Journal of Nutritional Biochemistry最新文献

{"title":"Association between maternal obesity and neonatal folate and vitamin B12 status: functional biomarkers and placental transporters.","authors":"Erika Castaño-Moreno, Karina Carrasco-Negue, Rocío Díaz de la Garza, Víctor Treviño, Chittaranjan S Yajnik, Yvonne Lamers, María L Garmendia, Ana M Ronco, Paola Casanello","doi":"10.1016/j.jnutbio.2026.110393","DOIUrl":"https://doi.org/10.1016/j.jnutbio.2026.110393","url":null,"abstract":"<p><strong>Background: </strong>Pregestational obesity increases the risk of vitamin deficiencies in mothers, yet its impact on neonatal status and placental transporters is unclear. This study investigates the association between pregestational obesity and neonatal folate and vitamin B12 levels, as well as their biomarkers and the expression of placental transporters.</p><p><strong>Methods: </strong>This cross-sectional study included women with pregestational overweight or obesity (BMI >25 kg/m²; Ob group) and healthy weight (BMI <25 kg/m²; HW group). In mothers and newborns, folate status was measured in plasma and RBCs using LC-MS/MS to identify six chemical forms, and total vitamin B12 was quantified by ECLIA, holotranscobalamin (holoTC) by CMIA, methylmalonic acid (MMA) by LC-MS/MS, and total homocysteine (tHCY) by HPLC-FD in plasma. Placental FOLR1 and TCblR/CD320 were examined using RT-qPCR and Western blot. A p-value <0.05 was considered statistically significant.</p><p><strong>Results: </strong>Women in the Ob-group had lower RBC folate status than those in the HW-group. Newborns of Ob-groups had decreased folate forms, total vitamin B12, holoTC, and higher MMA. Female newborns displayed greater folate and vitamin B12 depletion than females in the HW. Placental expression of FOLR1 (protein) and TCblR/CD320 (mRNA) was lower in the Ob. Conversely, FOLR1 and TCblR/CD320 (mRNA and protein) were higher in female compared to male placentas (p<0.05).</p><p><strong>Conclusions: </strong>Maternal obesity is associated with decreased neonatal folate and vitamin B12 levels, as confirmed by functional biomarkers. Altered placental FOLR1 and CD320 expression suggests impaired vitamin transport in obesity. The sex-specific differences may indicate an adaptive response in the female placenta, but further studies of mechanisms are warranted.</p>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":" ","pages":"110393"},"PeriodicalIF":4.9,"publicationDate":"2026-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147838888","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Leptin Mediates the Effects of Sulfur Amino Acid Restriction on Food Intake and Body Weight in Mice.","authors":"Diana Cooke, Amadou Ouattara, Gene P Ables","doi":"10.1016/j.jnutbio.2026.110396","DOIUrl":"https://doi.org/10.1016/j.jnutbio.2026.110396","url":null,"abstract":"<p><p>Sulfur amino acid restriction (SAAR) paradoxically increases food intake while inducing weight loss, but the mechanisms underlying these outcomes remain unclear. To investigate the role of leptin in this response, we assessed food intake, body weight, and metabolic markers in diet-induced obese (DIO), leptin-deficient (ob/ob), and leptin receptor-deficient (db/db) mice. In DIO-SAAR mice, increased food intake was associated with hypothalamic upregulation of orexigenic (Agrp, Npy, and Mchr1) and downregulation of anorexigenic (Pomc, Cartpt, and Bdnf) mRNA levels. This orexigenic profile is accompanied by reduced adiposity and lower circulating leptin levels, suggesting that decreased leptin may induce compensatory increased food intake. Despite increased food intake, SAAR also induces weight loss, which is associated with enhanced β3-adrenergic signaling in brown and inguinal white AT (BAT and iWAT), as reflected by elevated Adrb3 and Ucp1 mRNA levels but downregulated protein expression, suggesting post-transcriptional regulation. These phenotypes induced by SAAR may possibly involve thyroid hormone metabolism, as indicated by increased circulating T3 and T4 concentrations and upregulation of BAT deiodinase 2 (D2) mRNA. Importantly, these metabolic effects of SAAR are attenuated in ob/ob and abolished in db/db mice, despite reductions in circulating SAA levels. Furthermore, leptin treatment during SAAR reduced food intake, induced weight loss, demonstrating preserved leptin sensitivity in low fat diet-fed and ob/ob mice. These findings reveal that leptin is required for both increased food intake and weight loss during SAAR.