Journal of Nutritional Biochemistry最新文献

{"title":"Exposure to bisphenol A and sodium nitrate found in processed meat induces endocrine disruption and dyslipidemia through PI3K/AKT/SREBP pathway in zebrafish larvae","authors":"Santosh Pushpa Ramya Ranjan Nayak ,&nbsp;Anamika Das ,&nbsp;Karthikeyan Ramamurthy ,&nbsp;Mukesh Pasupuleti ,&nbsp;Rajakrishnan Rajagopal ,&nbsp;Jesu Arockiaraj","doi":"10.1016/j.jnutbio.2025.109887","DOIUrl":"10.1016/j.jnutbio.2025.109887","url":null,"abstract":"<div><div>Meat is a staple in many cultural diets, and the consumption of processed meats has increased significantly worldwide. The widespread use of sodium nitrate (NaNO₃) as a preservative and the unintentional leaching of bisphenol A (BPA) from packaging into meats have raised health concerns. This study evaluates the combined toxicity of BPA and NaNO₃ despite their individual safety assessments. Our findings reveal that coexposure to BPA and NaNO₃ at levels found in processed meats induces mortality and malformations in zebrafish larvae. The combined exposure triggers oxidative stress, lipid peroxidation, dyslipidemia, inflammation, and apoptosis. Network toxicology analysis elucidates the molecular mechanisms underlying metabolic dysfunction caused by these substances. Dysregulation of genes related to thyroid function (<em>tsh-β, dio-1, thr-b</em>) and inflammation (<em>tnf-α, il-1β, il-6, nfκb</em>) was observed in the co-exposure group. Additionally, this group exhibited increased lipid accumulation, elevated cholesterol and triglyceride levels, and dysregulation of essential lipid metabolism genes (<em>srebp2, pcsk9</em>). Co-exposure also impaired larval motility and behavior, evidenced by hypolocomotion and reduced acetylcholinesterase levels. Further gene expression analysis showed increased levels of <em>pi3k</em> and <em>akt,</em> two major signaling molecules. Ultimately, the simultaneous exposure to BPA and NaNO₃ leads to disruptions in the endocrine system and abnormal lipid levels via activating the PI3K/AKT/SREBP pathway.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"140 ","pages":"Article 109887"},"PeriodicalIF":4.8,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143537297","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":"Diosgenin alleviates lipid accumulation in NAFLD through the pathways of ferroptosis defensive and executive system","authors":"Linya Wang ,&nbsp;Hongzhuan Yu ,&nbsp;Dongxian Wang ,&nbsp;Guoliang Yin ,&nbsp;Suwen Chen ,&nbsp;Xin Zhang ,&nbsp;Wenfei Yu ,&nbsp;Decheng Meng ,&nbsp;Hongshuai Liu ,&nbsp;Wenying Jiang ,&nbsp;Fengxia Zhang","doi":"10.1016/j.jnutbio.2025.109886","DOIUrl":"10.1016/j.jnutbio.2025.109886","url":null,"abstract":"<div><div>The most prevalent liver condition globally is non-alcoholic fatty liver disease (NAFLD), for which no approved therapies currently exist. Diosgenin, an important component in plants from the <em>Leguminosae, Dioscoreaceae</em>, and <em>Solanaceae</em> families, has demonstrated considerable anti-inflammatory and antioxidant effects. Nonetheless, the specific mechanism by which it may act in managing NAFLD remains unclear. Our research aims to explore the effects and molecular mechanisms of DG on NAFLD by utilizing both in vivo and in vitro experimental approaches. To investigate the effect of DG on hepatic steatosis, we used Sprague-Dawley rats induced by a high-fat diet (HFD) and HepG2 cells exposed to free fatty acids. Oil red O staining and hematoxylin-eosin (H&amp;E) staining were used to explore lipid accumulation and hepatic degeneration. ROS staining, SOD, MDA, and Fe²⁺kits were used to detect the indexes related to oxidative stress in ferroptosis in hepatic tissues and cells. IFSP1 and pcDNA3.1-ACSL4 plasmid were used to knock down Ferroptosis suppressor protein1 (FSP1) and promote the expression of acyl-CoA synthetase long-chain family member 4 (ACSL4) in HepG2 cells. DG improved lipid metabolism disorders and liver damage induced by a high-fat diet in rats with NAFLD. Furthermore, the administration of DG notably decreased oxidative stress levels and liver Fe²⁺ concentrations in rats. Additionally, in vitro experiments demonstrated that DG treatment markedly attenuated ferroptosis and ROS accumulation in HepG2 cells induced by FFAs. Moreover, overexpression of hepatic ACSL4 expression by pcDNA3.1-ACSL4 plasmid promoted the regulatory effects of DG on LPCAT3 and ALOX15. Our research shows that DG can alleviate NAFLD by regulating the FSP1/COQ10 pathway of the ferroptosis defense system and the ACSL4/LPCAT3/ALOX15 pathway of the ferroptosis execution system. Therefore, DG may serve as a novel inhibitor of ferroptosis for the treatment of NAFLD.