Molecular Nutrition & Food Research最新文献

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Probiotics in the Management of Chemotherapy-Induced Gastrointestinal Complications: Underlying Mechanisms and Potential Applications 益生菌治疗化疗引起的胃肠道并发症:潜在的机制和潜在的应用
IF 5.2 2区 农林科学
Molecular Nutrition & Food Research Pub Date : 2026-04-20 DOI: 10.1002/mnfr.70421
Faeze Mazloom, Mahsa Mottaghizadeh-Jazi, Amin Sadeghi Dousari, Alireza Farsinejad, Alireza Khanahmad
{"title":"Probiotics in the Management of Chemotherapy-Induced Gastrointestinal Complications: Underlying Mechanisms and Potential Applications","authors":"Faeze Mazloom, Mahsa Mottaghizadeh-Jazi, Amin Sadeghi Dousari, Alireza Farsinejad, Alireza Khanahmad","doi":"10.1002/mnfr.70421","DOIUrl":"https://doi.org/10.1002/mnfr.70421","url":null,"abstract":"The intestinal microbial population safeguards the gut's health through dynamic interactions with adjacent epithelial and immune cells. Therefore, microbial imbalance in the gastrointestinal (GI) tract may lead to impaired immune system function, disrupted epithelial integrity, and elevated susceptibility to systemic health issues. Chemotherapy, a nonspecific, widely used therapeutic option in cancer treatment, can harm rapidly proliferating intestinal epithelial cells and disrupt intestinal microbial balance, leading to chemotherapy-induced GI adverse events, including mucositis, diarrhea, constipation, bowel inflammation, nausea, vomiting, flatulence, dyspepsia, gastritis, stomatitis, and abdominal pain and distention. These adverse events significantly impair the quality of life of cancer patients. Clinical evidences show promising efficacy for probiotics, especially <i>Lactobacillus</i> spp. and <i>Bifidobacterium</i> spp., in restoring gut microbiota diversity, enhancing mucosal integrity, and modulating inflammatory cytokines (e.g., IL-10, IL-6, and TNF-a). However, study design variabilities, strain-specific effects, and safety concerns in immunocompromised cases remain challenging. This review explores the underlying mechanisms of preventing chemotherapy-induced GI complications using probiotics. Understanding these mechanisms can facilitate probiotic integration into supportive oncology care protocols. This review also highlights the need for standard protocols, personalized therapies, and advanced multi-omics approaches to discover the host–microbe interactions.","PeriodicalId":212,"journal":{"name":"Molecular Nutrition & Food Research","volume":"16 1","pages":"e70421"},"PeriodicalIF":5.2,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147719802","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}
引用次数: 0
Tannin Phytocomplex Improves IBS-D Symptoms and Gut-Brain Markers: Prospective Pilot Study 单宁植物复合物改善IBS-D症状和肠-脑标志物:前瞻性试点研究
IF 5.2 2区 农林科学
Molecular Nutrition & Food Research Pub Date : 2026-04-20 DOI: 10.1002/mnfr.70451
Silvia Molino, María M. Piskorz, Alberto Lerma-Aguilera, Fabiana López Mingorance, Cielo Gutierrez, Juan M. Montero, Tatiana Uehara, Harumi Hashimoto, Esteban González Ballerga, Jorge A. Olmos
{"title":"Tannin Phytocomplex Improves IBS-D Symptoms and Gut-Brain Markers: Prospective Pilot Study","authors":"Silvia Molino, María M. Piskorz, Alberto Lerma-Aguilera, Fabiana López Mingorance, Cielo Gutierrez, Juan M. Montero, Tatiana Uehara, Harumi Hashimoto, Esteban González Ballerga, Jorge A. Olmos","doi":"10.1002/mnfr.70451","DOIUrl":"https://doi.org/10.1002/mnfr.70451","url":null,"abstract":"Diarrhea-predominant irritable bowel syndrome (IBS-D) is a multifactorial disorder involving gut-brain axis dysregulation, altered barrier integrity, microbial imbalance, and stress-related mechanisms, with limited nutritional strategies targeting these pathways. Tannin-rich extracts may exert barrier-protective, microbiota-modulating, and stress-related effects.","PeriodicalId":212,"journal":{"name":"Molecular Nutrition & Food Research","volume":"135 1","pages":"e70451"},"PeriodicalIF":5.2,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147719707","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}
