PharmaNutrition最新文献

{"title":"Vitamin D does not mitigate monocyte adhesion to vascular endothelial cells in an in vitro pro-inflammatory model","authors":"Mirko Marino ,&nbsp;Samuele Venturi ,&nbsp;Peter Møller ,&nbsp;Marco Rendine ,&nbsp;Daniela Martini ,&nbsp;Patrizia Riso ,&nbsp;Cristian Del Bo'","doi":"10.1016/j.phanu.2025.100454","DOIUrl":"10.1016/j.phanu.2025.100454","url":null,"abstract":"<div><div>Vitamin D deficiency has been associated with cardiovascular risk factors, including endothelial dysfunction, a critical step in the pathogenesis of atherosclerosis. This study aimed to evaluate the effects of 1α,25-dihydroxycholecalciferol (VD3) on monocyte (THP-1) adhesion to human umbilical vein endothelial cells (HUVECs) under a pro-inflammatory condition. Endothelial cell activation was induced with tumor necrosis factor-alpha (TNF-α, 100 ng/mL), and cells were treated with VD3 at concentrations ranging from 0.1 to 100 nM. Monocyte adhesion was quantified spectrophotometrically, while levels of vascular cell adhesion molecule 1 (VCAM-1), E-selectin, and cluster of differentiation 15 (CD15) were assessed using ELISA. TNF-α significantly increased THP-1 cell adhesion to HUVECs compared to the control group (p &lt; 0.05). Co-treatment with VD3 at all concentrations tested did not reduce monocyte adhesion, showing levels similar to the TNF-α only group, and significantly higher than the negative control (p &lt; 0.05). Furthermore, TNF-α significantly upregulated VCAM-1 expression (p &lt; 0.05), which was unaffected by VD3. E-selectin and CD15 levels remained unchanged under all experimental conditions. These results do not support a modulatory role for VD3 in the early stages of atherogenesis, specifically in reducing endothelial cell activation and monocyte adhesion. While vitamin D has shown beneficial effects in other aspects of cardiovascular health, its impact on vascular inflammation and adhesion processes remains uncertain and needs further investigation.</div></div>","PeriodicalId":20049,"journal":{"name":"PharmaNutrition","volume":"34 ","pages":"Article 100454"},"PeriodicalIF":2.4,"publicationDate":"2025-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145183786","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Functional food prevents diabetic nephropathy in a rat model through inhibition of aldose reductase and accumulation of advanced glycation end-products","authors":"Krishna Kalyan Kalahasti,&nbsp;Marka Nagaraju,&nbsp;Sneha Jakhotia,&nbsp;S.Sreenivasa Reddy,&nbsp;G.Bhanuprakash Reddy","doi":"10.1016/j.phanu.2025.100446","DOIUrl":"10.1016/j.phanu.2025.100446","url":null,"abstract":"<div><div>Diabetic nephropathy (DN) is a chronic microvascular complication of diabetes mellitus, characterized by glomerulomegaly, podocytopathy, and proteinuria. Among the many molecular mechanisms, accumulation of advanced glycation end-products (AGEs) due to non-enzymatic glycation and sorbitol accumulation due to increased aldose reductase (AR) activity are implicated in DN. We previously identified some functional foods and their bioactive molecules for inhibitory potential against AGE formation and, AR activity. Based on those studies, in this study, we formulated a functional food (FF) mix- composed of amla, turmeric, cinnamon, ginger, and black pepper in a specific proportion and tested its efficacy against DN in a rat model. Two-month-old Sprague Dawley rats were grouped into control (C), streptozotocin-induced diabetes (D), and diabetes treated with FF at two doses (FF1–0.85 g and FF2–4.25 g/ 100 g diet). The animals were maintained for 20 weeks on respective diets after the induction of diabetes. Elevated serum albumin, creatinine, and urea were observed in the untreated diabetic group compared to the control. These changes were significantly ameliorated by FF supplementation. FF2 showed better efficacy than FF1 in preventing proteinuria, as reflected in the albumin and creatinine ratio. Further, FF prevented diabetes induced AGE accumulation, inflammation, and activation of the polyol pathway in the kidney. The FF decreased the expression of TGF-β in the diabetic kidney and prevented fibrotic changes. Most importantly, FF prevented the depletion of podocyte slit diaphragm proteins and histological changes. These results provide a mechanistic basis of FF and its potential against progression of DN in a rat model.