</p>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":" ","pages":"110396"},"PeriodicalIF":4.9,"publicationDate":"2026-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147838892","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"L-Theanine Activates the mTOR Signaling Pathway through TAS1R1-FRMD6 To Promote Milk Synthesis in Bovine Mammary Epithelial Cells.","authors":"Xiechen Zhou, Mingyang Sun, Naiyuan Jiang, Ji Cheng, Feng Li, Jiaxin Wang, Wenjin Guo, Juxiong Liu, Yu Cao, Shoupeng Fu","doi":"10.1016/j.jnutbio.2026.110395","DOIUrl":"https://doi.org/10.1016/j.jnutbio.2026.110395","url":null,"abstract":"<p><p>L-Theanine (LT), a characteristic amino acid found in tea, possesses diverse biological activities, including antioxidant, growth-promoting, and immune-enhancing effects, and is widely used in supplements. However, the regulatory role of LT in milk synthesis in dairy cows remains unclear. This study aimed to elucidate the effects of LT on milk synthesis and its underlying molecular mechanisms in primary bovine mammary epithelial cells (BMECs). We isolated primary BMECs and investigated the effects of LT treatment (100 μM), utilizing overexpression and knockdown techniques for TAS1R1, FERM domain containing 6 (FRMD6), and mTOR. Results showed that 100 μM LT significantly promoted BMECs proliferation and the synthesis of milk protein and fat. Knockdown of its putative receptor, TAS1R1, reversed these stimulatory effects of LT. Transcriptome sequencing analysis revealed FRMD6 as a key target gene mediating the LT-induced promotion of BMEC proliferation and milk synthesis. Mechanistic studies further indicated that LT enhanced the interaction between FRMD6 and mTOR, promoted mTOR translocation from the cytoplasm to the lysosomal surface, subsequently leading to the activation of the mTORC1 signaling pathway, ultimately promoting milk synthesis. The clinical experiment results on dairy cows show that Rumen-Protected LT can significantly increase the milk production of mid-lactation cows and improve the quality of their milk. In conclusion, our research provides strong preclinical evidence for LT as a potential functional feed additive to promote milk synthesis.</p>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":" ","pages":"110395"},"PeriodicalIF":4.9,"publicationDate":"2026-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147838852","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Microbial-derived Mediators of the Gut-Brain Axis: Implications for Neurological Disorders.","authors":"Mariam M Abady, Amal M Shawky, Dina Mostafa Mohammed","doi":"10.1016/j.jnutbio.2026.110394","DOIUrl":"https://doi.org/10.1016/j.jnutbio.2026.110394","url":null,"abstract":"<p><p>Gut-brain communication is mediated by metabolic and signaling pathways that play important roles in brain development and cognitive function. Recently, the bidirectional role of the gut microbiota in the Gut-Brain axis has drawn greater scientific attention. The gut microbiota, a group of bacteria that naturally colonize the gastrointestinal tract of mammals, may play a role in healthcare burden neurodegeneration, which affects many of the body's activities. Lately, it has been reported that some mediators produced by changes in the gut microbiota are associated with neurodegenerative diseases. Additionally, the host immune system plays a role in Gut-Brain communication, as gut microbiota are potent modulators of immune cells that reside in the central nervous system. Unfortunately, the majority of current strategies are based on pre-clinical studies, with little known about the causes and molecular mechanisms. Herein, we summarize the evidence supporting an integrated hypothesis of mediators in neurodegenerative diseases and Gut-Brain communication, which result from biologically conserved interactions and factors related to the distinct composition of the gut microbiota. We also mention the need for establishing a standardized approach for particular focal parts of the microbiota-Gut-Brain Axis, thorough biological sample analyses, dietary strategies, and recognition of a new therapeutic paradigm. A stronger emphasis on omics technologies and on advanced in vitro and in vivo models is also urgently needed. This will enable research on the microbiota- Gut-Brain axis to proceed to the next stage, allowing us to identify practical opportunities to modify the microbiota for enhanced brain health.</p>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":" ","pages":"110394"},"PeriodicalIF":4.9,"publicationDate":"2026-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147838975","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Niacin enhances erythropoiesis and attenuates oxidative stress and ferroptosis through the modulation of Nrf2/HO-1/GPX4 pathway in phenylhydrazine-induced hemolytic anemia in rats.","authors":"Muhammed Ramadan Galal, Ayman Saber Mohamed, Ahmed Abdel Aziz Bayoumi, Shaymaa Mohamed Eissa","doi":"10.1016/j.jnutbio.2026.110392","DOIUrl":"https://doi.org/10.1016/j.jnutbio.2026.110392","url":null,"abstract":"<p><p>Anemia is a public health issue affecting people of all ages worldwide. 