Journal of Nutritional Biochemistry最新文献_第3页

Lycopene protects against myocardial ischemia-reperfusion injury by inhibiting FABP3-mediated pyroptosis in cardiac microvascular endothelial cells 番茄红素通过抑制fabp3介导的心肌微血管内皮细胞焦亡来保护心肌缺血再灌注损伤。

IF 4.9 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Journal of Nutritional Biochemistry

Pub Date : 2026-05-01 Epub Date: 2026-01-15 DOI: 10.1016/j.jnutbio.2026.110270

Yuetong Sha , Yawen Xie , Xue Guan , Xinran Wang , Qianhui Zhang , Yonggang Cao , Pilong Shi , Hongli Sun

Cardiac microvascular damage exhibits a significant association with myocardial ischemia/reperfusion injury (MI/RI) development, which correlates with mitochondrial dysfunction. Lycopene has demonstrated pharmacological efficacy against cardiovascular diseases. Nevertheless, the potential roles and underlying mechanisms through which lycopene influences MI/RI remain incompletely understood. This study aimed to investigate the effect of lycopene on cardiac microvascular endothelial cells (CMECs) function in a rat model of MI/RI. This investigation sought to elucidate lycopene’s role in MI/RI and its mechanistic foundation. A rat MI/RI model was employed, and multiple experimental approaches were conducted, encompassing quantitative real-time polymerase chain reaction, western blot analysis, immunofluorescence microscopy, enzyme-linked immunosorbent assay, molecular docking, and molecular dynamics simulations. In vitro studies involved the establishment of a hypoxia-reoxygenation model using CMECs to evaluate lycopene’s contribution to pyroptosis suppression and mitochondrial dysfunction prevention. Lycopene was found to enhance mitochondrial function through inhibition of the YTHDF1/E2F8/FABP3 axis in CMECs, suppress cGAS-STING signaling pathway activation, reduce cellular inflammatory responses, and inhibit cellular pyroptosis. These effects ultimately resulted in improved CMECs function, enhanced microvascular integrity, and increased perfusion and oxygen delivery to cardiomyocytes.

心肌微血管损伤与心肌缺血/再灌注损伤（MI/RI）的发展密切相关，而心肌缺血/再灌注损伤与线粒体功能障碍相关。番茄红素已被证明对心血管疾病具有药理功效。然而，番茄红素影响MI/RI的潜在作用和潜在机制仍不完全清楚。本研究旨在探讨番茄红素对心肌梗死/心肌梗死大鼠心肌微血管内皮细胞（CMEC）功能的影响。本研究旨在阐明番茄红素在MI/RI中的作用及其机制基础。采用大鼠MI/RI模型，采用实时定量聚合酶链反应、Western blot分析、免疫荧光显微镜、酶联免疫吸附实验、分子对接、分子动力学模拟等多种实验方法。体外研究包括使用cmec建立缺氧-再氧化模型，以评估番茄红素在抑制焦亡和预防线粒体功能障碍方面的作用。发现番茄红素通过抑制CMECs中YTHDF1/E2F8/FABP3轴增强线粒体功能，抑制cGAS-STING信号通路激活，减少细胞炎症反应，抑制细胞焦亡。这些作用最终导致CMEC功能改善，微血管完整性增强，心肌细胞灌注和氧输送增加。

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引用次数: 0

Dietary inulin mediates the molecular mechanism of intestinal metabolites to alleviate high salt diet-induced chronic kidney disease in mice 饲粮菊糖介导肠道代谢物缓解高盐饮食诱导的小鼠慢性肾病的分子机制

IF 4.9 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Journal of Nutritional Biochemistry

Pub Date : 2026-05-01 Epub Date: 2026-01-15 DOI: 10.1016/j.jnutbio.2026.110269

Qinglin Qu, Huajing Gao, Xue Gao, Peihua Li, Yanquan Mou, Xiangrui Kong, Xintong Tan