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"140 ","pages":"Article 109886"},"PeriodicalIF":4.8,"publicationDate":"2025-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143537296","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":"Ginsenoside Rg1 alleviated experimental colitis in obesity mice by regulating memory follicular T cells via Bcl-6/Blimp-1 pathway","authors":"Zeyun Zhang ,&nbsp;Jiaqi Huang ,&nbsp;Xiyan Zhu ,&nbsp;Bailin Deng ,&nbsp;Haimei Zhao ,&nbsp;Haiyan Wang ,&nbsp;Duanyong Liu","doi":"10.1016/j.jnutbio.2025.109880","DOIUrl":"10.1016/j.jnutbio.2025.109880","url":null,"abstract":"<div><div>The pathological mechanisms of ulcerative colitis (UC) are closely related with abnormal memory follicular helper T (mTfh) cell subsets and the Bcl-6/Blimp-1 signaling pathway. Ginsenoside Rg1 (G-Rg1) has been confirmed to exhibit therapeutic effects in obese mice with dextran sulfate sodium (DSS)-induced ulcerative colitis. The aim of this study was to investigate the mechanism of action of G-Rg1 in obese mice with UC by observing mTfh cell subsets and the Bcl-6/Blimp-1 signaling pathway. Obese mice with UC were treated with G-Rg1 at a dose of 200 mg/kg. Disease activity was assessed macroscopically and microscopically, and cytokine levels were measured using enzyme-linked immunosorbent assay (ELISA). Flow cytometry was employed to analyze mTfh cell subsets, and Western blotting to assess protein expression related to the Bcl-6/Blimp-1 pathway. qPCR was used to detect the expression of Bcl-6/Blimp-1, and immunofluorescence was utilized to compare Bcl-6/Blimp-1 expression between different groups. G-Rg1 treatment ameliorated the symptoms of DSS-induced colitis, alleviated the pathological changes in the colonic tissue of obese mice with ulcerative colitis, and reduced the levels of inflammatory cytokines in these mice. Furthermore, flow cytometry analysis indicated that G-Rg1 modulated the balanceof mTfh cells subsets by increasing central memory Tfh (cmTfh) cells and decreasing effector memory Tfh (emTfh) cells, thereby mitigating ulcerative colitis in obese mice. qPCR results revealed the significant upregulation of Bcl-6 and the downregulation of Blimp-1 expression in the DSS group, which was effectively reversed by G-Rg1 treatment. These findings were further confirmed by Western blot and immunofluorescence assays. Collectively, the qPCR, Western blot, and immunofluorescence results demonstrated the pivotal role of the Bcl-6/Blimp-1 signaling pathway in the therapeutic process of G-Rg1 for ulcerative colitis in obese mice. Ginsenoside Rg1 alleviates experimental colitis in obese mice by modulating the proportion of mTfh cell subsets via the Bcl-6/Blimp-1 signaling pathway.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"140 ","pages":"Article 109880"},"PeriodicalIF":4.8,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143531522","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":"Alpha-aminobutyric acid ameliorates diet-induced metabolic dysfunction-associated steatotic liver disease (MASLD) progression in mice via enhancing AMPK/SIRT1 pathway and modulating the gut-liver axis","authors":"Felicianna ,&nbsp;Emily Kwun Kwan Lo ,&nbsp;Congjia Chen ,&nbsp;Marsena Jasiel Ismaiah ,&nbsp;Fangfei Zhang ,&nbsp;Hoi Kit Matthew Leung ,&nbsp;Hani El-Nezami","doi":"10.1016/j.jnutbio.2025.109885","DOIUrl":"10.1016/j.jnutbio.2025.109885","url":null,"abstract":"<div><div>Alpha-aminobutyric acid (ABA) is a nonproteinogenic amino