43% of children under five in Egypt are suffering from anemia. Hemolytic anemia (HA), characterized by the premature destruction of red blood cells, is often associated with oxidative stress. Phenylhydrazine (PHZ) is a chemical substance frequently used to induce HA in experimental animal models. Studies indicate that niacin (nicotinic acid) activates antioxidant pathways through nuclear factor erythroid 2-related factor 2 (Nrf2). This study aimed to evaluate the anti-anemic effects of niacin in PHZ-induced hemolytic anemia in rats. Twenty-four rats were divided into four groups (n=6). The control group received saline for two days, then 5% CMC. The anemia group received PHZ (40 mg/kg/day, i.p.) for two days, followed by 5% CMC. The low- and high-dose niacin groups received PHZ for two days, then niacin (100 or 360 mg/kg/day, orally) for six days. Niacin-treated groups showed hematological parameters close to normal levels, affected the expression of Nrf2/ARE genes, preserved histological architecture, and reduced caspase-3 protein expression. Niacin protected rats from hemolytic anemia by restoring blood parameters and promoting red blood cell survival. It may serve as a potential treatment by reducing oxidative stress, ferroptosis, and inflammation, while supporting erythropoiesis.</p>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":" ","pages":"110392"},"PeriodicalIF":4.9,"publicationDate":"2026-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147838971","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vitamin E and related tocols in cancer: Unraveling the paradox of antioxidant and pro-oxidant roles","authors":"Fen Xiao ,&nbsp;Zhi-Bin Wang ,&nbsp;Nayiyuan Wu ,&nbsp;Xiu Zhang ,&nbsp;Xing Yu ,&nbsp;Zu-Ping He ,&nbsp;Jing Wang","doi":"10.1016/j.jnutbio.2026.110265","DOIUrl":"10.1016/j.jnutbio.2026.110265","url":null,"abstract":"<div><div>Vitamin E, strictly defined as α-tocopherol, exhibits a complex dual role in cancer pathogenesis through its context-dependent pro-oxidant and antioxidant activities. Other members of the tocopherol and tocotrienol families (collectively referred to as tocols) have also been extensively studied for their bioactivities. At physiological levels, certain tocols such as γ-tocopherol and δ-tocotrienol act as potent antioxidants by neutralizing reactive oxygen species, inhibiting lipid peroxidation, and activating NRF2-mediated defenses, thereby suppressing tumor initiation, proliferation, and metastasis in models of colon, breast, and prostate cancers. On the contrary, under conditions such as high concentration of vitamin E in plasma, metabolic dysregulation, and the presence of transition metals (<em>e.g.</em>, Cu²⁺), or specific genetic backgrounds, vitamin E exerts pro-oxidant effects. However, such effects are relatively rare and more often documented <em>in vitro</em> than <em>in vivo</em>. These include promoting reactive oxygen species generation, reducing p53 expression, enhancing angiogenesis, and facilitating cancer cell survival—ultimately driving tumor progression and metastasis. Critically, vitamin E modulates ferroptosis, a regulated cell death pathway pivotal in cancer; it inhibits ferroptosis via GPX4 upregulation and NRF2 activation but may paradoxically promote it in certain settings. Clinical studies highlight isomer-specific outcomes, with tocotrienols showing promise in adjuvant therapy. The dichotomy hinges on dosage, cellular microenvironment, redox balance, and vitamin E isoform. Overall, the biological impact of vitamin E is highly context-dependent, influenced by dosage, cellular microenvironment, redox status, and the specific tocol studied. Future research must prioritize isoform-specific mechanisms, optimal dosing strategies, and interactions with conventional therapies to harness vitamin E and related tocols’s anticancer potential while mitigating risks.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"151 ","pages":"Article 110265"},"PeriodicalIF":4.