It is recognized that excessive dietary salt intake is a critical factor contributing to chronic kidney disease (CKD). A high-salt diet (HSD) disrupts the balance of the gut microbiota, but the molecular mechanisms linking gut dysbiosis to target organ damage remain unclear. This study identified dietary prebiotic inulin (INU) as a potent regulator of the gut-short-chain fatty acid-kidney axis, capable of counteracting HSD-induced CKD. Sequencing analysis showed that INU selectively enriched Bifidobacterium and Faecalibaculum while downregulating Desulfovibrio. This microbiome shift restored intestinal tight junction proteins and reduced serum lipopolysaccharide (LPS) levels, thereby inhibiting TLR4/NF-κB-mediated renal inflammation. Notably, the effects of direct SCFA supplementation align with the renal protective effects of INU, confirming the critical role of the gut-kidney axis. Our study reveals INU as a dietary strategy that combats HSD-induced CKD via SCFAs produced by the microbiota, offering new insights into the gut-SCFAs-kidney axis as a therapeutic target.

人们认识到，过量的饮食盐摄入是导致慢性肾脏疾病（CKD）的关键因素。高盐饮食（HSD）会破坏肠道微生物群的平衡，但肠道生态失调与靶器官损伤之间的分子机制尚不清楚。本研究发现膳食益生元菊糖（INU）是肠-短链脂肪酸-肾轴的有效调节剂，能够对抗hsd诱导的CKD。测序分析显示，INU选择性富集双歧杆菌和粪杆菌，下调Desulfovibrio。这种微生物群的转移恢复了肠道紧密连接蛋白，降低了血清脂多糖（LPS）水平，从而抑制了TLR4/NF-κ b介导的肾脏炎症。值得注意的是，直接补充SCFA的效果与INU的肾脏保护作用一致，证实了肠肾轴的关键作用。我们的研究揭示了INU作为一种饮食策略，通过微生物群产生的SCFAs对抗hsd诱导的CKD，为肠道-SCFAs-肾脏轴作为治疗靶点提供了新的见解。

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引用次数: 0

Dietary eicosapentaenoic and docosahexaenoic acids reduce oxylipins that provide early mediators of colonic inflammation induced by chemotherapy 饮食中的二十碳五烯酸和二十二碳六烯酸可减少氧脂素，而氧脂素是化疗引起的结肠炎症的早期介质。

IF 4.9 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Journal of Nutritional Biochemistry

Pub Date : 2026-04-01 Epub Date: 2025-11-23 DOI: 10.1016/j.jnutbio.2025.110192

Sarah Ruth Parsons , Irma Magaly Rivas-Serna , Peter Odion Isesele , Md Monirujjaman , Abha Dunichand-Hoedl , Aducio Leonel Thiesen , Michael Thomas Clandinin , Vera Christine Mazurak

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.

伊立替康+5-氟尿嘧啶联合化疗治疗晚期结直肠癌，但引起细胞因子和氧化脂类介导的肠道毒性。本研究的目的是确定饮食中添加二十碳五烯酸（EPA）和二十二碳六烯酸（DHA）对化疗后结肠组织细胞因子和氧化脂平衡的影响。将Ward结肠肿瘤植入雌性Fischer 344大鼠（13-14周龄，n=56），生长2周后开始化疗（第0天）。随后，将大鼠维持在对照饮食（n=32）或切换到EPA+DHA饮食（n=24），这是一种主要在EPA和DHA含量上有所不同的等热量饮食。在第0天（基线）、第2天、第4天和第8天对大鼠实施安乐死。参考组（无肿瘤，n=8）和基线组（有肿瘤，n=8）不接受化疗。细胞因子、磷脂脂肪酸和氧化脂素在饮食和化疗后几天的结肠组织中进行比较。饲喂EPA+DHA导致第8天结肠磷脂增加9倍和2倍，同时EPA和DHA衍生的总氧化脂分别增加10倍和2倍。在第2天，EPA和DHA的掺入阻止了化疗后促炎花生四烯酸（AA）衍生的氧化脂类的增加，包括前列腺素（PG） D2、PGE2、6-酮- pgf1 α、血栓素B2和5-羟基二碳四烯酸。EPA和DHA在结肠膜中置换AA可减轻早期炎性脂质氧化脂质。膳食EPA+DHA可能减轻伊立替康+5-氟尿嘧啶治疗的结直肠癌患者肠道紊乱。