引用次数: 0
Cocoa Attenuates Gluten-induced Pathogenesis in a Preclinical Model of Celiac Disease 在乳糜泻临床前模型中,可可可减弱谷蛋白诱导的发病机制
IF 5.2 2区 农林科学
Molecular Nutrition & Food Research Pub Date : 2026-04-20 DOI: 10.1002/mnfr.70472
Marina Girbal-González, María José Rodríguez-Lagunas, Arturo Rodríguez-Banqueri, Ulrich Eckhard, F. Xavier Gomis-Rüth, Àngels Franch-Masferrer, Francisco J. Pérez-Cano
{"title":"Cocoa Attenuates Gluten-induced Pathogenesis in a Preclinical Model of Celiac Disease","authors":"Marina Girbal-González, María José Rodríguez-Lagunas, Arturo Rodríguez-Banqueri, Ulrich Eckhard, F. Xavier Gomis-Rüth, Àngels Franch-Masferrer, Francisco J. Pérez-Cano","doi":"10.1002/mnfr.70472","DOIUrl":"https://doi.org/10.1002/mnfr.70472","url":null,"abstract":"Celiac disease (CeD) is an autoimmune-mediated disorder triggered by gluten ingestion. Strict adherence to a gluten-free diet (GFD) is currently the only available treatment, yet it presents nutritional and lifestyle challenges. Polyphenols and other bioactive food compounds have shown potential in modulating inflammation and gut health. This study evaluated the impact of cocoa, a polyphenol-rich food, on CeD pathogenesis in a preclinical model. DQ8-D<sup>d</sup>-villin-IL-15tg mice with predisposition to CeD were fed either a GFD (REF), a gluten-containing diet (GLI), or a gluten-containing diet supplemented with cocoa (GLI+COCOA) for 25 days. Outcomes assessed included intestinal histology, antibody (Ab) levels, cytokine and immunoglobulin profiles and mesenteric lymph node lymphocytes’ phenotypes. Cocoa administration limited gluten-induced intestinal villous atrophy and reduced anti-gliadin Abs, while significantly decreasing the secretion of pro-inflammatory cytokines. Moreover, cocoa normalized the Ig isotype profile dysregulated by gluten intake. Cocoa intake exerts a protective effect against key hallmarks of CeD, attenuating inflammation and limiting the damage to the intestinal structure. These findings support cocoa as a promising complementary dietary strategy to modulate CeD-related manifestations, although additional translational studies are warranted","PeriodicalId":212,"journal":{"name":"Molecular Nutrition & Food Research","volume":"49 1","pages":"e70472"},"PeriodicalIF":5.2,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147719654","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}
引用次数: 0
Paternal Malnutrition has Organ-Specific Intergenerational Effects on Mitochondrial Function and Oxidative Stress Induced DNA Damage in Male Mouse Offspring 父亲营养不良对雄性小鼠后代线粒体功能和氧化应激诱导的DNA损伤具有器官特异性代际影响
IF 5.2 2区 农林科学
Molecular Nutrition & Food Research Pub Date : 2026-04-17 DOI: 10.1002/mnfr.70470
Esther S. Lenssen, Sonia de Assis, Alex Remels, Raquel Santana da Cruz, Frederik-Jan van Schooten, Roger W. L. Godschalk
