, the exact role of P3C on glucose metabolism in the IR state remains unexplored. Methods and results: To induce IR, AML12 cells were exposed to glucose (27 mM) and insulin (10 µg/mL) and then incubated with P3C (0.25 or 0.5 µM) for 24 h. The effects of P3C on glucose metabolism in insulin-resistant AML12 cells were evaluated through glucose consumption assays, real-time quantitative polymerase chain reaction (qPCR), Western blotting, and metabolic analysis for extracellular acidification rate (ECAR) and oxygen consumption rate (OCR). Our data showed that P3C significantly improved insulin sensitivity in AML12 hepatocytes with high glucose-induced IR. P3C stimulated insulin sensitivity and glucose uptake by activating the IRS/PI3K/Akt signaling pathway, which enhances glycogen synthesis and suppresses gluconeogenesis in insulin-resistant AML12 cells. In addition, P3C treatment increased the protein expression of p-AMPK and PGC1α, as well as the expression of oxidative phosphorylation complex proteins, potentially enhancing mitochondrial oxidative respiration. Conclusions: Our findings imply that P3C could be a therapeutic option for improving metabolic abnormalities associated with IR.
{"title":"Improvement of Glucose Metabolism by Pennogenin 3-O-β-Chacotrioside via Activation of IRS/PI3K/Akt Signaling and Mitochondrial Respiration in Insulin-Resistant Hepatocytes","authors":"Jae-In Lee, Hee Min Lee, Jae-Ho Park, Yu Geon Lee","doi":"10.1002/mnfr.70010","DOIUrl":"https://doi.org/10.1002/mnfr.70010","url":null,"abstract":"Scope: Insulin resistance (IR), which causes chronic hyperglycemia, has been one of the most prevalent components of metabolic syndrome over the centuries. Pennogenin 3-<i>O</i>-β-chacotrioside (P3C), the main steroid glycoside derived from <i>Paris polyphylla</i>, has been found to exert various biological activities. However, the exact role of P3C on glucose metabolism in the IR state remains unexplored. Methods and results: To induce IR, AML12 cells were exposed to glucose (27 mM) and insulin (10 µg/mL) and then incubated with P3C (0.25 or 0.5 µM) for 24 h. The effects of P3C on glucose metabolism in insulin-resistant AML12 cells were evaluated through glucose consumption assays, real-time quantitative polymerase chain reaction (qPCR), Western blotting, and metabolic analysis for extracellular acidification rate (ECAR) and oxygen consumption rate (OCR). Our data showed that P3C significantly improved insulin sensitivity in AML12 hepatocytes with high glucose-induced IR. P3C stimulated insulin sensitivity and glucose uptake by activating the IRS/PI3K/Akt signaling pathway, which enhances glycogen synthesis and suppresses gluconeogenesis in insulin-resistant AML12 cells. In addition, P3C treatment increased the protein expression of p-AMPK and PGC1α, as well as the expression of oxidative phosphorylation complex proteins, potentially enhancing mitochondrial oxidative respiration. Conclusions: Our findings imply that P3C could be a therapeutic option for improving metabolic abnormalities associated with IR.","PeriodicalId":212,"journal":{"name":"Molecular Nutrition & Food Research","volume":"14 5 1","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143653687","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}
Yi Wang, Suqing Lan, Laiming Zhang, Yunxuan Li, Ziyang Deng, Xingqian Ye, Haibo Pan, Shiguo Chen
Scope: Polyphenols reportedly possess strong in vitro α-glucosidase inhibitory activity, even higher than acarbose, but their in vivo regulation on postprandial hyperglycemia is poor. So far this typical problem of polyphenols remains unsolved, greatly hindering their application as α-glucosidase inhibitors. Methods and results: Here, we identify the small intestinal mucus layer acts as a barrier to significantly reduce in vivo α-glucosidase inhibitory activity of epigallocatechin gallate, prodelphinidin B digallate (proDB DG), and proanthocyanidins from Chinese bayberry leaves. Multispectroscopy, rheology, solvent method, and molecular docking analysis showed that these pyrogallol-based polyphenols, especially proDB DG strongly interacted with small intestinal mucins through hydrogen bonding, hydrophobic interactions, and electrostatic interactions. These interactions block polyphenols from penetrating the mucus layer, resulting in their low binding rates with α-glucosidase in vivo. Besides, polyphenol-driven aggregation of the mucins enhanced the barrier function and reduced the permeability of the mucus layer, resulting in delayed digestion and absorption of carbohydrates. Conclusions: The mucus barrier weakens the inhibitory activity of pyrogallol-based polyphenols against α-glucosidase. Hence, overcoming the mucus barrier is a promising strategy to improve the regulation of pyrogallol-based polyphenols against postprandial hyperglycemia in vivo, which helps them to become novel α-glucosidase inhibitors in the clinic.