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引用次数: 0

Ketogenic diet attenuates high fat diet induced obesity in rats: insights into hepatic and intestinal tissues 生酮饮食减轻大鼠高脂肪饮食引起的肥胖：对肝脏和肠道组织的见解。

IF 4.9 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Journal of Nutritional Biochemistry

Pub Date : 2026-04-01 Epub Date: 2025-12-13 DOI: 10.1016/j.jnutbio.2025.110237

Nada F. Abo El-Magd , Nehal M. Ramadan , Yomna F. Hassan , Amr M. Mahmoud , Maha M. Azzam , Salma M. Eraky

The rising global prevalence of obesity and its impact on health and economy make finding available safe treatment an urgent need. Ketogenic diet represents trendy dietary intervention, while underlying molecular mechanisms remains unclear. Twenty-four male Sprague-Dawley rats were randomized into three groups: Control (maintained on conventional chow diet for 24 weeks), HFD (fed High-fat diet (HFD) for 24 weeks), keto (fed HFD for 12 weeks, then ketogenic diet for additional 12 weeks). Effect of ketogenic diet on serum metabolomics using Ultra Performance Liquid Chromatography coupled with Liquid Chromatography on both positive and negative modes; hepatic tissue using histopathological examination, enzyme-linked immunosorbent assay (ELISA), Real time Polymerase Chain Reaction, proteome array detection; intestinal tissue using histopathological examination, ELISA and adipose tissue using histopathological examination were evaluated. The ketogenic diet reduced rat weight, food intake, epididymal fat mass, and blood glucose level compared to HFD group. Furthermore, it resulted in a decrease in serum methionine, linolenic acid, Lyso Phosphatidylcholine (PC) (15.0:0.0), Lyso PC (18.0:0.0) with hepatic repression of fibroblast growth factor 21 (FGF21), and type II cell surface protein/ Dipeptidyl peptidase 4, Intercellular Adhesion Molecule 1, Insulin growth factor-1, Lipocalin-2, Serpin E1, tissue inhibitor of matrix metalloproteinase-1, receptor for advanced glycation end products and induction of Farnesoid X receptor (FXR), hepatocyte growth factor (HGF) which leads to hepatic antioxidant effects and histopathological amelioration. In addition, the ketogenic diet caused intestinal induction of melanocortin-4 receptors/ glucagon-like peptide 1 pathway, which causes intestinal antioxidant effects and histopathological amelioration. Thus, ketogenic diet stated potential anti-obesity effect that mitigates HFD-induced organ damage through the modulation of key metabolic and signaling networks.

