Journal of Nutritional Biochemistry最新文献

{"title":"Zinc, Fe2+, and Fe3+ differentially influence IFN-γ production in human peripheral blood mononuclear cells","authors":"Evelyn Fast ,&nbsp;Jana Jakobs ,&nbsp;Jens Bertram ,&nbsp;Inga Weßels ,&nbsp;Judith Sailer ,&nbsp;Bernhard Michalke ,&nbsp;Lothar Rink","doi":"10.1016/j.jnutbio.2025.110194","DOIUrl":"10.1016/j.jnutbio.2025.110194","url":null,"abstract":"<div><div>Iron overload is a common phenomenon in patients undergoing transfusions or organ transplantation. Clinical studies indicate that iron overload interferes with immune function. Baseless supplementation of iron leads to higher morbidity and mortality. In iron overload T-cell differentiation is skewed towards a Th2 response, with lower levels of interferon (IFN)-γ. Zinc is known for its immune balancing abilities, e.g., by induction of regulatory T cells. This study aims to investigate the interaction of iron and zinc in mixed lymphocyte cultures (MLC). MLC, peripheral blood mononuclear cells (PBMC) stimulation with phytohemagglutinin, ELISA, PCR, and ICP-MS were used as methods. Zn²⁺ supplementation leads to a significantly lower IFN-γ production in MLC compared with control (<em>P</em>&lt;.03). Fe²⁺ supplementation lowers the IFN-γ production in MLC (<em>P</em>&lt;.0017), too. However, Fe³⁺ has a slightly increasing effect on IFN-γ release which differs significantly from Fe²⁺ (<em>P</em>&lt;.03). In 2,2-Bipyridyl-induced iron deficiency IFN-γ production is lowered (<em>P</em>&lt;.0003), whereas zinc deficiency does not significantly affect IFN-γ production. Examinations of Interleukin (IL)-2 and IL-6 show comparable tendencies. The Fe²⁺ effect can be imitated by sodium sulfite. Fe³⁺ treatment increases intracellular free iron in peripheral blood mononuclear cells (PBMC) significantly compared to Fe²⁺ treatment (<em>P</em>&lt;.02). Iron (II) and zinc both suppress cytokine production in MLC. Fe³⁺ shows a significantly different effect on IFN-γ production. The underlying mechanism is likely a donation of electrons by Fe²⁺ or oxidative stress. These findings provide mechanistic insights on how the oxidation state of iron differentially modulates human immune cell function and highlights the importance of iron speciation in nutritional immunology.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"149 ","pages":"Article 110194"},"PeriodicalIF":4.9,"publicationDate":"2025-11-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145634797","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":"Dietary eicosapentaenoic and docosahexaenoic acids reduce oxylipins that provide early mediators of colonic inflammation induced by chemotherapy","authors":"Sarah Ruth Parsons ,&nbsp;Irma Magaly Rivas-Serna ,&nbsp;Peter Odion Isesele ,&nbsp;Md Monirujjaman ,&nbsp;Abha Dunichand-Hoedl ,&nbsp;Aducio Leonel Thiesen ,&nbsp;Michael Thomas Clandinin ,&nbsp;Vera Christine Mazurak","doi":"10.1016/j.jnutbio.2025.110192","DOIUrl":"10.1016/j.jnutbio.2025.110192","url":null,"abstract":"<div><div>Combination chemotherapy, irinotecan+5-fluorouracil, treats advanced colorectal cancer but causes intestinal toxicity mediated by cytokines and oxylipins. The objective of this study is to determine the effect of dietary eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) on cytokines and the balance of oxylipins in colon tissue after chemotherapy. Ward colon tumors were implanted into female Fischer 344 rats (13–14 weeks old, n=56) and grew for 2 weeks before initiating chemotherapy (day 0). Subsequently, rats were maintained on the control diet (n=32) or switched to the EPA+DHA diet (n=24), an isocaloric diet that differed mainly in EPA and DHA content. Rats were euthanized on day 0 (baseline), 2, 4 and 8. The reference (no tumor, n=8) and baseline D0 (with tumor, n=8) groups did not receive chemotherapy. Cytokines, phospholipid fatty acids, and oxylipins in colon tissue were compared between the diets and over days