范围：据报道，多酚具有很强的体外α-葡萄糖苷酶抑制活性，甚至高于阿卡波糖，但其体内对餐后高血糖的调节作用却很差。迄今为止，多酚的这一典型问题仍未得到解决，这极大地阻碍了它们作为α-葡萄糖苷酶抑制剂的应用。方法和结果：在此，我们发现小肠粘液层作为一种屏障，显著降低了没食子儿茶素没食子酸酯、原鹅掌楸素 B 二没食子酸酯（proDB DG）和杨梅叶中原花青素的体内α-葡萄糖苷酶抑制活性。多光谱、流变学、溶剂法和分子对接分析表明，这些以焦花色酚为基础的多酚，尤其是原DB DG，通过氢键、疏水作用和静电作用与小肠粘蛋白发生了强烈的相互作用。这些相互作用阻碍了多酚类物质穿透粘液层，导致它们在体内与 α-葡萄糖苷酶的结合率较低。此外，多酚驱动的粘蛋白聚集增强了屏障功能，降低了粘液层的通透性，从而延迟了碳水化合物的消化和吸收。结论粘液屏障削弱了焦酚基多酚对α-葡萄糖苷酶的抑制活性。因此，克服粘液屏障是改善焦山梨醇类多酚对体内餐后高血糖的调节作用的一种有前途的策略，这有助于它们成为临床上新型的α-葡萄糖苷酶抑制剂。
{"title":"Mucus Barrier Weakens the Inhibitory Activity of Pyrogallol-Based Polyphenols Against α-Glucosidase","authors":"Yi Wang, Suqing Lan, Laiming Zhang, Yunxuan Li, Ziyang Deng, Xingqian Ye, Haibo Pan, Shiguo Chen","doi":"10.1002/mnfr.202400838","DOIUrl":"https://doi.org/10.1002/mnfr.202400838","url":null,"abstract":"Scope: Polyphenols reportedly possess strong in vitro α-glucosidase inhibitory activity, even higher than acarbose, but their in vivo regulation on postprandial hyperglycemia is poor. So far this typical problem of polyphenols remains unsolved, greatly hindering their application as α-glucosidase inhibitors. Methods and results: Here, we identify the small intestinal mucus layer acts as a barrier to significantly reduce in vivo α-glucosidase inhibitory activity of epigallocatechin gallate, prodelphinidin B digallate (proDB DG), and proanthocyanidins from Chinese bayberry leaves. Multispectroscopy, rheology, solvent method, and molecular docking analysis showed that these pyrogallol-based polyphenols, especially proDB DG strongly interacted with small intestinal mucins through hydrogen bonding, hydrophobic interactions, and electrostatic interactions. These interactions block polyphenols from penetrating the mucus layer, resulting in their low binding rates with α-glucosidase in vivo. Besides, polyphenol-driven aggregation of the mucins enhanced the barrier function and reduced the permeability of the mucus layer, resulting in delayed digestion and absorption of carbohydrates. Conclusions: The mucus barrier weakens the inhibitory activity of pyrogallol-based polyphenols against α-glucosidase. Hence, overcoming the mucus barrier is a promising strategy to improve the regulation of pyrogallol-based polyphenols against postprandial hyperglycemia in vivo, which helps them to become novel α-glucosidase inhibitors in the clinic.","PeriodicalId":212,"journal":{"name":"Molecular Nutrition & Food Research","volume":"91 1","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143660391","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}
Pengfei Li, Yong Zhang, Hedong Lang, Pengfei Hou, Yu Yao, Ruiliang Zhang, Xiaolan Wang, Qianyong Zhang, Mantian Mi, Long Yi
Insulin resistance is a common metabolic disease, and its pathogenesis is still unclear. The decrease of glucagon-like peptide-1 (GLP-1) level mediated by the alteration of gut microbiota may be the pathogenesis. The study was to investigate the regulatory effect of dihydromyricetin (DHM) on GLP-1 level and insulin resistance induced by high-fat diet (HFD), and to further explore its possible molecular mechanism. Mice were fed an HFD to establish the model of insulin resistance to determine whether DHM had a protective effect. DHM could improve insulin resistance. DHM increased serum GLP-1 by improving intestinal GLP-1 secretion and inhibiting GLP-1 decomposition, associated with the alteration of intestinal intraepithelial lymphocytes (IELs) proportions and decreased expression of CD26 in IELs and TCRαβ+ CD8αβ+ IELs in HFD-induced mice. DHM could ameliorate GLP-1 level and insulin resistance by modulation of gut microbiota and the metabolites, particularly the regulation of chenodeoxycholic acid (CDCA) content, followed by the inhibition of farnesoid X receptor (FXR) expression in intestinal L cells and increased glucagon gene (Gcg) mRNA expression and GLP-1 secretion. This research demonstrates the role of “gut microbiota-CDCA” pathway in the improvement of intestinal GLP-1 levels in HFD-induced mice by DHM administration, providing a new target for the prevention of insulin resistance.