{"title":"Paternal Malnutrition has Organ-Specific Intergenerational Effects on Mitochondrial Function and Oxidative Stress Induced DNA Damage in Male Mouse Offspring","authors":"Esther S. Lenssen, Sonia de Assis, Alex Remels, Raquel Santana da Cruz, Frederik-Jan van Schooten, Roger W. L. Godschalk","doi":"10.1002/mnfr.70470","DOIUrl":"https://doi.org/10.1002/mnfr.70470","url":null,"abstract":"Paternal pre-conceptional lifestyle may affect the offspring's levels of oxidative DNA damage. Therefore, we investigated whether paternal malnutrition affected mitochondrial function, oxidative stress, and DNA damage in lung and liver of mouse offspring at adult age. Adult male C57Bl6 mice received a control or low protein diet (LPD) and were mated with female mice reared on control diets. Offspring was kept under control feeding conditions until adult age. Compared to control, mitochondrial copy number and citrate synthase activity were higher in lung and liver of offspring whose fathers received LPD. Moreover, expression of genes involved in mitochondrial biogenesis was lower in lungs of offspring whose fathers received LPD, but no changes were observed in liver. Mitochondria may be a source of oxidative stress and indeed, levels of 8-oxo-deoxyguanosine (8-oxo-dG) were higher in lungs of offspring whose fathers received LPD. On the contrary, 8-oxo-dG levels in liver were lower in offspring whose father received LPD, which was associated with the tissue-specific expression of enzymatic antioxidants catalase, NAD(P)H: quinone oxidoreductase 1 and γ-glutamylcysteine synthetase. This study confirms that pre-conceptional paternal malnutrition can influence background levels of DNA damage and mitochondrial function in a tissue-specific manner in offspring.","PeriodicalId":212,"journal":{"name":"Molecular Nutrition & Food Research","volume":"18 1","pages":"e70470"},"PeriodicalIF":5.2,"publicationDate":"2026-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147695935","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}
引用次数: 0
Supercritically Extracted Mealworm Oil Alleviates High-Fat Diet-Induced Obesity by Modulating Gut Microbiota in Mice 超临界提取粉虫油通过调节小鼠肠道微生物群减轻高脂肪饮食引起的肥胖
IF 5.2 2区 农林科学
Molecular Nutrition & Food Research Pub Date : 2026-04-17 DOI: 10.1002/mnfr.70445
Ju-Hye Im, Yu-Jin Heo, Mi-Kyung Lee, Hae-In Lee
{"title":"Supercritically Extracted Mealworm Oil Alleviates High-Fat Diet-Induced Obesity by Modulating Gut Microbiota in Mice","authors":"Ju-Hye Im, Yu-Jin Heo, Mi-Kyung Lee, Hae-In Lee","doi":"10.1002/mnfr.70445","DOIUrl":"https://doi.org/10.1002/mnfr.70445","url":null,"abstract":"In this study, we investigated the effects of mealworm oil (MO) supplementation on gut microbiota composition and lipid metabolism in male C57BL/6 mice with high-fat diet (HFD)-induced obesity. The mice were divided into five groups: normal diet (NC), high-fat diet (HFD), HFD with low MO (MOL), HFD with high MO (MOH), and HFD with olive oil (PC). After 16 weeks, body fat composition was analyzed using dual-energy x-ray absorptiometry. MOH intake reduced fat mass and abdominal circumference. MO supplementation decreased body weight, fat mass, and serum lipid levels, and improved insulin resistance. Importantly, MANCOVA/ANCOVA analyses indicated that these metabolic improvements were not solely attributable to reduced food intake. Gut microbiota analysis was performed using 16S rRNA sequencing. <i>Firmicutes</i> were predominantly enriched in the HFD group, while <i>Verrucomicrobiota</i> were enriched in the MOH group. <i>Firmicutes</i> and <i>Deferribacterota</i> showed positive correlations with lipid content and related indicators, whereas <i>Bacteroidetes</i> and <i>Verrucomicrobiota</i> displayed negative correlations. As a result of these changes in microbiota composition, lipogenesis-related genes and proteins were downregulated in the MOH group compared to the HFD group. These findings suggest that MO alleviates obesity in HFD-fed mice by modulating gut microbiota composition and the lipid biosynthesis pathway.","PeriodicalId":212,"journal":{"name":"Molecular Nutrition & Food Research","volume":"5 1","pages":"e70445"},"PeriodicalIF":5.2,"publicationDate":"2026-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147695936","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}
