Emily Berg, Salma Moftah, Emad Yuzbashian, Catherine B Chan
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The metabolic phenotype and liver lipid metabolism pathways were studied and compared by one-way ANOVA; p ≤ 0.05 was considered significant.</p><p><strong>Results: </strong>NFM reduced body weight (BW) gain (46±2.5 vs 61±3.5 %BW, p <0.01) and hepatic triglyceride (TG) content (46.0±10.4 vs 71.7±14.4 mg/g, p <0.05) compared with HFD. Immunoblotting revealed that NFM feeding increased hepatic mitochondrial complex abundance (p < 0.05) compared with WFM. Compared with NFM, WFM had higher triglyceride content (69.2±16.5 vs 46.0±10.4 mg/g, p < 0.05) but reduced liver area covered by lipid droplets in comparsion to HFD (6.49±2.75 vs 13.61±2.75 % standard area, p = 0.051). De novo lipogenesis enzymes, fatty acid synthase (1.33±0.56 vs 0.76±0.56 AU, p < 0.05) and phosphorylated acetyl-CoA carboxylase (1.65±0.49 vs 0.02±0.49 AU, p < 0.05) were increased compared with NFM. Carnitine palmitoyl transferase 1α (1.48±0.19 vs 1.00±0.19 AU, p < 0.05) was increased in WFM compared to HFD animals and Opa1 mRNA expression was increased in WFM (1.26±0.21 vs 0.66±0.21 AU, p < 0.05) versus the NFM group.</p><p><strong>Conclusions: </strong>Compared with WFM, NFM mice had greater benefits on mitigating MASLD progression through increased capacity for oxidative phosphorylation and fatty acid export, leading to reduced hepatic fat accumulation.</p>","PeriodicalId":16620,"journal":{"name":"Journal of Nutrition","volume":" ","pages":""},"PeriodicalIF":3.8000,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Nonfat milk supplementation mitigates hepatic lipid accumulation and improves hepatic lipid metabolism in an early metabolic dysfunction-associated steatotic liver disease (MASLD) C57BL/6N mouse model.\",\"authors\":\"Emily Berg, Salma Moftah, Emad Yuzbashian, Catherine B Chan\",\"doi\":\"10.1016/j.tjnut.2025.09.020\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>Dairy products may mitigate metabolic dysfunction-associated steatotic liver disease (MASLD) progression but the role of dairy fat is unclear.</p><p><strong>Objective: </strong>This animal trial compares MASLD-related outcomes after feeding non- (NFM) or whole-fat milk (WFM) in a high-fat diet (HFD)-induced MASLD mouse model.</p><p><strong>Methods: </strong>Male C57Bl/6N mice were fed a HFD (45% kcal fat; n=40) for 9 wk. During the last 8 wk, 2 randomly-selected groups additionally consumed 0.425 mL NFM (0 g% fat; n=8) or WFM (3.25 g% fat; n=12), from a small dish, 5 d/wk. A low-fat diet (LFD) group (10% kcal fat; n=20) served as a reference. The metabolic phenotype and liver lipid metabolism pathways were studied and compared by one-way ANOVA; p ≤ 0.05 was considered significant.</p><p><strong>Results: </strong>NFM reduced body weight (BW) gain (46±2.5 vs 61±3.5 %BW, p <0.01) and hepatic triglyceride (TG) content (46.0±10.4 vs 71.7±14.4 mg/g, p <0.05) compared with HFD. Immunoblotting revealed that NFM feeding increased hepatic mitochondrial complex abundance (p < 0.05) compared with WFM. Compared with NFM, WFM had higher triglyceride content (69.2±16.5 vs 46.0±10.4 mg/g, p < 0.05) but reduced liver area covered by lipid droplets in comparsion to HFD (6.49±2.75 vs 13.61±2.75 % standard area, p = 0.051). De novo lipogenesis enzymes, fatty acid synthase (1.33±0.56 vs 0.76±0.56 AU, p < 0.05) and phosphorylated acetyl-CoA carboxylase (1.65±0.49 vs 0.02±0.49 AU, p < 0.05) were increased compared with NFM. Carnitine palmitoyl transferase 1α (1.48±0.19 vs 1.00±0.19 AU, p < 0.05) was increased in WFM compared to HFD animals and Opa1 mRNA expression was increased in WFM (1.26±0.21 vs 0.66±0.21 AU, p < 0.05) versus the NFM group.