Nutritional Neuroscience最新文献

{"title":"<i>Cornus mas</i> ameliorates AlCl₃-induced Alzheimer's disease in rats with metabolic syndrome by regulating inflammation and oxidative stress.","authors":"Zatiye Ayça Çevikelli Yakut, Elvan Bakar, Filiz Sanal, Dicle Çevik, Çetin Hakan Karadağ, Etil Güzelmeriç","doi":"10.1080/1028415X.2025.2460384","DOIUrl":"10.1080/1028415X.2025.2460384","url":null,"abstract":"<p><strong>Objectives: </strong>Alzheimer's disease (AD) results from different risk variables, such as metabolic syndrome (MetS) and environmental factors. The benefits of <i>Cornus mas</i> L. on diabetes are well-known. However, the impacts of <i>C. mas</i> fruits on AD or MetS-related cognitive dysfunction have not yet been studied. We evaluated the impact of <i>C. mas</i> fruit (80% ethanol) extract in an animal model of MetS and AD.</p><p><strong>Methods: </strong>Male Spraque-Dawley rats were administered a high-fat, high-sugar diet for 105 days alone or with an AlCl₃ intraperitoneal injection for the last 60 days. <i>C. mas</i> fruit extract (400, 700, and 1000 mg/kg peroral) was administered for 60 days. After conducting behavioral tests and measuring blood pressure, hippocampal tissues and serum samples were obtained. The phytochemical analyses were conducted on <i>C. mas</i> fruit extract.</p><p><strong>Results: </strong><i>C. mas</i> alleviated MetS by reducing blood glucose, total cholesterol, and systolic blood pressure levels. Behavioral tests demonstrated that <i>C. mas</i> improves AlCl₃-related cognitive decline in rats with MetS, which was supported by the neuroprotective effect of <i>C. mas</i> in histological analysis. <i>C. mas</i> dose-dependently reduced amyloid-β, malondialdehyde levels, acetylcholinesterase activity in the hippocampus, proinflammatory cytokines in serum, and elevated glutathione levels in the hippocampus. Phytochemical analyses revealed that <i>C. mas</i> fruit contains loganic acid, cornuside, and anthocyanins.</p><p><strong>Discussion: </strong><i>C. mas</i> fruit extract in every three doses given could improve cognitive decline due to MetS and AlCl₃ through alleviation of MetS, oxidative stress and inflammation, prevention of amyloid deposition, and increased cholinergic transmission.</p>","PeriodicalId":19423,"journal":{"name":"Nutritional Neuroscience","volume":" ","pages":"1034-1054"},"PeriodicalIF":3.6,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143414872","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exploring the impact of a high-fat diet on the serotonin signaling in gut-brain axis.","authors":"Taylor Gray, Yewande O Fasina, Scott H Harrison, Evelyn M Chang, Alex Y Chang, Antoinette Maldonado-Devincci, Jian Han","doi":"10.1080/1028415X.2025.2539320","DOIUrl":"https://doi.org/10.1080/1028415X.2025.2539320","url":null,"abstract":"<p><p>Serotonin is a critical neurotransmitter that regulates a wide range of physiological, neurological, and behavioral functions. While peripheral serotonin, primarily produced in the gut, modulates gastrointestinal motility and vascular tone, central serotonin that is synthesized in the brain governs processes such as food intake, emotion regulation, memory, learning, and sexual behavior. Chronic consumption of a high-fat diet (HFD) disrupts serotonin signaling across the gut, brain, and the gut-brain axis, which supports bidirectional communication between these systems. Although the underlying mechanisms remain incompletely understood, this review explores how HFD alters serotonin signaling in both the gut and the brain. We report that HFD triggers pathway-specific changes that elevate serotonin levels in the gut while eliciting region-specific effects in the brain. HFD increases serotonin biosynthesis in the brain's raphe nuclei; however, enhanced 5-HT1A autoreceptor activity within these nuclei inhibits serotonin release to downstream projection areas. Coupled with increased serotonin degradation in these regions, this results in reduced serotonin levels in the hippocampus and hypothalamus. Additionally, our findings highlight a central role for microbial metabolites in mediating HFD-induced serotonergic dysfunction. Notably, short-chain fatty acids produced by gut microbiota, significantly contribute to the dysregulation of serotonin release and signaling under HFD conditions. Understanding these mechanisms may reveal new therapeutic strategies for managing serotonergic dysfunctions associated with gastrointestinal disorders, mood disturbances, and obesity-related complications.