acid, a metabolite which could be generated from the metabolism of methionine, threonine, serine and glycine or as a gut-microbiome-derived metabolite. Changes in ABA levels have been embroiled in metabolic dysfunction-associated steatotic liver disease (MASLD) intervention studies, but their relation to MASLD pathogenesis remains unclear. Hence, this present study aimed to investigate the effect of oral ABA supplementation on the progression of a high fat/high cholesterol diet (HFD) induced MASLD mice model. ABA was found to remodel the gut microbiome composition and ameliorate MASLD parameters in HFD-fed mice. ABA mitigated HFD-induced gain in liver weight, hepatic steatosis, insulin resistance, serum and hepatic triglyceride levels, and liver cholesterol levels. Modulation of lipid metabolism was observed in the liver, in which expression of proteins and/or genes involved in <em>de novo</em> lipogenesis were suppressed, while those involved in fatty acid oxidation and autophagy were upregulated together with cellular antioxidant capacity, in addition to the enhancement of the AMPK/SIRT1 pathway. ABA reshaped the gut composition by enriching nine bacterial species, including <em>Helicobacter hepaticus, Desulfovibrio sp. G11, Parabacteroides distasonis</em>, and <em>Bacteroides fragilis</em>, while diminishing the abundance of 16 species, which included four <em>Helicobacter</em> species. KEGG pathway analysis of microbial functions found that ABA impeded secondary bile acid biosynthesis – which was reflected in the faecal BA composition analysis. Notably, ABA also inhibited ileal FXR-Fgf15 signaling, allowing for increased hepatic Cyp7a1 expression to eliminate cholesterol buildup in the liver. Overall, our findings indicate that ABA could be used as a promising therapeutic approach for the intervention of MASLD.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"140 ","pages":"Article 109885"},"PeriodicalIF":4.8,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143523733","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DNA hypermethylation-induced suppression of ALKBH5 is required for folic acid to alleviate hepatic lipid deposition by enhancing autophagy in an ATG12-dependent manner","authors":"Chaoqun Huang ,&nbsp;Yaojun Luo ,&nbsp;Youhua Liu ,&nbsp;Jiaqi Liu ,&nbsp;Yushi Chen ,&nbsp;Botao Zeng ,&nbsp;Xing Liao ,&nbsp;Yuxi Liu ,&nbsp;Xinxia Wang","doi":"10.1016/j.jnutbio.2025.109870","DOIUrl":"10.1016/j.jnutbio.2025.109870","url":null,"abstract":"<div><div>Nonalcoholic fatty liver disease (NAFLD) occurs when too much fat builds up in the liver. As a growing worldwide epidemic, NAFLD is strongly linked with multiple metabolic diseases including obesity, insulin resistance, and dyslipidemia. However, very few effective treatments are currently available. Folate, an essential B-group vitamin with important biological functions including DNA and RNA methylation regulation, has been shown to have a protective effect against NAFLD with its underlying mechanism remains largely unclear. Here, we show that administration of folic acid significantly improves glucose tolerance, insulin sensitivity, and dyslipidemia in high-fat diet (HFD) fed mice. Moreover, folic acid treatment significantly inhibits lipid deposition in hepatocytes both <em>in vivo</em> and <em>in vitro</em>. Mechanically, folic acid reduces the expression of m⁶A demethylase AlkB homolog 5 (ALKHB5) via promoter DNA hypermethylation. Decreased ALKBH5 causes increased m⁶A modification and increased expression of ATG12 in a demethylase activity-dependent manner, thereby promoting autophagy and preventing hepatic steatosis. Inhibition of ATG12 induced by overexpression of ALKBH5 could impair autophagy and the inhibitory effect of folic acid on lipid accumulation in hepatocytes. Together, these findings provide novel insights into understanding the protective role of folic acid in the treatment of NAFLD and suggest that folic acid may be a potential agent for combating NAFLD.