{"title":"Dihydromyricetin Promotes Glucagon-Like Peptide-1 Secretion and Improves Insulin Resistance by Modulation of the Gut Microbiota-CDCA Pathway","authors":"Pengfei Li, Yong Zhang, Hedong Lang, Pengfei Hou, Yu Yao, Ruiliang Zhang, Xiaolan Wang, Qianyong Zhang, Mantian Mi, Long Yi","doi":"10.1002/mnfr.202400491","DOIUrl":"https://doi.org/10.1002/mnfr.202400491","url":null,"abstract":"Insulin resistance is a common metabolic disease, and its pathogenesis is still unclear. The decrease of glucagon-like peptide-1 (GLP-1) level mediated by the alteration of gut microbiota may be the pathogenesis. The study was to investigate the regulatory effect of dihydromyricetin (DHM) on GLP-1 level and insulin resistance induced by high-fat diet (HFD), and to further explore its possible molecular mechanism. Mice were fed an HFD to establish the model of insulin resistance to determine whether DHM had a protective effect. DHM could improve insulin resistance. DHM increased serum GLP-1 by improving intestinal GLP-1 secretion and inhibiting GLP-1 decomposition, associated with the alteration of intestinal intraepithelial lymphocytes (IELs) proportions and decreased expression of CD26 in IELs and TCRαβ<sup>+</sup> CD8αβ<sup>+</sup> IELs in HFD-induced mice. DHM could ameliorate GLP-1 level and insulin resistance by modulation of gut microbiota and the metabolites, particularly the regulation of chenodeoxycholic acid (CDCA) content, followed by the inhibition of farnesoid X receptor (FXR) expression in intestinal L cells and increased glucagon gene (Gcg) mRNA expression and GLP-1 secretion. This research demonstrates the role of “gut microbiota-CDCA” pathway in the improvement of intestinal GLP-1 levels in HFD-induced mice by DHM administration, providing a new target for the prevention of insulin resistance.","PeriodicalId":212,"journal":{"name":"Molecular Nutrition & Food Research","volume":"87 1","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143608712","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}
Michael Leonidas Chikindas, Donald W. Schaffner, Svetoslav Dimitrov Todorov
The UN Sustainable Development Goal 2 (Zero Hunger) highlights the need to produce sufficient food commodities to meet the world's population demands and combat hunger, while also respecting the environment and adhering to sustainability principles. Since the beginning of the 21st century, new ideas, ingredients, and technologies have emerged that could significantly transform the food industry. These transformations may alter the rules of food production by integrating traditional knowledge with new technologies and scientific advancements. These innovative processes align to feed the world's growing population through sustainable production. The introduction of new ingredients in food products may necessitate new food safety and/or quality requirements. Using several examples of both traditional and new ingredients such as insects, plants, marine plants, mycoproteins, meat crops, cellulose, and chitin (as representative examples), we illustrate the need to determine which microorganisms to look for when it comes to the microbiological quality and safety of such food products. This opinion does not seek to establish new microbiological guidelines or standards for safety and quality. Instead, our goal is to emphasize the need for a process to define new microbiological criteria, ensuring the quality and safety of emerging food products.