post-chemotherapy. Feeding EPA+DHA resulted in a 9- and 2-fold increase in colon phospholipid by day 8 mirrored by a 10- and 2-fold increase in total oxylipins derived from EPA and DHA, respectively. Incorporation of EPA and DHA by day 2 prevented an increase in pro-inflammatory arachidonic acid (AA)-derived oxylipins after chemotherapy, including prostaglandin (PG) D₂, PGE₂, 6-keto-PGF_1α, thromboxane B₂, and 5-hydroxyeicosatetraenoic acid. Displacement of AA by EPA and DHA in colonic membrane attenuates early inflammatory lipid oxylipins. Dietary EPA+DHA may mitigate intestinal perturbations in colorectal cancer patients receiving irinotecan+5-fluorouracil.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"150 ","pages":"Article 110192"},"PeriodicalIF":4.9,"publicationDate":"2025-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145604641","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":"Dietary galactose enhances systemic lipid oxidation but decreases intestinal fatty acid oxidation in post-weaning female mice","authors":"Ferran S. Fos-Codoner,&nbsp;Jaap Keijer,&nbsp;Melissa Bekkenkamp-Grovenstein,&nbsp;Evert M. van Schothorst","doi":"10.1016/j.jnutbio.2025.110193","DOIUrl":"10.1016/j.jnutbio.2025.110193","url":null,"abstract":"<div><div>Replacing part of dietary glucose with galactose in the early post-weaning diet of mice, mimicking extended breastfeeding, improves both short- and long-term physiological and metabolic health parameters. As the primary organ for nutrient absorption, the small intestine was hypothesized to play a key role in these effects.</div><div>Young, weaned mice underwent a 3 week dietary intervention comparing isocaloric diets with a monosaccharide fraction of galactose+glucose <em>versus</em> glucose. Physiological parameters were assessed in both sexes, while metabolic analyses, transcriptomics, and immunohistochemistry of the proximal small intestine were conducted in fed female mice.</div><div>Dietary galactose increased whole-body 24 h fatty acid oxidation (FAO), both absolute and relative to carbohydrate oxidation, without changes in body weight or energy expenditure. Contrasting, the small intestine showed lower expression of transcripts involved in FAO, along with reduced enterocytic lipid droplets. Carbohydrate metabolism remained unaffected, while reduced expression of NADPH-dependent and -independent antioxidant enzymes and the pentose phosphate pathway suggested a shift in local metabolism. Despite these intestinal changes, the liver showed no alterations in lipid catabolism, implicating other organs in the observed systemic FAO increase. In addition, <em>Ppargc1a</em>, central regulator of mitochondrial biogenesis was upregulated, which is in line with the known role of galactose in upregulating mitochondrial oxidative phosphorylation.</div><div>In conclusion, replacing half of post-weaning dietary glucose with galactose, mimicking prolonged lactose intake, profoundly affects substrate metabolism at both systemic and intestinal levels. We propose that reduced intestinal FAO redirects fatty acid oxidation to extra-intestinal, extra-hepatic tissues, driving the observed systemic metabolic benefits.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"149 ","pages":"Article 110193"},"PeriodicalIF":4.9,"publicationDate":"2025-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145604597","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":"Coenzyme Q10 ameliorates obesity by promoting white adipose tissue browning and preserving mitochondrial dynamics in ovariectomized rats fed a high-fat diet","authors":"Tong Pan ,&nbsp;Shu-Ying Chen ,&nbsp;Ching-Wen Kung ,&nbsp;Hsuan-Yu Chen ,&nbsp;Pao-Yun Cheng ,&nbsp;Hsin-Hsueh Shen ,&nbsp;Ing-Luen Shyu ,&nbsp;Yen-Mei Lee","doi":"10.1016/j.jnutbio.2025.110187","DOIUrl":"10.1016/j.jnutbio.2025.110187","url":null,"abstract":"<div><div>Estrogen deficiency caused by menopause leads to obesity in women. In obesity, excessive visceral