全球肥胖流行率不断上升及其对健康和经济的影响，迫切需要找到可用的安全治疗方法。生酮饮食代表了流行的饮食干预，但其潜在的分子机制尚不清楚。将24只雄性Sprague-Dawley大鼠随机分为3组：对照组（喂食常规饲料24周）、高脂饲料（喂食高脂饲料24周）、酮饲料（喂食高脂饲料12周，再喂食生酮饲料12周）。生酮饮食对血清代谢组学的影响——超高效液相色谱-正、负两种模式肝组织采用组织病理学检查、酶联免疫吸附试验（ELISA）、实时聚合酶链反应、蛋白质组阵列检测；采用组织病理学检查对大鼠肠道组织、ELISA和脂肪组织进行评价。与HFD组相比，生酮饮食降低了大鼠体重、食物摄入量、附睾脂肪量和血糖水平。此外，它还导致血清蛋氨酸、亚麻酸、Lyso磷脂酰胆碱（PC）（15.0:0.0）、Lyso磷脂酰胆碱（PC）（18.0:0.0）的降低，并抑制成纤维细胞生长因子21 （FGF21）、II型细胞表面蛋白/二肽基肽酶4、细胞间粘附分子1、胰岛素生长因子-1、脂钙素-2、丝氨酸蛋白酶E1、基质金属蛋白酶-1组织抑制剂、晚期糖基化终产物受体和Farnesoid X受体（FXR）的诱导。肝细胞生长因子（HGF），导致肝脏抗氧化作用和组织病理学改善。此外，生酮饮食引起肠道诱导黑素皮质素-4受体/胰高血糖素样肽1通路，引起肠道抗氧化作用和组织病理改善。因此，生酮饮食表明了潜在的抗肥胖作用，通过调节关键的代谢和信号网络来减轻hfd诱导的器官损伤。

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引用次数: 0

Jujuboside A ameliorates glomerular podocytes lipotoxicity in diabetic mice by YY1-mediated promotion of intracellular cholesterol transport and efflux 红枣苷A通过yy1介导的促进细胞内胆固醇转运和外溢改善糖尿病小鼠肾小球足细胞脂毒性。

IF 4.9 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Journal of Nutritional Biochemistry

Pub Date : 2026-04-01 Epub Date: 2025-12-13 DOI: 10.1016/j.jnutbio.2025.110231

Ying Liu , Dandan Pan , Pinyan Zhang , Yuting Shao , Yinhua Kong , Zhenzhou Jiang , Wenjing Zhu , Houwen Wang , Xinghan Liu , Sitong Qian , Tao Wang , Xia Zhu , Tingting Yang , Qian Lu

Glomerular podocytes injury represents a critical pathological hallmark of diabetic kidney disease (DKD), in which lipotoxicity plays a central pathogenic role. Our previous investigations in type 2 diabetes mellitus (T2DM) have demonstrated that Jujuboside A (Ju A), a triterpene saponin isolated from Semen Ziziphi Spinosae (SZS), exerted dual therapeutic effects in T2DM by ameliorating hepatic steatosis and renal dysfunction. However, the role of podocytes lipid metabolism in Ju A-mediated protection against DKD remain undefined prior to the present study. In this work, we reported that Ju A significantly attenuated glomerular podocytes injury and lipotoxicity in DKD, while concurrently improving renal function and preserving glomerular morphology. Mechanistically, Yin Yang 1 (YY1)-mediated alleviation of lipotoxicity contributed to the protective effect of Ju A against glomerular podocytes injury, primarily by promoting intracellular cholesterol transport and efflux. In conclusion, our findings demonstrated that Ju A mitigated lipid overload in glomerular podocytes by modulating cholesterol homeostasis via YY1, which not only intercepted the pathological progression of DKD but also provided a potential therapeutic target (YY1) and candidate agent (Ju A) for DKD intervention.

肾小球足细胞损伤是糖尿病肾病（DKD）的一个重要病理标志，其中脂肪毒性起着核心的致病作用。我们之前对2型糖尿病（T2DM）的研究表明，从紫皮子（SZS）中分离的三萜皂苷枣苷A （Ju A）通过改善肝脂肪变性和肾功能障碍，对T2DM具有双重治疗作用。然而，在本研究之前，足细胞脂质代谢在Ju a介导的抗DKD保护中的作用仍未明确。在这项工作中，我们报道了菊a显著减轻DKD肾小球足细胞损伤和脂肪毒性，同时改善肾功能和保持肾小球形态。在机制上，阴阳1 （YY1）介导的脂肪毒性减轻有助于菊a对肾小球足细胞损伤的保护作用，主要是通过促进细胞内胆固醇的运输和外排。总之，我们的研究结果表明Ju A通过YY1调节胆固醇稳态来减轻肾小球足细胞的脂质过载，这不仅阻断了DKD的病理进展，而且为DKD干预提供了潜在的治疗靶点（YY1）和候选药物（Ju A）。