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145984938","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Brown adipocyte-derived SAA3–CPT1A axis regulates diet-induced thermogenesis and protects against obesity","authors":"Pei-Chi Chan ,&nbsp;Chun-Han Jhuang ,&nbsp;Hsin-Yi Chang ,&nbsp;Po-Shiuan Hsieh","doi":"10.1016/j.jnutbio.2026.110263","DOIUrl":"10.1016/j.jnutbio.2026.110263","url":null,"abstract":"<div><div>Diet-induced thermogenesis (DIT), a critical component of energy expenditure driven by brown adipose tissue (BAT), is essential for maintaining metabolic health; however, its precise molecular regulation remains poorly understood. We investigated whether serum amyloid A3 (SAA3), a factor secreted by brown adipocytes, regulates DIT and protects against diet-induced obesity. Using two distinct mouse models: mice with brown adipocyte-specific Saa3 deletion and mice with lentiviral-mediated Saa3 overexpression in BAT, we examined energy expenditure, substrate utilization, and thermogenic responses under chow or short-term high-fat diet feeding. SAA3 expression in BAT was acutely induced by refeeding. Loss of SAA3 severely diminished postprandial DIT and total energy expenditure, leading to accelerated weight gain on a high-fat diet. Mechanistically, Saa3 deletion compromised uncoupling protein‑1 induction, chiefly by impairing adipose triglyceride lipase-driven lipolysis and, critically, by inhibiting carnitine palmitoyltransferase 1A (CPT1A)-dependent fatty acid oxidation (FAO). Conversely, SAA3 overexpression robustly enhanced DIT, stimulated lipolysis and FAO, and promoted mitochondrial oxidative phosphorylation. Studies in primary brown adipocytes confirmed that SAA3 deficiency reduced CPT1A expression, palmitate-stimulated lipolysis, and mitochondrial respiration. Together, these findings identify the SAA3–CPT1A axis as a novel, BAT-intrinsic mechanism that couples nutrient sensing to uncoupling protein‑11 function via enhanced FAO. By promoting lipid utilization and postprandial energy dissipation, SAA3 optimizes postprandial thermogenesis and defends against obesity, highlighting conserved SAA signaling as a potential nutritional and therapeutic target in metabolic disease.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"151 ","pages":"Article 110263"},"PeriodicalIF":4.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145984980","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chronic theobromine administration attenuates short-term memory decline via neurotrophic, anti-inflammatory and antioxidant mechanisms in senescence-accelerated mouse prone 8 (SAMP8)","authors":"Eri Sumiyoshi ,&nbsp;Kentaro Matsuzaki ,&nbsp;Masanori Katakura ,&nbsp;Shadman Nazib ,&nbsp;Shahdat Hossain ,&nbsp;Sho Maejima ,&nbsp;Ying Zhang ,&nbsp;Hiroko Kishi ,&nbsp;Naotoshi Sugimoto ,&nbsp;Osamu Shido","doi":"10.1016/j.jnutbio.2025.110258","DOIUrl":"10.1016/j.jnutbio.2025.110258","url":null,"abstract":"<div><div>Aging-related cognitive decline is a major concern in aging societies. Theobromine (TB), a cacao-derived methylxanthine, exerts neuroprotective effects through anti-inflammatory, antioxidant, and neurotrophic mechanisms; however, its efficacy in aging models remains unclear. This study investigated the mechanisms underlying neuroprotective effects of chronic TB administration in senescence-accelerated mouse prone 8 (SAMP8), a model of age-related memory impairment. SAMP8 and SAMR1 mice were fed either a control diet or a diet supplemented with 0.05% TB for 50 d. Cognitive performance was evaluated by the novel object recognition (NOR) test. Neurotrophic factors (BDNF and NT-3), synaptic proteins (PSD95 and synaptophysin), and plasticity-related signaling molecules (phosphorylated CREB and TrkB) were analyzed in the prefrontal cortex and hippocampus. Inflammatory cytokines, lipid peroxides, and antioxidant enzymes were quantified. Molecular docking was used to assess TB’s interaction with phosphodiesterase (PDE) enzymes. TB improved short-term memory in SAMP8, increasing discrimination index in the NOR test. This was accompanied by increased BDNF, NT-3, PSD95, and synaptophysin levels and enhanced CREB and TrkB phosphorylation. Furthermore, TB lowered the levels of pro-inflammatory cytokines (IL-1β, TNF-α) and phosphorylated NF-κB, reduced lipid peroxidation, and increased the levels of antioxidant markers (HO-1, GSH). These effects were minimal in SAMR1. No adverse effects on body weight or blood parameters were observed. Molecular docking indicated that TB binds to PDE enzymes with weaker inhibitory activity than selective inhibitors. TB enhances short-term memory and synaptic function in aged mice via neurotrophic, antioxidant, and anti-inflammatory mechanisms, supporting its potential as a safe dietary intervention for age-related cognitive decline.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"151 ","pages":"Article 110258"},"PeriodicalIF":4.