</p>","PeriodicalId":19423,"journal":{"name":"Nutritional Neuroscience","volume":" ","pages":"1-15"},"PeriodicalIF":3.6,"publicationDate":"2025-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144963328","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Choline intake during pregnancy influences maternal cognitive function and hippocampal gene expression in late adulthood.","authors":"Qian Yee Woo, Bernett T K Lee, Lee Wei Lim, Jingtao Zhang, Ayumu Tashiro, Pheck Khee Lau, Guillaume Thibault, Yulan Wang, Valerie C L Lin","doi":"10.1080/1028415X.2025.2546946","DOIUrl":"https://doi.org/10.1080/1028415X.2025.2546946","url":null,"abstract":"<p><strong>Background and objective: </strong>Women are twice as likely to have Alzheimer's disease (AD) than men and multiparity has been suggested to be a risk factor for dementia. The present study evaluated whether the lack of certain nutrients during pregnancy influences cognition while pregnant and in late adulthood using mouse model.</p><p><strong>Methods: </strong>Non-targeted NMR analysis was conducted to assess changes in plasma nutrients and metabolites on gestation day 7.5 compared to day 1. Effects of choline intake during pregnancy on cognition and general health were evaluated in consecutive pregnancies. Mice were assigned to groups with normal diet, cholinesupplemented diet, or choline-deficient diet during pregnancy. Non-pregnant mice were included as controls. Behavioral analyses were performed during the second half of the first and fourth pregnancies, as well as at 12 and 15 months of age. The hippocampus was collected for RNA-seq analysis at 15 months of age.</p><p><strong>Results and conclusion: </strong>Non-targeted NMR analysis revealed significantly lower levels of numerous plasma nutrients and metabolites including choline and its derivatives on gestation day 7 compared to day 1. Novel object recognition and Morris Water Maze tests revealed impaired cognition in pregnant mice compared to nonpregnant controls. Choline deprivation worsened the cognitive impairment during pregnancy and choline supplementation alleviated it. Furthermore, choline availability during pregnancy affected cognition and general health in late adulthood, with mice given a choline-deficient diet during pregnancy performed more poorly. RNA-Seq analysis indicates lasting effect of choline intake during pregnancy on hippocampal gene signatures in late adulthood. Choline deprivation was associated with more upregulation of proinflammatory genes, whereas choline supplementation showed upregulation of neuroprotective genes such as <i>Prl</i>, <i>Gh</i>, and hemoglobin (<i>Hba</i> and <i>Hbb</i> subunits). Together, the study shows that choline supplementation benefits cognitive health in women during pregnancy and in late adulthood.</p>","PeriodicalId":19423,"journal":{"name":"Nutritional Neuroscience","volume":" ","pages":"1-26"},"PeriodicalIF":3.6,"publicationDate":"2025-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144963330","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Morin hydrate: a comprehensive review on therapeutic potential in treating neurological diseases.","authors":"Shaik Mohammad Noor, Dontiboina Harikrishna Reddy, Yadava Srikanth, Matte Kasi Viswanadh, Naresh Dumala, Guntupalli Chakravarthy, Buchi N Nalluri, Alla Naryanarao, Sajusha Duguluri, Ganesh Yadagiri, Vani Sai Prasanna, Shyam Sundaram, Lohitha Gujjari, Kakarla Ramakrishna","doi":"10.1080/1028415X.2025.2544605","DOIUrl":"https://doi.org/10.1080/1028415X.2025.2544605","url":null,"abstract":"<p><p><b>Background:</b> Morin hydrate is a polyphenolic flavonoid present in various vegetables, fruits, nuts, and sea products. It has been reported to offer multiple protective effects against a range of diseases, including cancer, cardiovascular, liver, neurological, metabolic, and renal disorders.