fat accumulation induces a chronic, low-grade inflammatory response, thereby increasing the risk of cardiovascular disease, insulin resistance, and type 2 diabetes mellitus. Browning of white adipose tissue (WAT) has emerged as a promising strategy to counteract obesity and related metabolic disorders. Coenzyme Q10 (CoQ10) has been reported to reduce oxidative stress, enhance mitochondria function and improve metabolic syndrome in obese and diabetic animals and patients. In this study, we evaluated whether long-term CoQ10 supplementation could induce WAT browning to ameliorate obesity in ovariectomized (OVX) rats fed a high-fat diet (HFD), and explored the underlying mechanisms. Supplementation with CoQ10 (20 and 40 mg/kg, once daily by gavage) for 12 weeks in OVX rats significantly reduced weight gain, excessive visceral fat accumulation, white adipocyte hypertrophy, plasma triglyceride levels, and glucose intolerance, while increasing energy expenditure compared to OVX rats treated with vehicle (<em>P</em>&lt;.05). High dose CoQ10 (40 mg/kg) significantly lowered plasma insulin levels, reduced HIF-1α, MCP-1 and IL-6 protein expression, and increased phosphorylated AKT in retroperitoneal WAT (<em>P</em>&lt;.05). In inguinal WAT (iWAT), CoQ10 enhanced the expression of browning-related proteins including UCP-1, CIDEA, PRDM16, PGC-1α, and phosphorylated AMPK, and elevated plasma irisin levels (<em>P</em>&lt;.05). CoQ10 also regulated mitochondria dynamics of iWAT, as evidenced by increased MFN1, MFN2, and OPA1, and decreased FIS1 protein expression compared with the OVX group (<em>P</em>&lt;.05). In 3T3-L1 adipocytes, CoQ10-induced expression of browning markers (UCP-1, TBX1 and PRDM16) was significantly suppressed by dorsomorphin, an AMPK inhibitor, and by AMPK knockdown (<em>P</em>&lt;.05). In conclusion, long-term CoQ10 supplementation ameliorates weight gain, white adipocyte hypertrophy and inflammation in WAT, and metabolic disorders caused by combined estrogen deficiency and HFD, likely through its WAT browning effect. AMPK activation is suggested to contribute to the browning effect and enhance the expression of proteins involved in mitochondrial dynamics. Therefore, CoQ10 supplementation could be an effective intervention for preventing postmenopausal obesity.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"149 ","pages":"Article 110187"},"PeriodicalIF":4.9,"publicationDate":"2025-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145587635","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":"Decoding the anti-obesity mechanisms of isoliquiritigenin: AMPK activation modulates adipogenesis, lipolysis, oxidative stress, and inflammation in high-fat diet rat models","authors":"Mohammed Abdo Yahya ,&nbsp;Ghedeir M. Alshammari ,&nbsp;Samy M. Eleawa ,&nbsp;Kawther Amawi ,&nbsp;Mahmoud Alkhateeb ,&nbsp;Ammar M. AL-Farga ,&nbsp;Hisham Alshaikhli ,&nbsp;Nora A. AlFaris ,&nbsp;Setah Naif Alotaibi","doi":"10.1016/j.jnutbio.2025.110190","DOIUrl":"10.1016/j.jnutbio.2025.110190","url":null,"abstract":"<div><div>This study investigated the effects of Isoliquiritigenin (ISL) on adiposity in Wistar rats fed a high-fat diet (HFD), positing that ISL mitigates adiposity by inhibiting adipogenesis and promoting lipolysis via AMPK activation. Adult male Wistar rats were divided into six groups (<em>n</em>=8): Control (vehicle), Control + ISL (40 mg/kg), HFD (vehicle), HFD + ISL (20 mg/kg), HFD + ISL (40 mg/kg), and HFD + ISL (40 mg/kg) + Dorsomorphin (0.2 mg/kg) for 12 weeks. In a dose-dependent manner, ISL (thrice a week) significantly attenuated the increase in body weight and adipocyte size, improving glucose and insulin tolerance, HbA1c, and HOMA-IR without affecting food intake in HFD rats. Particularly, the higher dose of ISL (40 mg/kg) significantly increased the phosphorylation of AMPK (+193.3%), resulting in a p-AMPK/AMPK activity ratio increase of 191.0% in the white adipose tissue (WAT) of HFD rats. This