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"140 ","pages":"Article 109870"},"PeriodicalIF":4.8,"publicationDate":"2025-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143492371","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":"Alteration of the microbiota with vancomycin and high-fiber diet affects short-chain fatty acid/free fatty acid receptor signaling in rat caecum","authors":"Jasmin Ballout ,&nbsp;Yasutada Akiba ,&nbsp;Jonathan D. Kaunitz ,&nbsp;Andreas Schwiertz ,&nbsp;Gemma Mazzuoli-Weber ,&nbsp;Gerhard Breves ,&nbsp;Martin Diener","doi":"10.1016/j.jnutbio.2025.109881","DOIUrl":"10.1016/j.jnutbio.2025.109881","url":null,"abstract":"<div><div>Microbial short-chain fatty acids (SCFA) regulate intestinal functions via free-fatty acid (FFA) receptors type 2 and 3. Though the caecum is the most important fermentation chamber in many species, it is unknown whether this signaling system is modulated in dependence on the rate of fermentation within the lumen of this part of the large intestine. Thus, we asked the question whether alteration of the microbiota composition by antibiotic treatment or high-fiber diet affects the SCFA/FFA signaling using rat caecum as model system. SCFA concentrations and microbiota were analyzed in caecal samples from untreated rats, following vancomycin treatment, or after feeding with a high-fiber diet. Oral and aboral caecal segments were harvested for Ussing chamber experiments paralleled by Ca²⁺ imaging experiments with Fura-2 loaded crypts, immunofluorescence, and qPCR. Vancomycin treatment reduced total SCFA concentrations in the caecal content, whereas the high-fiber diet increased the concentration of acetate, but reduced that of propionate and butyrate. Propionate-induced anion secretion was abolished in the vancomycin group, whereas it nearly doubled in the high-fiber group. These effects could not be explained by changes in the expression of FFA2 receptor or in Ca²⁺ signaling evoked by FFA2 receptor activation. Parallel changes in ion secretion evoked by carbachol suggest that alterations in cholinergic signaling might be responsible for the observed changes in epithelial ion transport. Additionally, mucosal mast cell and enterochromaffin cell density increased after vancomycin and high-fiber diet, respectively. This study emphasizes the complex interactions between the microbiota and the caecal epithelium focusing on SCFA/FFA signaling.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"140 ","pages":"Article 109881"},"PeriodicalIF":4.8,"publicationDate":"2025-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143492365","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cannabidiol and sphingolipid metabolism - an unexplored link offering a novel therapeutic approach against high-fat diet-induced hepatic insulin resistance.","authors":"Karolina Konstantynowicz-Nowicka, Klaudia Sztolsztener, Adrian Chabowski, Ewa Harasim-Symbor","doi":"10.1016/j.jnutbio.2025.109865","DOIUrl":"https://doi.org/10.1016/j.jnutbio.2025.109865","url":null,"abstract":"<p><p>Despite extensive research on insulin resistance, which is associated with type 2 diabetes and obesity, there remains a lack of effective and safe methods to treat it. Thus, we hypothesized that cannabidiol (CBD), which influences lipid accumulation and inflammatory response, may interact with sphingolipid metabolism and insulin signaling. To investigate the effects of CBD, male Wistar rats were fed a standard rodent chow or high-fat diet for 7 weeks to induce IR and were treated with CBD or its vehicle administered intraperitoneally for the last two weeks of the experiment. High-Performance Liquid Chromatography (HPLC) was used to assess sphingolipid concentration in the liver, while multiplex assay and western blotting were used to investigate the level or expression of proteins in the insulin signaling pathway and sphingolipid metabolism. Our results revealed that CBD prevented ceramide deposition in the liver of high-fat-fed rats through inhibition of the ceramide de novo synthesis pathway. Moreover, the accumulation of sphingosine-1-phosphate was notably increased with impaired catabolic pathway. Observed changes in the sphingolipid pathway coincided with improved insulin signaling after CBD treatment in animals fed a high-fat diet. Considering the presented evidence, CBD exerted a beneficial effect on insulin sensitivity in a state of lipid overload through the modification of sphingolipid deposition. Our study reveals the importance of broadening IR treatment methods, especially with natural substances that lack serious side effects such as CBD.