<b>Objective:</b> This review highlights the molecular mechanisms and therapeutic potential of Morin in neurological diseases, including Parkinson's disease, Alzheimer's disease, traumatic brain injury, neuropathic pain, stroke, Huntington's disease, multiple sclerosis, amyotrophic lateral sclerosis, depression, anxiety, sleep, encephalopathy, schizophrenia, and psychosis, etc.<b>Methods:</b> The research and review articles were collected from the Pubmed, Scopus, Web of Science, and Google Scholar databases using 'Morin' and the above-mentioned neurological diseases as keywords.<b>Results:</b> The neuroprotective effects of Morin are primarily attributed to its ability to mitigate oxidative stress, inflammation, excitotoxicity, calcium dysregulation, mitochondrial dysfunction, neurotransmitter alterations, protein modifications, and enzymatic inhibition.<b>Conclusion:</b> Despite its promising pharmacological profile, the clinical adaptation of Morin for combating neurological diseases requires further validation through comprehensive preclinical and clinical investigations.</p>","PeriodicalId":19423,"journal":{"name":"Nutritional Neuroscience","volume":" ","pages":"1-25"},"PeriodicalIF":3.6,"publicationDate":"2025-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144963282","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Supplementation with Jatobá-do-cerrado flour (<i>Hymenaea stigonocarpa</i> Mart.) decreased oxidative stress in amygdala and adipose tissue and reduced anxiety-like behaviors of Wistar male rats on a high-fat diet.","authors":"Alexandre Alves da Silva, Arthur Rocha-Gomes, Ítalo Gomes Reis, Pedro Ernesto de Pinho Tavares Leal, Mayara Rodrisgues Lessa, Nisia Andrade Villela Dessimoni Pinto, Tania Regina Riul, Daniel Campos Villela","doi":"10.1080/1028415X.2025.2544608","DOIUrl":"https://doi.org/10.1080/1028415X.2025.2544608","url":null,"abstract":"<p><p>In recent years, obesity has reached pandemic levels and has been associated with a range of comorbidities, including anxiety disorders. Several studies have shown that the inclusion of legumes rich in dietary fiber can attenuate the adverse effects induced by high-fat diets. Jatobá-do-cerrado (<i>Hymenaea stigonocarpa</i> Mart.) stands out as a legume with high levels of dietary fiber and antioxidant compounds. The current study aimed to evaluate the effects of supplementation with Jatobá-do-cerrado flour on anxiety-like behavior and redox state parameters in rats on a high-fat diet. Male Wistar rats were divided for 126 days: Control- standard diet during 126 days; High-fat diet (HFD)- standard diet with added lard (20% w/w) for 126 days; Jatobá-do-cerrado flour (JCF)- standard diet with added Jatobá-do-cerrado flour (20% w/w) from 63^rd to 126^th day; Jatobá-do-cerrado flour + High-fat diet (JCF + HFD)- standard diet with Jatobá-do-cerrado flour (20% w/w) and lard (20% w/w) from 63^rd to 126^th. After the dietary treatments, the animals performed the Elevated Plus Maze, Light-Dark Box, and Open Field tests. The redox state of the adipose tissue and amygdala were analyzed. The HFD group showed anxiety-like responses in the tests, low antioxidant activity and high levels of lipid peroxidation in the adipose tissue and amygdala. Conversely, JCF + HFD group reduced anxiety-like behaviors and improved the antioxidant activity (adipose tissue and amygdala). In summary, the supplementation with Jatobá-do-cerrado flour improved antioxidant activity and also promoted an anxiolytic effect, suggesting its potential as a functional food and may be useful as an adjunct in the management of obesity and its related comorbidities.