Glauser Jade Sancha de Oliveira, Santana-Oliveira Daiana Araujo, Silva-Veiga Flávia Maria, Fernandes-da-Silva Aline, Aguila Marcia Barbosa, Souza-Mello Vanessa
Laboratory of Morphometry, Metabolism, and Cardiovascular Diseases, Biomedical Center, Institute of Biology, Rio de Janeiro State University, Rio de Janeiro, Rio de Janeiro, Brazil.
Laboratory of Morphometry, Metabolism, and Cardiovascular Diseases, Biomedical Center, Institute of Biology, Rio de Janeiro State University, Rio de Janeiro, Rio de Janeiro, Brazil.
Nutrition. 2025 Sep;137:112805. doi: 10.1016/j.nut.2025.112805. Epub 2025 Apr 11.
To investigate the effects of comparable dietary excess of fat or fructose and the combination of these two insults (mimicking ultra-processed foods) on interscapular brown adipose tissue (iBAT) whitening and markers of mitochondrial dynamics in adult male mice.
Male C57BL/6 mice were randomly assigned into four groups according to the diet: control diet (C, following AIN-93M), high-fat diet (HF, 32% energy as lard), high-fructose diet (HFRU, 32% energy as fructose) or for high-fat/high-fructose diet (HF-HFRU, 32% as lard and 32% as fructose) for 12 weeks. Data were tested with one-way ANOVA and Dunnet T3 post-test (n=5 per analysis, significance level P < 0.05).
All diets caused insulin resistance and iBAT whitening, albeit with overweight only in the HF and HF-HFRU groups. Principal component analysis indicated that the HFRU scores loaded next to inflammation (Nlrp3) and adipogenesis markers (Pparg), and the HF diet influenced more a mitochondrial gene (Tomm20). However, iBAT whitening in all groups was associated with deficits in mitochondrial dynamics (Ppargc1a, Dnml1, and Pink1), vascularization (Vegfa), and thermogenic markers (Bmp8b, and Ucp1).
Similar increases in dietary saturated fat or fructose (32% as energy) and the combination of these two insults (32% / 32%) caused insulin resistance and brown adipocyte dysfunction (whitening) in adult mice after 12 weeks independent of being overweight. In comparison, the PC scores of the HFRU groups were closer to the HF-HFRU group than the HF group, implying a worse outcome and highlighting the importance of limiting saturated fat and fructose intake from ultra-processed foods.
研究成年雄性小鼠中,等量的膳食脂肪或果糖过量以及这两种损伤因素共同作用(模拟超加工食品)对肩胛间棕色脂肪组织(iBAT)变白及线粒体动力学标志物的影响。
雄性C57BL/6小鼠按饮食随机分为四组:对照饮食(C组,遵循AIN-93M标准)、高脂饮食(HF组,32%的能量来自猪油)、高果糖饮食(HFRU组,32%的能量来自果糖)或高脂/高果糖饮食(HF-HFRU组,32%来自猪油且32%来自果糖),持续12周。数据采用单因素方差分析和Dunnet T3事后检验(每次分析n = 5,显著性水平P < 0.05)。
所有饮食均导致胰岛素抵抗和iBAT变白,不过只有HF组和HF-HFRU组出现超重。主成分分析表明,HFRU组的得分与炎症(Nlrp3)和成脂标志物(Pparg)相近,而HF饮食对线粒体基因(Tomm20)影响更大。然而,所有组的iBAT变白均与线粒体动力学(Ppargc1a、Dnml1和Pink1)、血管生成(Vegfa)及产热标志物(Bmp8b和Ucp1)的缺陷有关。
膳食中饱和脂肪或果糖等量增加(占能量的32%)以及这两种损伤因素共同作用(各占32%),在12周后均会导致成年小鼠出现胰岛素抵抗和棕色脂肪细胞功能障碍(变白),且与超重无关。相比之下,HFRU组的主成分得分比HF组更接近HF-HFRU组,这意味着其结果更差,并突出了限制从超加工食品中摄入饱和脂肪和果糖的重要性。