dose also reduces body weight (24.6%), weight gain (28.7), fat deposit weight (−39.2% %), HOMA-IR (−67.62%), and serum triglycerides (−62.4%), cholesterol (56.7%), IL-6 (−66.1%) and TNF-α (−79.5%) in these HFD rats. It also increased p-ACC levels (+86.7%), Nrf2 mRNA (+392.7%), and PPARα mRNA (+255.0%), as well as the levels of HSL (+149.7%) and ATGL (139.62%). ISL (40 mg/kg) also decreased WAT levels of IL-6 (−57.86%), TNF-α (−74.96%), mRNA of SREBP1 (−38/8%), FAS (−50%) and NF-kB (58.8%), and levels of PLIN1 (−50.1) in these HFD rats. Dorsomorphin treatment reversed these effects in ISL + HFD rats. In conclusion, ISL demonstrates anti-obesity effects in HFD-induced rats through AMPK activation.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"149 ","pages":"Article 110190"},"PeriodicalIF":4.9,"publicationDate":"2025-11-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145582208","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":"Short-term effect of Ketogenic diet and Low-calorie diet on Ketometabolism and lipid metabolism","authors":"Flora Bahrami ,&nbsp;Elija Buetler ,&nbsp;Katrin Freiburghaus ,&nbsp;Patcharamon Seubnooch ,&nbsp;Lia Bally ,&nbsp;Jonathan Maurer ,&nbsp;Christa E Flück ,&nbsp;Reiner Wiest ,&nbsp;Mojgan Masoodi","doi":"10.1016/j.jnutbio.2025.110188","DOIUrl":"10.1016/j.jnutbio.2025.110188","url":null,"abstract":"<div><div>The ketogenic diet (KD) has shown therapeutic potential for epilepsy, neuroprotective effects, and, more recently, metabolic complications. In this study, we explored the impact of the KD on the promotion of ketometabolism and the improvement of dyslipidemia. To this end, we investigated the outcomes of two different diets, eucaloric KD and low-calorie diet (LCD), on ketogenesis, circulating intact lipids, bile acids, and neuro and pancreatic peptides. Based on our results, the concentration of ketone bodies, namely 3-hydroxybutyric acid, increased significantly by an average of ten and two times for KD and LCD, respectively. Additionally, the concentration of several triglyceride (TAG) species decreased up to 98.3% and 99.1% for KD and LCD, respectively, while these reductions were only significant for LCD. Moreover, our results showed that 3 d of KD led to an increase in the baseline concentration of pancreatic polypeptide 3-36, which suggests that short-term KD has the potential to suppress the appetite. Finally, no significant change in the baseline and kinetic postprandial concentration of bile acid species was observed during the KD. In conclusion, our findings suggest that the ketogenic diet, being less restrictive than the low-calorie diet, has a greater impact on ketometabolism. However, while KD reduces TAG species, this reduction is not statistically significant, unlike the significant decrease observed with LCD.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"149 ","pages":"Article 110188"},"PeriodicalIF":4.9,"publicationDate":"2025-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145564174","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":"Inducible trophoblast-specific knockdown of mechanistic target of rapamycin impairs placental folate transport in mice","authors":"Hiroshi Shimada ,&nbsp;Johann Urschitz ,&nbsp;Theresa L Powell ,&nbsp;Thomas Jansson ,&nbsp;Fredrick J Rosario","doi":"10.1016/j.jnutbio.2025.110189","DOIUrl":"10.1016/j.jnutbio.2025.110189","url":null,"abstract":"<div><div>Folate deficiency in pregnancy is strongly associated with fetal growth restriction (FGR). Fetal folate availability is determined by maternal folate intake and the capacity of the placenta to transport folate. However, the mechanisms regulating placental folate transport remain poorly understood. The mechanistic target of rapamycin (mTOR) regulates placental function and fetal growth, but it is unknown if mTOR regulates folate transport <em>in vivo.