{"title":"New Food Ingredients: The Challenge of Potential New Pathogens and Spoilage Issues","authors":"Michael Leonidas Chikindas, Donald W. Schaffner, Svetoslav Dimitrov Todorov","doi":"10.1002/mnfr.70022","DOIUrl":"https://doi.org/10.1002/mnfr.70022","url":null,"abstract":"The UN Sustainable Development Goal 2 (Zero Hunger) highlights the need to produce sufficient food commodities to meet the world's population demands and combat hunger, while also respecting the environment and adhering to sustainability principles. Since the beginning of the 21st century, new ideas, ingredients, and technologies have emerged that could significantly transform the food industry. These transformations may alter the rules of food production by integrating traditional knowledge with new technologies and scientific advancements. These innovative processes align to feed the world's growing population through sustainable production. The introduction of new ingredients in food products may necessitate new food safety and/or quality requirements. Using several examples of both traditional and new ingredients such as insects, plants, marine plants, mycoproteins, meat crops, cellulose, and chitin (as representative examples), we illustrate the need to determine which microorganisms to look for when it comes to the microbiological quality and safety of such food products. This opinion does not seek to establish new microbiological guidelines or standards for safety and quality. Instead, our goal is to emphasize the need for a process to define new microbiological criteria, ensuring the quality and safety of emerging food products.","PeriodicalId":212,"journal":{"name":"Molecular Nutrition & Food Research","volume":"54 1","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143608710","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}
Larissa de Mattos Manhães, Ludmilla Santana, Marcelo Ribeiro Alves, Priscila Mansur Leal, Patricia Coelho de Velasco, Isabelle Santana, Jessyca Sousa de Brito, Denise Mafra, Natália Alvarenga Borges
Scope: The uremic toxin trimethylamine N-oxide (TMAO) accumulates in patients with chronic kidney disease (CKD) and is associated with its progression, cardiovascular disease, and other complications. The gut microbiota produces TMAO from substrates mainly found in red meat, eggs, and dairy. However, some saltwater fish also contain high levels of TMAO. Although fish consumption is generally linked to beneficial effects, its effects on CKD patients require further research. Methods and results: This study compares the effect of red meat and cod fish intake on TMAO plasma levels in CKD patients undergoing hemodialysis (HD). Participants received a single animal protein source (red meat vs. cod fish) for lunch and dinner for four consecutive days (each intervention), with a 2-week washout period in between. TMAO plasma levels were analyzed using LC-MS/MS. All 14 patients concluded the red meat intervention, while one refused to participate in the fish intervention. No significant difference in TMAO plasma levels was found post-red meat (p = 0.21) or fish intervention (p = 0.91), as well as between groups (p = 0.43). Conclusion: In this study, 4 days of red meat and cod fish intake did not significantly impact TMAO levels in HD patients, while other factors may be associated with their circulating levels.
{"title":"Trimethylamine N-Oxide Plasma Levels Following Red Meat and Cod Fish Intake: A Pilot Crossover Trial in Hemodialysis Patients","authors":"Larissa de Mattos Manhães, Ludmilla Santana, Marcelo Ribeiro Alves, Priscila Mansur Leal, Patricia Coelho de Velasco, Isabelle Santana, Jessyca Sousa de Brito, Denise Mafra, Natália Alvarenga Borges","doi":"10.1002/mnfr.70031","DOIUrl":"https://doi.org/10.1002/mnfr.70031","url":null,"abstract":"Scope: The uremic toxin trimethylamine <i>N</i>-oxide (TMAO) accumulates in patients with chronic kidney disease (CKD) and is associated with its progression, cardiovascular disease, and other complications. The gut microbiota produces TMAO from substrates mainly found in red meat, eggs, and dairy. However, some saltwater fish also contain high levels of TMAO. Although fish consumption is generally linked to beneficial effects, its effects on CKD patients require further research. Methods and results: This study compares the effect of red meat and cod fish intake on TMAO plasma levels in CKD patients undergoing hemodialysis (HD). Participants received a single animal protein source (red meat vs. cod fish) for lunch and dinner for four consecutive days (each intervention), with a 2-week washout period in between. TMAO plasma levels were analyzed using LC-MS/MS. All 14 patients concluded the red meat intervention, while one refused to participate in the fish intervention. No significant difference in TMAO plasma levels was found post-red meat (<i>p</i> = 0.21) or fish intervention (<i>p</i> = 0.91), as well as between groups (<i>p</i> = 0.43). Conclusion: In this study, 4 days of red meat and cod fish intake did not significantly impact TMAO levels in HD patients, while other factors may be associated with their circulating levels.","PeriodicalId":212,"journal":{"name":"Molecular Nutrition & Food Research","volume":"68 1","pages":""},"PeriodicalIF":5.2,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143608711","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}
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