</div></div>","PeriodicalId":20049,"journal":{"name":"PharmaNutrition","volume":"33 ","pages":"Article 100446"},"PeriodicalIF":2.4,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144770805","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Enhanced therapeutic efficacy of nanocurcumin over free curcumin in the management of diabetes mellitus","authors":"Pratibha Chauhan ,&nbsp;GBKS Prasad","doi":"10.1016/j.phanu.2025.100445","DOIUrl":"10.1016/j.phanu.2025.100445","url":null,"abstract":"<div><h3>Objectives</h3><div>Numerous scientific studies have revealed that curcumin is a pleiotropic molecule and influences multiple signaling pathways but is rapidly eliminated from the body due to its poor bioavailability. In the present study, nanocurcumin was synthesized and evaluated the therapeutic efficacy of nanocurcuminin comparison to those of free curcumin in human subjects with type II diabetes mellitus.</div></div><div><h3>Design</h3><div>Curcumin nanoparticles (NPs) have been synthesized then analyzed employing particle size analyzer and X-ray diffraction, while therapeutic efficacy of nanocurcumin has been assessed by evaluating blood glucose level (BGL), lipid profiles, as well as oxidative stress markers. This randomized trial included subjects (n = 60) with criteria of type II diabetes mellitus(T2DM). Subjects had been allocated randomly for receiving either curcumin or nanocurcumin capsules (1000 mg/day and 600 mg/day, accordingly) for 12 weeks. Nanocurcumin capsules' therapeutic function has been investigated by monitoring blood glucose, lipid profile, oxidative stress biomarkers, and glycosylated hemoglobin, along with DNA damage, prior to and after therapy.</div></div><div><h3>Results</h3><div>Particle size analysis indicated an average particle size of 78 nm of nanocurcumin. 'Nanocurcumin capsules' daily administration for 12 weeks drastically reduced BGLs. Compared to free curcumin, nanocurcumin exhibited a markedly enhanced antihyperglycemic effect. It could additionally preserve lipid homeostasis. Subject demonstrated improvements in enzymatic as well as non-enzymatic biochemical indicators of oxidative stress. When compared directly with free curcumin, nanocurcumin proved to be a more effective antioxidant, indicating enhanced bioavailability and efficacy in mitigating oxidative damage.</div></div><div><h3>Conclusion</h3><div>Current research results demonstrated ‘Nanocurcumin capsules’ anti-hyperglycemic, anti-hyperlipidemic and anti-oxidative potential in subjects with diabetes mellitus (DM). Nanocurcumin therapeutic potential had been prominent than curcumin.</div></div>","PeriodicalId":20049,"journal":{"name":"PharmaNutrition","volume":"33 ","pages":"Article 100445"},"PeriodicalIF":2.4,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144770806","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The regulation of gut microbiota and urate lowering: A study on the mechanisms of action of probiotics and plant components","authors":"Zhihua Xing ,&nbsp;Yue Xu ,&nbsp;Wen Jiang ,&nbsp;Mingyu Gao ,&nbsp;Guanghuan Shen ,&nbsp;Yingjie Liu ,&nbsp;Na Ling ,&nbsp;Linlin Cui","doi":"10.1016/j.phanu.2025.100450","DOIUrl":"10.1016/j.phanu.2025.100450","url":null,"abstract":"<div><div>The gut microbiota system serves as a \"barometer\" of human health, with significant differences observed in the intestinal microbiome between individuals with hyperuricemia (HUA) and gout compared to those in the general population. This article comprehensively reviews the correlation between gut microbiota and HUA and uric acid-lowering substances that regulate the gut microbiota. It elucidates the mechanisms underlying the occurrence and progression of HUA associated with the gut microbiota. It summarizes the effects and mechanisms through which probiotics, plant polysaccharides, and plant small molecular compounds reduce serum uric acid by modulating the gut microbiota. It is hoped that this review will provide a theoretical basis for the development of strategies for uric acid-lowering drugs targeting the gut microbiota, serving as a reference for subsequent in-depth research.