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引用次数: 0

Lnc-Gm26626 in visceral adipose tissues participates in energy metabolism via IDH3α-associated tricarboxylic acid cycle activity 内脏脂肪组织中的Lnc-Gm26626通过idh3 α-相关三羧酸循环活性参与能量代谢。

IF 4.9 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Journal of Nutritional Biochemistry

Pub Date : 2026-04-01 Epub Date: 2025-12-21 DOI: 10.1016/j.jnutbio.2025.110243

Haoneng Tang , Fen Xiao , Yaru Chen , Chenyi Tang , Yue Guo , Huixuan Wu , Yinghui Zhou , Houde Zhou

The identification of novel long noncoding RNAs (lncRNAs) is involved in visceral adipose tissue development under fasting and refeeding conditions may be unravel the mechanisms of diet induced obesity. In this study, adult mice were subjected to fasting and refeeding intervention and mesenteric adipose tissue was extracted for transcriptome sequencing. Lnc-Gm26626 was identified and its role on tricarboxylic acid cycle (TCA) and isocitrate dehydrogenase 3α (IDH3α) expression was investigated using adenovirus-mediated gene interference. In vivo experiments were further performed to clarify whether lnc-Gm26626 affected the plasticity of adipose tissues. A total of 3,570 differentially expressed lncRNAs and 5,032 differentially expressed mRNAs were identified, lnc-Gm26626 was regulated by external nutritional stimulation and was observed to translocate from the nucleus to the cytoplasm under high glucose conditions. The knockdown of lnc-Gm26626 could inhibit the expression of IDH3α in vitro; AAV-mediated lnc-Gm26626 knockdown increased the fat content of mesenteric adipose tissues and alleviated the fluctuations in glucose and lipid metabolism during fasting and refeeding. Collectively, we identified lnc-Gm26626 as a novel regulator of energy metabolism that participate in the response to energy restriction by regulating IDH3α expression in the TCA cycle, thereby affecting visceral adipose tissue plasticity in male mice.

背景：在禁食和再喂养条件下，发现参与内脏脂肪组织发育的新型长链非编码rna （lncRNAs）可能有助于揭示饮食诱导肥胖的机制。方法：对成年小鼠进行禁食和再喂养干预，提取肠系膜脂肪组织进行转录组测序。鉴定了Lnc-Gm26626，并利用腺病毒介导的基因干扰研究了其在三羧酸循环（TCA）和异柠檬酸脱氢酶3α (IDH3α)表达中的作用。进一步进行体内实验，明确lnc-Gm26626是否影响脂肪组织的可塑性。结果：共鉴定出3570个差异表达lncrna和5032个差异表达mrna， lnc-Gm26626受外部营养刺激调控，并在高糖条件下观察到从细胞核向细胞质转运。lnc-Gm26626的敲低可抑制体外IDH3α的表达；aav介导的lnc-Gm26626基因敲低增加了肠系膜脂肪组织的脂肪含量，缓解了禁食和再喂养时糖脂代谢的波动。结论：我们发现lnc-Gm26626是一种新的能量代谢调节剂，通过调节TCA循环中IDH3α的表达参与能量限制的反应，从而影响雄性小鼠内脏脂肪组织的可塑性。

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引用次数: 0

Bovine milk fat and cancer risk: A double-edged sword? 牛乳脂肪与癌症风险：双刃剑？

IF 4.9 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Journal of Nutritional Biochemistry

Pub Date : 2026-04-01 Epub Date: 2025-12-11 DOI: 10.1016/j.jnutbio.2025.110233

Laura Elaine Strittmatter , Alban Piotrowsky , Luigi Marongiu , Sascha Venturelli , Christian Leischner

Among the many macro- and micronutrients contained in cow's milk, one of the most important is the lipid fraction. While the nutritional and physiological benefits of milk consumption after the first years of life are the subject of some debate, there also appear to be conflicting views on the health aspects of the milk lipids, including their involvement in cancer.