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145892525","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prebiotic fructan chain length influences enteric microbiota-host GABAergic signaling and intestinal motility","authors":"Benjamin A. Levine ,&nbsp;Alexis J. Lynch ,&nbsp;Michael T. Bailey ,&nbsp;Brett R. Loman","doi":"10.1016/j.jnutbio.2025.110234","DOIUrl":"10.1016/j.jnutbio.2025.110234","url":null,"abstract":"<div><div>Dietary fiber ingestion serves as a critical regulator of intestinal motility and the structure and function of the enteric microbiome. Yet, the extent to which subtle structural differences among fibers modulate motility via microbiota-host interactions remains undefined. GABA is a microbial metabolite intimately related to microbial fructan fermentation and host intestinal motility. The purpose of this study was to investigate how fructan chain length influenced microbiota-host signaling underlying ileal and colonic contractions. Male and female mice were pair-fed diets containing no fiber (fiber-free diet, FFD) or the same diet containing cellulose (CELL, fiber control), short-chain fructooligosaccharides (scFOS), or inulin (INU) for 2 weeks. scFOS and INU similarly enhanced total microbial load (fluorescence in situ hybridization), relative abundances of GABA-synthesizing bacteria (16S rRNA sequencing), and luminal GABA concentrations (ELISA) in the ileum and colon versus FFD. Conversely, scFOS altered expression (Fluidigm qPCR) of more motility- and GABA-related genes than INU in the ileum, whereas INU altered expression of more motility and GABA-related genes than scFOS in the colon. Incubation of ileal segments with GABA potentiated contraction force in INU but not scFOS ex vivo. Conversely, incubation of colon segments with GABA repressed contraction force in scFOS, reducing them to levels observed in INU with or without GABA. Notably, GABA altered contraction forces only in female mice. Our study highlights dietary fructan chain length as a determinant of segment- and sex-specific GABA-mediated intestinal motility and creates a rationale and framework for investigation of how prebiotic fiber structures influence microbiota-host interactions and physiology.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"151 ","pages":"Article 110234"},"PeriodicalIF":4.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145805016","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association between dairy-derived bioactive peptides and the risk of type 2 diabetes mellitus and cardiovascular diseases: Tehran lipid and glucose study","authors":"Fatemeh Ghasemi ,&nbsp;Farshad Teymoori ,&nbsp;Sajjad Roosta ,&nbsp;Mitra Kazemi Jahromi ,&nbsp;Hossein Farhadnejad ,&nbsp;Parvin Mirmiran ,&nbsp;Ebrahim Falahi ,&nbsp;Fereidoun Azizi","doi":"10.1016/j.jnutbio.2026.110260","DOIUrl":"10.1016/j.jnutbio.2026.110260","url":null,"abstract":"<div><div>Cardiometabolic diseases, including type 2 diabetes mellitus (T2DM) and cardiovascular diseases (CVDs) are escalating globally, posing significant health challenges. While dairy products and their bioactive peptides (BPs) may influence chronic diseases risk, the evidence remains inconsistent. These peptides may act via modulation of gut microbiota, reducing inflammation, and regulating lipid metabolism. The current study aimed to investigate the possible association between dairy-derived BPs (DDBPs) and the risk of T2DM and CVDs in Iranian adult population within the framework of Tehran Lipid and Glucose Study (TLGS). In this population-based cohort study, 5,469 participants (T2DM analysis) and 4,980 participants (CVDs analysis) from the TLGS were followed for a mean follow-up period of 6 years. Dietary intake data were determined using a validated food-frequency-questionnaire. Various types of DDBPs were estimated via in-silico proteolysis simulations. The association of bioactive peptides with T2DM and CVDs risk were determined using Cox proportional hazards regression models. Higher intake of k-casein-derived peptides (HR:1.21;95% CI: 1.01–1.64), Hepta-peptides (HR:1.31;95% CI:1.02–1.67), peptides with glycosylated residues (HR:1.29;95%CI: 1.01–1.65), glycosylated residues (HR:1.39;95% CI: 1.07–1.80), and disulfide bond- containing peptides (HR:1.34;95% CI: 1.05–1.71) was associated with an elevated T2DM risk in the adjusted model. Dairy protein intake (highest vs. lowest tertile: HR:1.29;95% CI: 1.02–1.62) Also increased T2DM risk, while total dairy intake showed no association. No significant associations were found between DDBPs, dairy intake, or dairy protein intake and the risk of CVDs. Our results showed that specific DDBPs particularly k-casein-derived fragments and structurally modified peptides (including hepta-peptides, glycosylated peptides, and peptides with disulfide bonds), were associated with an increased risk of T2DM in Tehranian adults. Further studies are warranted to elucidate these associations.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"151 ","pages":"Article 110260"},"PeriodicalIF":4.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145906260","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}