引用次数: 0
Lactational Western-Style Fat Exposure in Mice Programs Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) in Male Offspring 小鼠哺乳期西式脂肪暴露可导致雄性后代代谢功能障碍相关的脂肪变性肝病(MASLD)
IF 5.2 2区 农林科学
Molecular Nutrition & Food Research Pub Date : 2026-04-17 DOI: 10.1002/mnfr.70468
Amy Y. Zhao, Haijing Sun, Leyi Yan, Oyewale Shiyanbola, Dave Bridges, Brigid Gregg
{"title":"Lactational Western-Style Fat Exposure in Mice Programs Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) in Male Offspring","authors":"Amy Y. Zhao, Haijing Sun, Leyi Yan, Oyewale Shiyanbola, Dave Bridges, Brigid Gregg","doi":"10.1002/mnfr.70468","DOIUrl":"https://doi.org/10.1002/mnfr.70468","url":null,"abstract":"Metabolic dysfunction-associated steatotic liver disease (MASLD) is the leading cause of liver disease. Early-life exposure to maternal overnutrition during critical developmental windows, such as lactation, can predispose offspring to develop metabolic disease. We previously demonstrated that consumption of a high fat diet (60% fat) during lactation leads to the development of insulin resistance and MASLD in male offspring. However, no studies have investigated the role of a lactational Western-style fat (45% fat) exposure, which is more clinically relevant and representative of human food consumption habits. Dams were fed either a standard chow or Western-style fat diet from delivery through the 21-day lactation period. At weaning, all offspring were fed standard chow until 3 months of age, when a subset from each group was challenged with an additional high-fat stressor. Exposure to a Western-style fat diet during lactation increased male offspring susceptibility to weight gain, obesity, and insulin resistance when fed a high fat diet in adulthood. Furthermore, these offspring demonstrated hepatomegaly and hepatic triglyceride accumulation, which may be mediated by altered lipid metabolism. These findings indicate that an indirect neonatal exposure to a Western-style fat diet can program male offspring to develop MASLD later in life.","PeriodicalId":212,"journal":{"name":"Molecular Nutrition & Food Research","volume":"440 1","pages":"e70468"},"PeriodicalIF":5.2,"publicationDate":"2026-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147695971","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}
引用次数: 0
Chia Oil Supplementation Attenuates Obesity-Induced Hepatic Steatosis, PVAT Inflammation, and Endothelial Dysfunction in Mice 补充奇异油可减轻小鼠肥胖诱导的肝脂肪变性、PVAT炎症和内皮功能障碍
IF 5.2 2区 农林科学
Molecular Nutrition & Food Research Pub Date : 2026-04-17 DOI: 10.1002/mnfr.70469
Agatha de Assis-Ferreira, Gabrielly Muniz-Cassuce, Thaís Fonte-Faria, Thamiris de Souza, Marta Citelli, Lenize Costa Reis Marins de Carvalho, Dayane Teixeira Ognibene, Graziele Freitas de Bem, Angela Castro Resende, Christina Barja-Fidalgo, Simone Vargas da Silva