</div></div>","PeriodicalId":20049,"journal":{"name":"PharmaNutrition","volume":"33 ","pages":"Article 100450"},"PeriodicalIF":2.4,"publicationDate":"2025-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144722524","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Flavonoids and macrophage polarization: Key players in the immunomodulation of cardiometabolic syndrome and related therapies","authors":"Parisa Ahmadi ,&nbsp;Soroush Taherkhani ,&nbsp;Maryam Honardoost ,&nbsp;Atousa Janzadeh","doi":"10.1016/j.phanu.2025.100449","DOIUrl":"10.1016/j.phanu.2025.100449","url":null,"abstract":"<div><div>Cardiometabolic syndrome (CMS) is a major public health challenge characterized by obesity, insulin resistance, hypertension, and chronic inflammation, which increase the risk of type 2 diabetes (T2D) and cardiovascular disease. In this context, inflammatory M1 macrophages are pivotal, as they produce proinflammatory cytokines and contribute to oxidative stress, insulin resistance, and lipid accumulation in adipose tissue. Polyphenols with anti-inflammatory, antioxidant, and antiobesity properties alleviate CMS by promoting M2 macrophage differentiation and reprogramming M1 macrophages toward the M2 phenotype. Flavonoids inhibit inflammatory pathways such as NF-kB and activator protein-1 (AP-1); reduce the expression of proinflammatory markers such as TLR4, NOD-like receptor family pyrin domain-containing 3 (NLRP-3), and inducible nitric oxide synthase (iNOS); and enhance anti-inflammatory responses, including IL-10, Nrf-1, and peroxisome proliferator-activated receptor (PPAR) expression. They prevent foam cell formation by decreasing LPX-1, CD36, scavenger receptor-A, B1, and LOX-1 expression while increasing ABCA1 and ABCG1 levels. Flavonoids are antiobesity agents that decrease the infiltration of macrophages in adipose tissue and suppress the M1 phenotype in adipose tissue macrophages, lowering inflammation and leading to the suppression of lipogenesis and stimulation of lipolysis in adipocytes. This review highlights the importance of macrophage activation in metabolic imbalance and the potential of flavonoids in treating CMS through the induction of M2 macrophages.</div></div>","PeriodicalId":20049,"journal":{"name":"PharmaNutrition","volume":"33 ","pages":"Article 100449"},"PeriodicalIF":2.4,"publicationDate":"2025-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144770984","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hesperetin as a potential therapeutic agent for colorectal cancer: Targeting PI3K/AKT and EMT in cell lines through network pharmacology-guided strategies","authors":"Junyi Xue ,&nbsp;Jianmin Liao ,&nbsp;Haixing Ju ,&nbsp;Yuanyuan Lu","doi":"10.1016/j.phanu.2025.100447","DOIUrl":"10.1016/j.phanu.2025.100447","url":null,"abstract":"<div><div>Hesperetin is a naturally occurring flavonoid compound abundantly present in citrus fruit peels and Traditional Chinese Medicinal (TCM). It exhibits diverse pharmacological properties and represents a promising multi-target candidate for anticancer therapy. This study systematically investigated the molecular mechanisms underlying the anti-colorectal cancer (CRC) effects of hesperetin by integrating network pharmacology, molecular docking, and experimental validation. Network pharmacology analysis identified 42 core targets of hesperetin in CRC, with molecular docking confirming strong binding affinities (binding energy &lt; −7 kcal/mol) between hesperetin and key proteins, including Epidermal Growth Factor Receptor (EGFR), Threonine Kinase 1 (AKT1), Proto-oncogene Tyrosine-protein Kinase Src (SRC), Phosphatidylinositol-4,5-Bisphosphate 3-Kinase Catalytic Subunit Alpha (PIK3CA), and Matrix Metalloproteinase-9 (MMP9). In vitro experiments demonstrated that hesperetin dose-dependently inhibited the proliferation, migration, and invasion of HCT116 and Lovo cells. Mechanistically, hesperetin reversed epithelial-mesenchymal transition (EMT) by upregulating E-cadherin and downregulating N-cadherin, Vimentin, and Snail at both protein and mRNA levels. Western blot analysis revealed that hesperetin suppressed PI3K/AKT pathway activation by reducing phosphorylation of PI3K (Tyr458) and AKT (Ser473). Clinical data further validated the therapeutic relevance of these targets, showing that high expression of EGFR, AKT1, PIK3CA, and MMP9 correlated with poor prognosis in CRC patients. Collectively, these findings establish hesperetin as a promising multi-target nutritional supplement agent against CRC, demonstrating dual modulation of both PI3K/AKT signaling and EMT progression.