</p>","PeriodicalId":19423,"journal":{"name":"Nutritional Neuroscience","volume":" ","pages":"1-12"},"PeriodicalIF":3.6,"publicationDate":"2025-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144963022","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Obesity and Alzheimer´s disease: unraveling the impact of chronic consumption of high-fat or high-sucrose diets on neurodegeneration and mitochondrial dysfunction.","authors":"Carlos Francisco Aguilar Gamas, Norma Edith López Diaz-Guerrero, Nancy Patricia Gómez-Crisóstomo, Erick Natividad De la Cruz-Hernández, Cecilia Zazueta, Ixchel Ramírez-Camacho, Corazón de María Márquez-Álvarez, Eduardo Martínez-Abundis","doi":"10.1080/1028415X.2025.2546950","DOIUrl":"https://doi.org/10.1080/1028415X.2025.2546950","url":null,"abstract":"<p><strong>Background: </strong>The global incidence of obesity and metabolic disorders has been associated with alterations in the central nervous system, prominently featuring increased oxidative stress and heightened production of amyloid beta peptide (AB), stemming from mitochondrial dysregulations, which potentially contribute to the onset of neurodegenerative disorders like Alzheimer disease.</p><p><strong>Aims: </strong>In this study, we sought to ascertain whether chronic consumption of unbalanced diets by rats leads to elevated AB production and accumulation in brain structures, driving neuronal damage and mitochondrial dysfunction.</p><p><strong>Methods: </strong>Male Wistar rats were fed with unbalanced diets rich in sucrose or lard for 12 months. Subsequently, we evaluated zoometric and biochemical parameters, including glucose tolerance, serum cholesterol, and triglycerides, alongside spatial memory. Additionally, AB accumulation, oxidative stress markers, and mitochondrial respiratory chain activity were analyzed in mitochondria and homogenates from the hippocampus and cerebral cortex.</p><p><strong>Results: </strong>In our results, both dietary interventions induced abdominal obesity and spatial memory deterioration, associated to glucose metabolism disturbance, mitochondrial dysfunction, and increased oxidative stress. Nevertheless, AB accumulation was evident only in the mitochondria of rats fed with the sucrose-enriched diet.</p><p><strong>Conclusions: </strong>With these findings, we show that, although excessive consumption of fat or sucrose drives to obesity, only the last could potentially bridge the gap between obesity and neurodegenerative pathogenesis, thereby highlighting the relevance of lifestyle and diet quality, bringing a way to develop preventive strategies.</p>","PeriodicalId":19423,"journal":{"name":"Nutritional Neuroscience","volume":" ","pages":"1-15"},"PeriodicalIF":3.6,"publicationDate":"2025-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144963312","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The effect of 3',4'-dihydroxyflavonol (DiOHF) on endoplasmic reticulum stress in the cerebellum during brain ischemia-reperfusion.","authors":"Gizem Akkaya, Gozde Acar, Tugce Aladag, Saltuk Bugra Baltaci, Rasim Mogulkoc, Abdulkerim Kasim Baltaci","doi":"10.1080/1028415X.2025.2545513","DOIUrl":"https://doi.org/10.1080/1028415X.2025.2545513","url":null,"abstract":"<p><p>Ischemia is a condition occured when there is insufficient blood flow to the tissues, negatively affecting cellular energy production. Brain ischemia is a critical pathological process caused neuronal function to deteriorate and cell death due to the temporary or permanent interruption of cerebral blood circulation. During this process, triggering endoplasmic reticulum (ER) stress disrupts intracellular protein folding mechanisms, leading to increased neuronal damage. This study investigated the effect of a 1-week supplementation with 3',4'-Dihydroxyflavonol (DiOHF) on endoplasmic reticulum stress in cerebellum tissue after cerebral ischemia-reperfusion. The study was conducted on 28 male Wistar-albino rats. Control: No anesthesia or surgical procedure was applied. Sham: The carotid artery regions were opened and closed under general anesthesia. After the application, solvent application was performed for 1 week (1 ml DiOHF vehicle). Ischemia-Reperfusion: After isolating the carotid arteries, ischemia was performed by ligating them for 30 minutes, followed by reperfusion. Ischemia-Reperfusion + DiOHF: After ischemia was performed for 30 minutes, reperfusion was allowed. DiOHF supplementation was performed for 1 week. After one week of treatment, animals were killed and cerebellum tissues were taken to evaluate GRP78, HSP70, CHOP, Bcl-2 and Bax levels. While I/R increased GRP78 (<i>p</i> < 0,05), HSP70 (<i>p</i> < 0,05), CHOP (<i>p</i> < 0,05) and Bax (<i>p</i> < 0,05) values in the cerebellum, it resulted in significant downregulation of BCl-2 levels (<i>p</i> < 0,05). However, 3',4'-Dihydroxyflavonol application for 1 week corrected the deteriorations caused by I/R. The study results show that 1 week of 3',4'-Dihydroxyflavonol treatment after I/R provides significant correction in endoplasmic reticulum stress related parameters caused by focal brain I/R in the cerebellum, suggesting that DiOHF may serve as a promising therapeutic candidate for defending cerebellar tissue from ER stress-related post-ischemic damage.