{"title":"Chia Oil Supplementation Attenuates Obesity-Induced Hepatic Steatosis, PVAT Inflammation, and Endothelial Dysfunction in Mice","authors":"Agatha de Assis-Ferreira, Gabrielly Muniz-Cassuce, Thaís Fonte-Faria, Thamiris de Souza, Marta Citelli, Lenize Costa Reis Marins de Carvalho, Dayane Teixeira Ognibene, Graziele Freitas de Bem, Angela Castro Resende, Christina Barja-Fidalgo, Simone Vargas da Silva","doi":"10.1002/mnfr.70469","DOIUrl":"https://doi.org/10.1002/mnfr.70469","url":null,"abstract":"Obesity promotes metabolic disturbances that contribute to hepatic steatosis, adipose tissue dysfunction, and vascular impairments. Perivascular adipose tissue (PVAT) plays a critical role in vascular homeostasis, yet little is known about plant-derived omega 3 fatty acids modulate PVAT remodeling during obesity. Here, we investigated whether dietary chia oil supplementation, an abundant source of α-linolenic acid, attenuates metabolic, inflammatory, and vascular dysfunction in obese mice. Male C57BL/6J mice were fed a chow (C) or high-fat diet (HF) diet for 14 weeks and a subset of high-fat-fed mice received chia oil (1.5% v/v) from weeks 8–14 (HC). Chia oil improved insulin sensitivity, increased adiponectin levels, and reduced leptin and hepatic triglyceride accumulation. Histological and molecular analyses showed decreased macrovesicular steatosis and FABP4 expression beside increased CPT-1α and PGC-1α, indicating enhanced lipid oxidation. In mesenteric PVAT, chia oil reduced adipocyte hypertrophy and macrophage infiltration while increasing IL-10 and CD206 expression. Functionally, chia oil restored acetylcholine-induced vasodilation, reduced norepinephrine-mediated vasoconstriction, and increased AMPK phosphorylation. Chia oil supplementation ameliorates key features of obesity-associated metabolic dysfunction, supporting ALA-rich oils as promising nutritional strategies against metabolic disease.","PeriodicalId":212,"journal":{"name":"Molecular Nutrition & Food Research","volume":"23 1","pages":"e70469"},"PeriodicalIF":5.2,"publicationDate":"2026-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147695970","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}
引用次数: 0
Issue Information: Mol. Nutr. Food Res. 8'26 发布信息:Mol. Nutr。Food Res. 8'26
IF 4.2 2区 农林科学
Molecular Nutrition & Food Research Pub Date : 2026-04-16 DOI: 10.1002/mnfr.70474
{"title":"Issue Information: Mol. Nutr. Food Res. 8'26","authors":"","doi":"10.1002/mnfr.70474","DOIUrl":"https://doi.org/10.1002/mnfr.70474","url":null,"abstract":"","PeriodicalId":212,"journal":{"name":"Molecular Nutrition & Food Research","volume":"70 8","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/mnfr.70474","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147686040","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"农林科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Isoeugenol Inhibits Growth, Migration, and Invasion in Colorectal Cancer Cells With Distinct Molecular Characteristics 异丁香酚抑制结直肠癌细胞的生长、迁移和侵袭具有独特的分子特征
IF 4.2 2区 农林科学
Molecular Nutrition & Food Research Pub Date : 2026-04-16 DOI: 10.1002/mnfr.70466
Zih-Shuan Liou, Chih-Chun Kuo, Chien-Chih Yeh, Le Thi Bao Tran, Yi-Qi Chen, Li-Jane Shih, Chih-En Kao, Ching-Feng Cheng, Yung-Hsi Kao, Hui-Chen Ku
{"title":"Isoeugenol Inhibits Growth, Migration, and Invasion in Colorectal Cancer Cells With Distinct Molecular Characteristics","authors":"Zih-Shuan Liou,&nbsp;Chih-Chun Kuo,&nbsp;Chien-Chih Yeh,&nbsp;Le Thi Bao Tran,&nbsp;Yi-Qi Chen,&nbsp;Li-Jane Shih,&nbsp;Chih-En Kao,&nbsp;Ching-Feng Cheng,&nbsp;Yung-Hsi Kao,&nbsp;Hui-Chen Ku","doi":"10.1002/mnfr.70466","DOIUrl":"https://doi.org/10.1002/mnfr.70466","url":null,"abstract":"<div>\u0000 \u0000 <p>Colorectal cancer (CRC) is the second common cause of cancer death in the world and its development can be regulated by herbal compounds. Unfortunately, little information is known about the signal pathways of <i>Piper betle</i> isoeugenol in CRC cells (CRCCs). Using three CRC cell lines (SW480, SW620, and HCT116) that represent different molecular characteristics and serve as in vitro models of CRC progression, we