</div></div>","PeriodicalId":20049,"journal":{"name":"PharmaNutrition","volume":"33 ","pages":"Article 100447"},"PeriodicalIF":2.4,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144711055","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Neuroprotective potential of saffron metabolites in Parkinson's disease","authors":"Mohamed Ben El Caid ,&nbsp;Mohamed Ait Haddou ,&nbsp;Ouahid El Asri ,&nbsp;Laila Aboudlou ,&nbsp;Lalla Hadda Atyane ,&nbsp;Vikas Ramteke ,&nbsp;Rachid Ait Hammou","doi":"10.1016/j.phanu.2025.100448","DOIUrl":"10.1016/j.phanu.2025.100448","url":null,"abstract":"<div><div>Parkinson’s disease (PD) is a debilitating neurodegenerative disorder characterized by the progressive loss of dopaminergic neurons. Although current pharmaceutical treatments mitigate symptoms, these frequently induce adverse effects and may not prevent disease progression, highlighting the need for safer neuroprotective alternatives. Natural products like saffron (<em>Crocus sativus</em> L.) have emerged as promising candidates due to their pharmacological and nutritional properties. While prior studies have investigated saffron and its extracts in the context of PD, no review has comprehensively analyzed the specific roles of its major secondary metabolites. Saffron’s bioactive compounds, particularly crocetin, crocins, and safranal, have demonstrated significant therapeutic potential across <em>in vitro</em>, <em>in vivo</em>, and clinical studies. Crocetin has been shown to inhibit α-synuclein aggregation and preserve mitochondrial integrity. Crocins exhibit neuroprotective effects, including inhibition of amyloid fibril formation, protection of dopaminergic neurons, and enhancement of synaptic plasticity through pathways such as PI3K/Akt/mTOR. Notably, picrocrocin remains unstudied mainly, representing a significant research gap. Safranal has shown efficacy in preclinical PD models, with promising effects on dopaminergic neuron preservation, motor function improvement, and apoptosis regulation. However, clinical trials are warranted to validate its therapeutic potential further. This review highlights existing findings, critically examines the literature, and identifies underexplored mechanisms, including neurotrophic and mitochondrial pathways, as promising targets for future research, ultimately paving the way for innovative therapeutic strategies in PD management.</div></div>","PeriodicalId":20049,"journal":{"name":"PharmaNutrition","volume":"33 ","pages":"Article 100448"},"PeriodicalIF":2.4,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144711054","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"L-Arginine mitigates high glucose-induced podocyte injury via NRF2 pathway activation","authors":"Xiandeng Li ,&nbsp;Huiting Chen ,&nbsp;Hang Han,&nbsp;Guojiang Zhang,&nbsp;Xiao Zhang,&nbsp;Qinjian Zhao","doi":"10.1016/j.phanu.2025.100439","DOIUrl":"10.1016/j.phanu.2025.100439","url":null,"abstract":"<div><div>L-Arginine, a semi-essential amino acid involved in the ornithine cycle, exhibits therapeutic potential in diabetes through benefits demonstrated in both animal models and human studies. However, the precise mechanisms underlying its effects remain incompletely understood. Podocytes play a crucial role in the pathogenesis of diabetic nephropathy (DN), with podocyte injury contributing significantly to disease progression. In this study, we demonstrated that L-arginine treatment improved podocyte viability, decreased oxidative stress and inflammation markers, and upregulated nuclear factor erythroid 2-related factor 2 (NRF2) expression and its nuclear translocation, along with its downstream antioxidant enzymes, heme oxygenase-1 (HO-1) and NAD(P)H quinone dehydrogenase 1 (NQO1), in a dose-dependent manner. Importantly, these protective effects were reversed by the NRF2 inhibitor ML385 and <em>Nrf2</em> RNA interference (RNAi), suggesting that L-arginine’s protective mechanism is likely mediated through the NRF2 pathway. These findings emphasize the potential of L-arginine as a therapeutic agent for DN by protecting podocytes from high glucose-induced oxidative stress and injury.