Positive in vitro and/or in vivo data on growth-inhibiting or cytotoxic effects are available for lipid components of milk such as sphingomyelins and their degradation products or various hydroxy fatty acids. Isomers of linoleic acid and branched-chain fatty acids have also been shown to have anticarcinogenic potential in animal models by inducing apoptosis.

On the other hand, there is evidence of an association between increased cancer mortality and the consumption of high-fat milk, which contradicts the tumor-protecting effects observed in vitro and in vivo. Consumption of high-fat dairy products appears to be associated with an increased risk of developing types of cancer compared to low-fat dairy or other topical soy-based alternatives.

There are ambiguous results for an anticarcinogenic effect of various lipid constituents of cow's milk as well as for an association between general milk fat consumption and the occurrence especially of breast, colorectal, and prostate tumors.

Whether the effects observed in epidemiological studies can be attributed to milk lipids or whether the promising preclinical data on their anti-cancer efficacy can be transferred to humans remains unclear at present, therefore this review summarizes the latest findings.

牛奶中含有许多宏量和微量营养素，其中最重要的是脂质部分。虽然一岁以后喝牛奶的营养和生理益处是一些争论的主题，但关于牛奶脂质的健康方面，包括它们与癌症的关系，似乎也存在相互矛盾的观点。牛奶中的脂质成分，如鞘磷脂及其降解产物或各种羟基脂肪酸，具有抑制生长或细胞毒性作用的体外和/或体内阳性数据。在动物模型中，亚油酸和支链脂肪酸的异构体也显示出通过诱导细胞凋亡而具有抗癌潜力。另一方面，有证据表明癌症死亡率增加与食用高脂牛奶之间存在关联，这与体外和体内观察到的肿瘤保护作用相矛盾。与低脂乳制品或其他以大豆为基础的替代品相比，食用高脂乳制品似乎与患各种癌症的风险增加有关。关于牛奶中各种脂质成分的抗癌作用，以及一般牛奶脂肪摄入量与特别是乳房、结肠直肠和前列腺肿瘤的发生之间的关系，目前的结果并不明确。目前尚不清楚流行病学研究中观察到的效果是否归因于牛奶脂质，或者其抗癌功效的临床前数据是否可以转移到人类身上，因此本文综述了最新发现。

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引用次数: 0

Effects of pubertal dietary energy-protein levels and breeding strategies on mammary gland development and lactational performance in mice 青春期饲粮能量蛋白水平和饲养策略对小鼠乳腺发育和泌乳性能的影响。

IF 4.9 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Journal of Nutritional Biochemistry

Pub Date : 2026-04-01 Epub Date: 2025-12-15 DOI: 10.1016/j.jnutbio.2025.110236

Xusheng Dong , Siyu Tian , Wenjing Yu, Xueyan Lin, Zhonghua Wang, Qiuling Hou

Determining dietary energy and protein level to accelerate heifer growth while ensuring mammary development remains challenging. Technical and economic constraints in cattle hinder defining optimal energy protein levels and breeding timing. Thus, we used mice as a model to examine how post-weaning diets differing in energy and protein concentrations, combined with two breeding strategies, affect mammary development and lactation. Two hundred forty female mice (21 d) were divided into five dietary groups: high-energy moderate-protein, high-energy low-protein, moderate-energy moderate-protein, low-energy moderate-protein and low-energy low-protein. Mammary tissue and serum were collected at target mating weight (27±1 g) and body maturity (56 d). Breeding was initiated either upon attainment of target weight or at 63 d of age, with collection of mammary and serum samples at gestation 15 d as well as serum samples at lactation 13 d. The results showed that moderate increases in dietary energy accelerate growth, enhance mammary development, and improve lactational performance in mice. Under low-energy intake, maintaining adequate protein is critical for mammary and overall growth. High-energy feeding combined with a weight-based mating strategy markedly increased milk yield, whereas age-based mating provided nutrient-restricted mice with the necessary developmental window. These findings provide a theoretical foundation for advancing age at first calving through high energy feeding strategies in heifer management.