</p><p><strong>Conclusions: </strong>Compared with WFM, NFM mice had greater benefits on mitigating MASLD progression through increased capacity for oxidative phosphorylation and fatty acid export, leading to reduced hepatic fat accumulation.</p>\",\"PeriodicalId\":16620,\"journal\":{\"name\":\"Journal of Nutrition\",\"volume\":\" \",\"pages\":\"\"},\"PeriodicalIF\":3.8000,\"publicationDate\":\"2025-09-25\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Journal of Nutrition\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1016/j.tjnut.2025.09.020\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"NUTRITION & DIETETICS\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of Nutrition","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1016/j.tjnut.2025.09.020","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"NUTRITION & DIETETICS","Score":null,"Total":0}
引用次数: 0
摘要
背景：乳制品可以缓解代谢功能障碍相关的脂肪变性肝病（MASLD）的进展，但乳制品脂肪的作用尚不清楚。目的：本动物试验比较在高脂饮食（HFD）诱导的MASLD小鼠模型中饲喂非（NFM）或全脂牛奶（WFM）后MASLD的相关结果。方法：雄性C57Bl/6N小鼠饲喂高热量脂肪（45% kcal fat, n=40） 9周。在最后8周，随机选择2个组，从一个小盘中额外摄入0.425 mL NFM （0 g%脂肪，n=8）或WFM (3.25 g%脂肪，n=12)， 5 d/周。低脂饮食（LFD）组（10% kcal脂肪，n=20）作为参考。采用单因素方差分析对代谢表型和肝脏脂质代谢途径进行研究和比较；P≤0.05被认为是显著的。结果：NFM降低了体重（BW）增加（46±2.5 vs 61±3.5 %BW, p）。结论：与WFM相比，NFM小鼠通过增加氧化磷酸化和脂肪酸输出能力，减少肝脏脂肪积累，在缓解MASLD进展方面具有更大的益处。
Nonfat milk supplementation mitigates hepatic lipid accumulation and improves hepatic lipid metabolism in an early metabolic dysfunction-associated steatotic liver disease (MASLD) C57BL/6N mouse model.
Background: Dairy products may mitigate metabolic dysfunction-associated steatotic liver disease (MASLD) progression but the role of dairy fat is unclear.
Objective: This animal trial compares MASLD-related outcomes after feeding non- (NFM) or whole-fat milk (WFM) in a high-fat diet (HFD)-induced MASLD mouse model.
Methods: Male C57Bl/6N mice were fed a HFD (45% kcal fat; n=40) for 9 wk. During the last 8 wk, 2 randomly-selected groups additionally consumed 0.425 mL NFM (0 g% fat; n=8) or WFM (3.25 g% fat; n=12), from a small dish, 5 d/wk. A low-fat diet (LFD) group (10% kcal fat; n=20) served as a reference. The metabolic phenotype and liver lipid metabolism pathways were studied and compared by one-way ANOVA; p ≤ 0.05 was considered significant.
Results: NFM reduced body weight (BW) gain (46±2.5 vs 61±3.5 %BW, p <0.01) and hepatic triglyceride (TG) content (46.0±10.4 vs 71.7±14.4 mg/g, p <0.05) compared with HFD. Immunoblotting revealed that NFM feeding increased hepatic mitochondrial complex abundance (p < 0.05) compared with WFM. Compared with NFM, WFM had higher triglyceride content (69.2±16.5 vs 46.0±10.4 mg/g, p < 0.05) but reduced liver area covered by lipid droplets in comparsion to HFD (6.49±2.75 vs 13.61±2.75 % standard area, p = 0.051). De novo lipogenesis enzymes, fatty acid synthase (1.33±0.56 vs 0.76±0.56 AU, p < 0.05) and phosphorylated acetyl-CoA carboxylase (1.65±0.49 vs 0.02±0.49 AU, p < 0.05) were increased compared with NFM. Carnitine palmitoyl transferase 1α (1.48±0.19 vs 1.00±0.19 AU, p < 0.05) was increased in WFM compared to HFD animals and Opa1 mRNA expression was increased in WFM (1.26±0.21 vs 0.66±0.21 AU, p < 0.05) versus the NFM group.
Conclusions: Compared with WFM, NFM mice had greater benefits on mitigating MASLD progression through increased capacity for oxidative phosphorylation and fatty acid export, leading to reduced hepatic fat accumulation.
期刊介绍：
The Journal of Nutrition (JN/J Nutr) publishes peer-reviewed original research papers covering all aspects of experimental nutrition in humans and other animal species; special articles such as reviews and biographies of prominent nutrition scientists; and issues, opinions, and commentaries on controversial issues in nutrition. Supplements are frequently published to provide extended discussion of topics of special interest.
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