</p>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":" ","pages":"109865"},"PeriodicalIF":4.8,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143476614","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":"TAS2R5 and TAS2R38 are bitter taste receptors whose colonic expressions could play important roles in age-associated processes","authors":"Florijan Jalševac ,&nbsp;Helena Segú ,&nbsp;Francesc Balaguer ,&nbsp;Teresa Ocaña ,&nbsp;Rebeca Moreira ,&nbsp;Laia Abad-Jordà ,&nbsp;Jordi Gràcia-Sancho ,&nbsp;Anabel Fernández-Iglesias ,&nbsp;Cristina Andres-Lacueva ,&nbsp;Miriam Martínez-Huélamo ,&nbsp;Raul Beltran-Debon ,&nbsp;Esther Rodríguez-Gallego ,&nbsp;Ximena Terra ,&nbsp;Anna Ardévol ,&nbsp;Montserrat Pinent","doi":"10.1016/j.jnutbio.2025.109872","DOIUrl":"10.1016/j.jnutbio.2025.109872","url":null,"abstract":"<div><div>Ageing disrupts how our bodies process nutrients, leading to deregulation of nutrient-sensing and increased inflammation. Dietary interventions can promote healthy ageing, which demonstrates the importance of both metabolism and the gastrointestinal tract for our health. Bitter taste receptors (TAS2R) present in the intestine are key members of metabolic regulation. TAS2R are involved in controlling enterohormonal secretion, detect phenolic compounds in our diet, and potentially have a great impact on the ageing process.</div><div>Here, we aimed to analyze the potential role of intestinal TAS2R on the ageing process and establish potential impact of these receptors on the biomarkers.</div><div>Healthy subjects were divided into two age cohorts: young (38.9±6) and aged (63.6±6). TAS2R expression was analyzed in the colon. Analyses of metabolomics and of phenolic markers were performed in plasma. Best discriminatory parameters were obtained using three machine-learning methods. Finally, Spearman's rank correlation was performed.</div><div>The best separators of the age cohorts were docosahexaenoic acid and multiple lipoprotein fractions. Two TAS2R were also identified: TAS2R5 and TAS2R38. TAS2R5 correlated with multiple lipoprotein-derived fractions, inflammatory marker IL-6 and polyunsaturated fatty acids. TAS2R38 was much more selective, correlating with a few parameters, including membrane lipid sphingomyelin, ketone body acetone, and omega acids. Both TAS2R5 and TAS2R38 correlated with β-hydroxybutyrate.</div><div>The parameters that correlated with TAS2R have known effects on the ageing process. This suggests that TAS2R5 and TAS2R38 are the bitter receptors most likely to play a role in the development and progress of ageing.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"140 ","pages":"Article 109872"},"PeriodicalIF":4.8,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143476627","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":"Unsaturated fatty acids enhance mitochondrial function and PGC1-α expression in brown adipose tissue of obese mice on a low-carbohydrate diet","authors":"Yasmin Alaby Martins Ferreira ,&nbsp;Aline Boveto Santamarina ,&nbsp;Laís Vales Mennitti ,&nbsp;Esther Alves de Souza ,&nbsp;Carla Maximo Prado ,&nbsp;Luciana Pellegrini Pisani","doi":"10.1016/j.jnutbio.2025.109873","DOIUrl":"10.1016/j.jnutbio.2025.109873","url":null,"abstract":"<div><div>Brown adipose tissue (BAT) exhibits greater resilience against inflammation compared to white adipose tissue. However, chronic consumption of a high-fat diet can render brown adipocytes vulnerable to proinflammatory conditions, leading to a decline in their thermogenic capacity and subsequent dysfunction. The analysis of the effects of type fatty acids intake must be important in the context of the