</em> We hypothesized that trophoblast-specific mTOR knockdown inhibits placental folate transport in mice. We generated transgenic mice with a doxycycline-inducible, trophoblast-specific <em>Mtor</em> knockdown using PiggyBac transposase-enhanced pronuclear injection. Doxycycline administration on embryonic day (E) 14.5 induced placental-specific <em>Mtor</em> knockdown, resulting in reduced fetal weight, placental weight, and fetal-to-placental weight ratio. Functionally, mTOR knockdown reduced folate uptake in isolated trophoblast plasma membranes (TPM), decreased the TPM protein expression of the three main placental folate transporters (FRα, RFC, and PCFT) without affecting protein expression of theses transporters in placental homogenates, and lowered fetal plasma folate concentration. In conclusion, mTOR signaling is a positive regulator of the three main placental folate transporters <em>in vivo</em> mediated by posttranslational mechanisms, likely involving effects of plasma membrane trafficking. Trophoblast mTOR signaling is essential for maintaining adequate fetal folate supply and we propose that the inhibition of placental mTOR signaling reported in FGR contributes to fetal folate deficiency and decreased fetal growth in this pregnancy complication. Our data supports the potential to target placental mTOR signaling as a novel intervention in pregnancies affected by abnormal fetal growth.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"149 ","pages":"Article 110189"},"PeriodicalIF":4.9,"publicationDate":"2025-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145557089","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":"Dietary supplementation of n - 3 PUFAs ameliorates UV-induced photoaging and skin tumor via GPR120 activation","authors":"Shuzhan Shen,&nbsp;Qihang Chang,&nbsp;Yiting Zhao,&nbsp;Xidie Yin,&nbsp;Zhi Cao,&nbsp;Huan Xue,&nbsp;Qingyu Zeng,&nbsp;Xiuli Wang,&nbsp;Peiru Wang","doi":"10.1016/j.jnutbio.2025.110186","DOIUrl":"10.1016/j.jnutbio.2025.110186","url":null,"abstract":"<div><div>Chronic ultraviolet (UV) radiation induces cutaneous inflammation and immunosuppression, driving photoaging and skin carcinogenesis. <em>n</em> - 3 polyunsaturated fatty acids (PUFAs) have shown clinical efficacy in mitigating various inflammatory cutaneous diseases and neoplastic diseases via dietary supplementation. However, the precise molecular mechanisms by which <em>n</em> - 3 PUFAs prevent photoaging and carcinogenesis remain incompletely defined. In this study, transcriptomic analysis revealed that <em>n</em> - 3 PUFAs exert antiphotoaging effects by sustaining skin homeostasis through coordinated immunomodulation and anti-inflammatory actions. Multitimepoint sampling in murine models was employed to dynamically characterize stage-specific effects of <em>n</em> - 3 PUFAs during photoaging progression. Mechanistically, <em>n</em> - 3 PUFAs were noted to restore balanced M1/M2 ratios in both early and advanced stage of photoaged murine skin, thereby maintaining microenvironmental homeostasis. Moreover, <em>n</em> - 3 PUFAs were shown to counteract UV-induced immunosuppression by diminishing immunosuppressive cell accumulation. Overall, our findings highlight the crucial role of G protein-coupled receptor 120 (GPR120) as the pivotal mediator: its activation inhibits TAK1/NF-κB signaling and directs M2 macrophage skewing after UV exposure. This study elucidates the mechanism through which <em>n</em> - 3 PUFAs reverse photoaging, and lays the groundwork for enhancing the clinical applications of <em>n</em> - 3 PUFAs.