</p>","PeriodicalId":19423,"journal":{"name":"Nutritional Neuroscience","volume":" ","pages":"1-13"},"PeriodicalIF":3.6,"publicationDate":"2025-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144855931","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Extra virgin olive oil supplementation reduces inflammation in the arcuate nucleus of the hypothalamus and improves metabolic parameters in obese rats.","authors":"Ariadni Peres, Ricardo Dantas, Aline Ferreira, Ana Caroline Silveira, Giovana Raphaelli, Laís Felipe, Letícia Souza, Mariana Costa, Alessandra Machado, Diorlon Machado, Rodrigo Herrmann, Jade de Oliveira, Carlos Alexandre Netto, Angela Wyse, Carla Dalmaz, Rachel Bast","doi":"10.1080/1028415X.2025.2544609","DOIUrl":"https://doi.org/10.1080/1028415X.2025.2544609","url":null,"abstract":"<p><strong>Objectives: </strong>Obesity is a common public health problem, affecting 2.5 billion adults. Chronic high-fat diet (HFD) exposure, an experimental obesity model, strongly impacts the hypothalamic arcuate nucleus (ARC), a structure vulnerable to dietary-induced inflammation. Extra-virgin olive oil (EVOO) supplementation can be an interesting nutritional strategy to understand and/or treat obesity: EVOO has high nutritional quality, and acts on multiple molecular targets. We investigated EVOO supplementation's impact on metabolic parameters, satiety and hypothalamic inflammation in adult rats exposed to HFD from weaning, considering sex-specific outcomes.</p><p><strong>Methods: </strong>21-day-old Wistar rats were allocated into groups: (1) standard chow (SC); (2) SC+EVOO; (3) HFD; (4) HFD + EVOO. EVOO was administered daily by gavage. In adulthood, the behavioral satiety sequence was evaluated. Plasma leptin and ARC inflammatory markers levels were measured by ELISA technique. The immunofluorescence intensity of Toll-like receptor-4 (TLR-4) and ionized calcium-binding adaptor molecule-1 (IBA-1) were measured in the ARC.</p><p><strong>Results: </strong>Chronic HFD-induced obesity was evidenced in both sexes, with increased body weight, body mass index, fasting blood glucose, caloric efficiency, and plasma leptin levels. EVOO supplementation prevented HFD-induced increase in weight gain and BMI in both sexes. HFD-fed animals had altered satiety. EVOO supplementation decreased immunoreactivity of IBA-1 in the ARC, also attenuates TLR-4 immunoreactivity, interleukin (IL)-6, IL-1β, and tumor necrosis factor-α levels in the ARC of obese animals.</p><p><strong>Conclusion: </strong>Our results demonstrate that EVOO supplementation seemed promising, improving hypothalamic inflammation in obese animals, therefore might lead to the restoration of adverse metabolic consequences.</p>","PeriodicalId":19423,"journal":{"name":"Nutritional Neuroscience","volume":" ","pages":"1-16"},"PeriodicalIF":3.6,"publicationDate":"2025-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144835888","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Potential benefits of vitamin D on brain pathologies and cognitive function in metabolic syndrome: evidence from <i>in vivo</i> and clinical studies.","authors":"Houzhi Cheng, Jirapas Sripetchwandee, Wasana Pratchayasakul, Nipon Chattipakorn, Siriporn C Chattipakorn","doi":"10.1080/1028415X.2025.2544615","DOIUrl":"https://doi.org/10.1080/1028415X.2025.2544615","url":null,"abstract":"<p><strong>Objectives: </strong>Metabolic syndrome (MetS) is a global health issue linked to cardiovascular diseases, type 2 diabetes mellitus, and cognitive impairment. Chronic inflammation and oxidative stress associated with MetS condition contribute to cognitive decline, highlighting the need for therapeutic strategies to mitigate these complications. Vitamin D, a fat-soluble vitamin, plays a crucial role in physiological functions. Recent researches have highlighted the neuroprotective roles of vitamin D in several pathological conditions. Therefore, this review aims to summarize and discuss evidence from <i>in vivo</i> and clinical studies on the effects of vitamin D on brain pathologies and cognitive function in the context of MetS condition.