dietary pattern and obesity. This study aims to investigate the impact of a low-carbohydrate/high-fat diet, enriched with different types of fatty acids, on mitochondrial activity on brown adipose tissue in obese mice. Male mice were allocated into different dietary groups: a control diet (CTL), and a high-fat diet (HFD) for a duration of 10 weeks to induce obesity. Subsequently, the HFD group was subdivided into the following categories for an additional 6 weeks: HFD with a low carbohydrate content enriched with saturated fatty acids; HFD with a low carbohydrate content enriched with fish oil; HFD with a low carbohydrate content enriched with soybean oil; and HFD with a low carbohydrate content enriched with olive oil. The findings indicated that in comparison to a low-carbohydrate diet rich in saturated fats, diets rich in unsaturated fatty acids—particularly omega-6 (n-6) and omega-9 (n-9)—resulted in elevated expression of UCP1, a marker of BAT activity. Moreover, there was an increase in the expression of PGC1-α, a protein involved in mitochondrial biogenesis, and enhanced functionality of the oxidative phosphorylation system within BAT mitochondria. These results suggest that n-6 and n-9 fatty acids may confer greater benefits to BAT functionality than saturated fats within the context of a low-carbohydrate diet. Therefore, this study revealed some molecular components that mediate BAT mitochondria function influenced by different fatty acids in a low carbohydrate diet, making it an important therapeutic target in obesity</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"140 ","pages":"Article 109873"},"PeriodicalIF":4.8,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143476628","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":"Enhanced in-vitro bioavailability of curcumin, lutein and isoflavones through interaction with spearmint (Mentha spicata) via its bioactive component (R)-(−)-carvone","authors":"Lisa Haider ,&nbsp;Bernhard Blank-Landeshammer ,&nbsp;Nadine Reiter ,&nbsp;Mara Heckmann ,&nbsp;Marcus Iken ,&nbsp;Julian Weghuber ,&nbsp;Clemens Röhrl","doi":"10.1016/j.jnutbio.2025.109868","DOIUrl":"10.1016/j.jnutbio.2025.109868","url":null,"abstract":"<div><div>Numerous dietary phytochemicals such as curcumin, lutein and isoflavones are associated with health beneficial activities, however their application is often limited by their low bioavailability. Therefore, bioenhancers represent a feasible approach to increase the absorption efficiency of bioactive compounds. Here, we combined uptake and transport studies in differentiated Caco-2 cells with high resolution analytics and fractionation to evaluate the impact of spearmint (<em>Mentha spicata</em>) on the cellular uptake of curcumin. Additionally, we utilized mechanistic studies in native and overexpressing cell systems to assess P-glycoprotein (P-gp) and breast cancer resistance protein (BCRP) efflux transporter activity as well as <em>in-silico</em> molecular docking simulations. We found significantly elevated intracellular curcuminoid levels mediated by spearmint. Fractionation and functional assays identified (R)-(-)-carvone as a putative candidate for the biologically active compound mediating increased curcumin uptake via BCRP inhibition. Inhibition of P-gp-mediated efflux might additionally be involved. Molecular docking simulations suggest a common binding site of curcumin and (R)-(-)-carvone in BCRP. Further, spearmint significantly increased cellular uptake of lutein and transintestinal transport of isoflavones <em>in-vitro</em>. In summary, spearmint was identified as a novel bioenhancer for curcumin, lutein and isoflavones. Our findings suggest that spearmint increases bioavailability of a wide range of nutrients and drugs at least partially due to interference with BCRP via its active compound (R)-(-)-carvone.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"139 ","pages":"Article 109868"},"PeriodicalIF":4.8,"publicationDate":"2025-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143472502","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}