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"149 ","pages":"Article 110186"},"PeriodicalIF":4.9,"publicationDate":"2025-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145534750","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-linolenic acid regulates white adipose tissue lipolysis independent of background dietary protein","authors":"Siobhan E. Woods ,&nbsp;Melissa Gonzalez-Soto ,&nbsp;Alexa N. King ,&nbsp;Frédéric Capel ,&nbsp;David C. Wright ,&nbsp;David M. Mutch","doi":"10.1016/j.jnutbio.2025.110185","DOIUrl":"10.1016/j.jnutbio.2025.110185","url":null,"abstract":"<div><div>White adipose tissue (WAT) is an endocrine organ essential for maintaining whole-body energy balance by regulating fatty acid uptake, storage, and release. Emerging evidence indicates that omega-3 fatty acids have a role in modulating WAT lipid metabolism. While most studies have focused on marine-derived omega-3s, considerably less is known about alpha-linolenic acid (ALA). Previous research suggests that ALA may prevent or restore impaired lipolysis in dysfunctional WAT. The primary objective of this study was to examine the effects of ALA on WAT lipolytic activity and whether this varied with background dietary protein. Male C57BL/6N mice (<em>n</em>=16/group) were fed moderate-fat diets containing either 1% (low-ALA) or 3% (high-ALA) energy from ALA (provided by flaxseed oil), and either skim milk protein or a soy protein isolate for 8 weeks. Mice fed high-ALA diets showed increased body weight gain and WAT depot weights, reduced serum triglycerides, and increased serum glycerol levels. The higher serum glycerol levels in high-ALA fed mice were reflected in higher glycerol release from cultured adipose tissue explants stimulated with a β-adrenergic agonist. Markers of WAT lipolysis, including ATGL and phosphorylated HSL, were either lower or unchanged in mice fed high-ALA diets. Background dietary protein (from either dairy or soy) had little-to-no-effect on study endpoints. Our data suggests that increased dietary ALA intake improves circulating TAG levels while reducing markers of lipolysis in WAT depots. The increase in glycerol observed with high-ALA intake may point to a potential regulation of WAT glycerogenesis and/or aquaporin expression that warrants future investigation.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"149 ","pages":"Article 110185"},"PeriodicalIF":4.9,"publicationDate":"2025-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145530736","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 alleviates muscle oxidative damage by improving mitochondrial function, maintaining calcium homeostasis, and inhibiting ferroptosis","authors":"Yu Huang,&nbsp;Zhiqing Huang,&nbsp;Gang Jia,&nbsp;Hua Zhao,&nbsp;Xiaoling Chen","doi":"10.1016/j.jnutbio.2025.110182","DOIUrl":"10.1016/j.jnutbio.2025.110182","url":null,"abstract":"<div><div>Oxidative stress represents a critical driver of impaired muscle integrity and compromised meat quality. This study investigates the protective effects and underlying mechanisms of <span>l</span>-theanine against oxidative stress-induced muscle damage. Our results DEMONSTRATED that diquat exposure triggered significant histopathological lesions, oxidative stress (elevated reactive oxygen species and malondialdehyde, decreased muscle antioxidant capacity), mitochondrial dysfunction (reduced adenosine triphosphate levels, mitochondrial membrane potential and gene expression related to mitochondrial biogenesis and function), calcium dyshomeostasis (cytosolic and mitochondrial Ca²⁺ overload), iron accumulation (increased free Fe²⁺), increased acyl-CoA synthetase long chain family member 4 expression and decreased glutathione peroxidase 4 expression. <span>l</span>-theanine pretreatment effectively reversed these pathological alterations. Collectively, <span>l</span>-theanine alleviated oxidative stress-induced muscle damage by enhancing antioxidant capacity, improving mitochondrial function, maintaining calcium homeostasis, and inhibiting ferroptosis. These findings provide a novel theoretical foundation for developing <span>l</span>-theanine-based nutritional strategies to enhance muscle health.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"149 ","pages":"Article 110182"},"PeriodicalIF":4.9,"publicationDate":"2025-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145523654","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}