</p><p><strong>Methods: </strong>We searched articles published only in English, on PubMed Central from January 2000 to December 2023 using the following keywords: 1) \"vitamin D\", \"metabolic syndrome\", \"brain\"; 2) \"vitamin D\", \"metabolic syndrome\", \"cognition\"; 3) \"vitamin D\", \"obesity\", \"cognition\"; 4) \"vitamin D\", \"obesity\", \"brain\"; 5) \"vitamin D\", \"hyperglycemia\", \"brain\"; and 6) \"vitamin D\", \"dyslipidemia\", \"brain\", 7) \"vitamin D\", \"T2DM\", \"brain\"; and 8) \"vitamin D\", \"T2DM\", \"cognition\".</p><p><strong>Results: </strong>Vitamin D treatment in animals with the MetS condition attenuated metabolic disturbances including inflammation, oxidation, hyperglycemia, obesity, and insulin resistance, and ameliorated cognitive dysfunction, suggesting the beneficial effects of vitamin D in the MetS condition.</p><p><strong>Discussion: </strong>All the evidence indicates that vitamin D may be a potential therapeutic option to reduce cognitive dysfunction caused by metabolic syndrome.</p>","PeriodicalId":19423,"journal":{"name":"Nutritional Neuroscience","volume":" ","pages":"1-18"},"PeriodicalIF":3.6,"publicationDate":"2025-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144835889","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The possible antioxidative effects of ketogenic diet by modifying brain klotho expression: a rat model study.","authors":"Nasrin Ranjbar, Bahador Ebrahimi Behnam, Mehran Mesgari Abbasi, Mahsa Esmaeili, Fatemeh Jolfaei, Jamal Mohammadian, Nadereh Rashtchizadeh, Amir Ghorbanihaghjo, Sina Raeisi","doi":"10.1080/1028415X.2024.2436817","DOIUrl":"10.1080/1028415X.2024.2436817","url":null,"abstract":"<p><p><b>Objectives:</b> The ketogenic diet (KD) has long been used as an alternative nonpharmacological therapy to manage pharmacoresistant epilepsy. The anticonvulsant mechanisms of KD have yet to be fully elucidated. The present study explored whether a KD could exert antioxidative effects by altering brain Klotho (Kl) gene expression.<b>Methods:</b> Thirty male rats were divided into three groups: the normal diet (ND) group received standard rat chow; the calorie-restricted diet (CRD) group was maintained at 90% of the calculated energy need; and the KD group received a diet composed of 8% protein, 2% carbohydrates, and 90% fat (per calorie macronutrient). The levels of β-hydroxybutyrate (BHB) in the serum, <i>Kl</i> gene expression in the brain, and Kl protein, malondialdehyde (MDA), and protein carbonyl (PC) levels in the serum and brain were evaluated by standard methods.<b>Results:</b> The serum BHB levels in the KD group were significantly greater than those in the ND and CRD groups (<i>p</i> < 0.001). The Kl expression in the brain was significantly greater in the KD group than in the ND group (<i>p</i> = 0.028). The brain MDA levels in the KD group were significantly lower than those in the ND group (<i>p</i> = 0.006). Elevated BHB was positively correlated with brain <i>Kl</i> expression (r = 0.668, <i>p</i> < 0.001). The brain MDA levels were negatively correlated with brain <i>Kl</i> expression (r = -0.531, <i>p</i> = 0.003) and serum BHB levels (r = 0.472, <i>p</i> = 0.020).<b>Discussion:</b> KD might exert antioxidative effects by increasing BHB and upregulating <i>Kl</i> in the brain. This could be considered a possible anticonvulsant mechanism of KD.</p>","PeriodicalId":19423,"journal":{"name":"Nutritional Neuroscience","volume":" ","pages":"968-974"},"PeriodicalIF":3.6,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142829596","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}