found that isoeugenol inhibited cell growth. Wound healing and Boyden chamber assays indicated that isoeugenol inhibited the migration and invasion in CRCCs. Mechanistically, isoeugenol suppressed key regulators of cell cycle progression and epithelial–mesenchymal transition (EMT), including pAKT, CDK4, CDK6, cyclin D1, N-cadherin, and Snail, while increasing the levels of pAMPK, pJNK, pp38 MAPK, and E-cadherin. Cell line-specific modulation of CDK2, cyclin D3, p21, p27, and pERK proteins was also observed. Furthermore, isoeugenol inhibited the enzymatic activities of MMP-2 and MMP-9. Pharmacological inhibition of AMPK or p38 antagonized isoeugenol-suppressed cell growth, migration, invasion, and associated signaling events. In conclusion, these data suggest that isoeugenol may inhibit CRCC growth, migration, and invasion through activations of AMPK and p38 MAPK pathways and modulating pathways involved in cell cycle regulation and EMT.</p>\u0000 </div>","PeriodicalId":212,"journal":{"name":"Molecular Nutrition & Food Research","volume":"70 8","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147686042","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}
引用次数: 0
Anacardic Acid Inhibits Pde2a to Enhance Colonic Epithelial Barrier Integrity in the Improvement of Diabetic Cardiomyopathy 无心酸抑制Pde2a增强结肠上皮屏障完整性改善糖尿病性心肌病
IF 4.2 2区 农林科学
Molecular Nutrition & Food Research Pub Date : 2026-04-16 DOI: 10.1002/mnfr.70464
Rui Ge, Jialin Yin, Huali Meng, Xiaoli Huang, Lei Sun, Yan Zheng, Jianjun Yang, Hao Wu
{"title":"Anacardic Acid Inhibits Pde2a to Enhance Colonic Epithelial Barrier Integrity in the Improvement of Diabetic Cardiomyopathy","authors":"Rui Ge,&nbsp;Jialin Yin,&nbsp;Huali Meng,&nbsp;Xiaoli Huang,&nbsp;Lei Sun,&nbsp;Yan Zheng,&nbsp;Jianjun Yang,&nbsp;Hao Wu","doi":"10.1002/mnfr.70464","DOIUrl":"https://doi.org/10.1002/mnfr.70464","url":null,"abstract":"<div>\u0000 \u0000 <p>Diabetic cardiomyopathy (DCM) results in high mortality with surprisingly rare therapeutic approaches. Anacardic acid (AA) shows broad pharmacological properties, but its effect on DCM was unknown. This study aims to investigate the effect and molecular action of AA on DCM. KKAy mice, a model of spontaneous type 2 diabetes, were fed a high-fat diet, and were subsequently administered with AA by gavage at 5 mg/kg for 14 weeks. AA attenuated cardiac dysfunction, pathological injuries, inflammation, fibrosis, oxidative stress, and apoptosis. Mechanistically, AA was enriched in the colon, but not serum and heart, improving colonic histopathological scores, enhancing colonic tight junction protein expression and reducing serum lipopolysaccharide level, suggesting colonic epithelial barrier integrity (CEBI) as a key target of AA. In vitro experiment employed high glucose and palmitic acid-challenged colonic epithelial cells as a cell model of CEBI, showing that AA at 5 µmol/L reversed the impaired expression of tight junction proteins. RNA-sequencing identified <i>Pde2a</i> gene to be significantly inhibited by AA. Lentivirus-induced <i>Pde2a</i> overexpression in colonic epithelial cells abolished the protective effect of AA on CEBI. The present study reports that AA enhances CEBI to attenuate DCM, possibly through inhibiting colonic epithelial expression of <i>Pde2a</i>.</p>\u0000 </div>","PeriodicalId":212,"journal":{"name":"Molecular Nutrition & Food Research","volume":"70 8","pages":""},"PeriodicalIF":4.2,"publicationDate":"2026-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147686041","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}
引用次数: 0
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