确定膳食能量和蛋白质水平以加速小母牛生长，同时确保乳房发育仍然具有挑战性。牛的技术和经济限制阻碍了确定最佳能量蛋白质水平和繁殖时间。因此，我们使用小鼠作为模型来研究断奶后不同能量和蛋白质浓度的饮食，结合两种繁殖策略，如何影响乳房发育和泌乳。将240只雌性小鼠（21 d）分为5组：高能中蛋白组（HM）、高能低蛋白组（HL）、中能量中蛋白组（MM）、低能量中蛋白组（LM）和低能量低蛋白组（LL）。在目标交配体重（27±1 g）和体成熟（56 d）时采集乳腺组织和血清。在达到目标体重时或在63日龄时开始饲养，在妊娠15d时采集乳腺和血清样本，在哺乳13d时采集血清样本。结果表明，适度增加饲粮能量可促进小鼠生长，促进乳腺发育，提高泌乳性能。在低能量摄入的情况下，维持足够的蛋白质对乳房和整体生长至关重要。高能量喂养与基于体重的交配策略相结合显著提高了产奶量，而基于年龄的交配为营养受限的小鼠提供了必要的发育窗口。这些研究结果为在母牛管理中采用高能喂养策略来提高初产犊龄提供了理论基础。

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引用次数: 0

3,3′-Diindolylmethane ameliorate obesity-related skeletal muscle atrophy via regulating mitochondrial function 3,3'-二吲哚甲烷通过调节线粒体功能改善肥胖相关的骨骼肌萎缩。

IF 4.9 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Journal of Nutritional Biochemistry

Pub Date : 2026-04-01 Epub Date: 2025-12-15 DOI: 10.1016/j.jnutbio.2025.110223

Yuquan Zhong , Siyuan Chen , Jingyun Pan , Ruomei Niu , Junqiang Du , Qiuxia Dong , Yanxi Liu , Yilu Yao , Yunfeng Lin , Heng Fang , Jiewen Su , Xudong Li , Yan Zhang , Guangyu Yang , Jinyin Wu , Juntao Li , Weiwen Liu , Bing Huang , Jie Tang , Wei Zhu

Skeletal muscle is the primary storage and metabolic site for amino acids and proteins in the body, and its mass and function are affected by various pathological factors. Studies have shown that mitochondrial dysfunction is associated with skeletal muscle atrophy. Indole-3-carbinol (I3C) and its active metabolite 3,3′-Diindolylmethane (DIM) have bioactivities such as inhibiting fat formation, but it is unclear whether they can affect skeletal muscle atrophy in obesity by improving mitochondrial function. Our research found that high-fat factors can induce obesity-related skeletal muscle atrophy, characterized by decreased muscle mass and function, reduced mitochondrial number, and impaired function in muscle cells. DIM can improve obesity-related skeletal muscle atrophy caused by a high-fat diet, and the mechanism may be related to the regulation of AMPK/SIRT1/PGC-1α pathway protein expression and improved mitochondrial function in muscle cells.