</div></div>","PeriodicalId":20049,"journal":{"name":"PharmaNutrition","volume":"31 ","pages":"Article 100439"},"PeriodicalIF":2.4,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143519103","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Opportunities and challenges associated with rheumatoid arthritis: The role of natural polyphenol products","authors":"Kai Chen ,&nbsp;Hua Zhang ,&nbsp;Qinwei Fu ,&nbsp;Chunli Wu ,&nbsp;Jianlin Wu","doi":"10.1016/j.phanu.2025.100438","DOIUrl":"10.1016/j.phanu.2025.100438","url":null,"abstract":"<div><div>RA is a chronic inflammatory disease commonly found in industrialized nations, characterized by ongoing joint destruction. Its pathogenesis involves a complex interaction between the innate and adaptive immune systems, resulting in the excessive production of inflammatory mediators. These mediators contribute to various chronic diseases, including RA, which necessitates drug interventions to regulate their release. Herbal plants have historically been a rich source of bioactive compounds with therapeutic potential, many of which are now widely used as medications. Treatments for RA focus on inhibiting oxidative stress, downregulating pro-inflammatory cytokines such as IL-1, IL-6, TNF-α, and NF-κB, suppressing matrix metalloproteinases that damage cartilage, enhancing antioxidant activity, and modulating macrophage phenotypes. Flavonoids, a subclass of polyphenols, stand out for their antioxidant and anti-inflammatory properties. They help alleviate RA by inhibiting the production of inflammatory cytokines, reducing oxidative stress, suppressing the proliferation of lymphocytes and synovial cells, inducing apoptosis, and regulating energy metabolism. This review emphasizes the potential of natural polyphenols, primarily flavonoids, as promising candidates for RA treatment, providing insights into their mechanisms and the prospects for future drug development.</div></div>","PeriodicalId":20049,"journal":{"name":"PharmaNutrition","volume":"32 ","pages":"Article 100438"},"PeriodicalIF":2.4,"publicationDate":"2025-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143815761","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Aloe vera and its byproducts as sources of valuable bioactive compounds: Extraction, biological activities, and applications in various food industries","authors":"Emmanuel Ofosu Mensah ,&nbsp;Parise Adadi ,&nbsp;Richard Vincent Asase ,&nbsp;Opoku Kelvin ,&nbsp;Fatemeh Jalil Mozhdehi ,&nbsp;Isaac Amoah ,&nbsp;Dominic Agyei","doi":"10.1016/j.phanu.2025.100436","DOIUrl":"10.1016/j.phanu.2025.100436","url":null,"abstract":"<div><div>Aloe vera (AV) is a succulent plant renowned for its medicinal properties, containing numerous bioactive compounds that offer significant health benefits. Aligning with the United Nations Sustainable Development Goals, particularly Goal 12 on Responsible Consumption and Production, utilizing AV and its byproducts in the food industry can promote sustainability by reducing waste and maximizing resource efficiency. This review provides an in-depth analysis of AV and its byproducts as sources of functional compounds for the food industry. It focuses on various extraction methods for isolating bioactive compounds. The biological activities of these compounds, such as antioxidant, antimicrobial, anti-inflammatory, and gut microbiome properties, were discussed to highlight their potetial health benefits. Additionally, the review explores the diverse applications of AV and its byproducts in the food industry, including their use as natural preservatives, functional ingredients, and nutraceuticals. Effective extraction techniques preserve the functional properties of isolated compounds, which exhibit a wide range of biological activities. Ultimately, AV and its byproducts can enhance the nutritional profiles of food products and contribute to the development of health-promoting formulations. By harnessing these benefits, the food industry can create innovative products that align with sustainable practices while improving consumer health.</div></div>","PeriodicalId":20049,"journal":{"name":"PharmaNutrition","volume":"31 ","pages":"Article 100436"},"PeriodicalIF":2.4,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143420320","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}