骨骼肌是人体氨基酸和蛋白质的主要储存和代谢部位，其质量和功能受到多种病理因素的影响。研究表明，线粒体功能障碍与骨骼肌萎缩有关。吲哚-3-甲醇（I3C）及其活性代谢物3,3′-二吲哚基甲烷（DIM）具有抑制脂肪形成等生物活性，但是否通过改善线粒体功能影响肥胖骨骼肌萎缩尚不清楚。我们的研究发现，高脂因子可诱导肥胖相关的骨骼肌萎缩，表现为肌肉质量和功能下降，线粒体数量减少，肌肉细胞功能受损。DIM可改善高脂饮食引起的肥胖相关性骨骼肌萎缩，其机制可能与调节AMPK/SIRT1/PGC-1α通路蛋白表达及改善肌肉细胞线粒体功能有关。

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引用次数: 0

Dietary fiber-derived butyrate ameliorates pulmonary fibrosis by inhibiting YBX1 ubiquitination 膳食纤维来源的丁酸盐通过抑制YBX1泛素化改善肺纤维化。

IF 4.9 2区医学 Q1 BIOCHEMISTRY & MOLECULAR BIOLOGY

Journal of Nutritional Biochemistry

Pub Date : 2026-04-01 Epub Date: 2025-12-02 DOI: 10.1016/j.jnutbio.2025.110210

Mengyu Li , Tianyu Pan , Xiaoli Ma , Xiaofang Hu , Ji Jiang , Yafei Zhang , Lei Zhang , Xin Pan , Yuanyuan Wang

Pulmonary fibrosis (PF) is a progressive and fatal interstitial lung disease characterized by aberrant epithelial-mesenchymal transition (EMT) and extracellular matrix deposition. Dietary fiber, fermented by gut microbiota into butyrate, exerts anti-fibrotic effects, yet the underlying mechanisms are not fully elucidated. YBX1 plays a crucial role in the regulation of fibrosis and EMT. However, its function in PF remains unclear. This study aims to investigate the role of dietary fiber in PF and whether YBX1 mediates the anti-fibrotic effect of butyrate in PF. The roles of the high fiber (HF) diet and butyrate in PF and the changes in butyrate content were evaluated using RT-qPCR, Western blotting, immunofluorescence (IF) and GC-MS. RNA sequencing was used to analyze the downstream action sites of butyrate. The function of YBX1 in PF was elucidated through overexpression of YBX1, RNA sequencing, and KEGG pathway analysis. The interaction between YBX1 and butyrate was examined using ubiquitination and CHX assays. The results showed that the HF diet increased butyrate levels, thereby ameliorating PF by inhibiting EMT. The expression of YBX1 was downregulated in PF and overexpression of YBX1 inhibited EMT by regulating CYP1A1/NF-κB signaling pathway, thereby improving the progression of PF. Butyrate upregulated YBX1 protein expression by reducing its ubiquitination. This work provides new insights and promising strategies for the prevention and treatment of PF through dietary interventions.

肺纤维化（PF）是一种进行性和致死性间质性肺疾病，其特征是异常的上皮-间质转化（EMT）和细胞外基质沉积。膳食纤维经肠道菌群发酵生成丁酸盐，具有抗纤维化作用，但其作用机制尚未完全阐明。YBX1在纤维化和EMT的调控中起着至关重要的作用。然而，其在PF中的作用尚不清楚。本研究旨在探讨膳食纤维在PF中的作用以及YBX1是否介导了丁酸盐在PF中的抗纤维化作用，采用RT-qPCR、Western blotting、免疫荧光（IF）和GC-MS等方法评价高纤维饲料和丁酸盐在PF中的作用以及丁酸盐含量的变化。利用RNA测序技术分析丁酸酯的下游作用位点。通过YBX1过表达、RNA测序和KEGG通路分析，阐明了YBX1在PF中的功能。通过泛素化和CHX检测YBX1与丁酸盐的相互作用。结果表明，HF饲粮通过抑制EMT，提高了丁酸盐水平，从而改善了PF。YBX1在PF中表达下调，YBX1过表达通过调节CYP1A1 / NF-κB信号通路抑制EMT，从而改善PF的进展，丁酸盐通过降低YBX1的泛素化而上调其表达。这项工作为通过饮食干预预防和治疗PF提供了新的见解和有希望的策略。

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