Research Service, Harry S Truman Memorial Veterans Medical Center, Columbia, MO.
Department of Nutrition and Exercise Physiology, University of Missouri, Columbia, MO.
Med Sci Sports Exerc. 2018 Oct;50(10):2040-2048. doi: 10.1249/MSS.0000000000001675.
Maternal exercise and physical activity during the gestational period can be protective against maternal high-fat diet-induced hepatic steatosis in older offspring. However, it is unknown whether these protective effects are seen in younger offspring. In this study, we investigated whether maternal physical activity would attenuate maternal western diet (WD)-induced steatosis in young adult rats.
Female Wistar rats (7-8 wk of age) were randomized into WD (42% fat, 27% sucrose) or normal chow diet (ND), and further randomized into physical activity (RUN) or sedentary (SED) conditions for a total of four groups. Dams returned to ND/SED conditions after parturition. Postweaning, offspring were maintained in ND/SED conditions for 18 wk.
Maternal WD-induced increases in male offspring body mass was attenuated in the WD/RUN offspring (P < 0.05). Maternal WD feeding significantly increased hepatic steatosis in male (but not female offspring), which was not attenuated by maternal RUN. However, maternal RUN increased (P < 0.05) hepatic markers of mitochondrial biogenesis and mitophagy (mitochondrial transcription factor A, peroxisome proliferator activator receptor γ, and nuclear factor E2-related factor 2) in all offspring and the mitophagy marker BCL2-interacting protein 3 in WD/RUN offspring. Interestingly, hepatic markers of de novo lipogenesis (fatty acid synthase and acetyl coenzyme A carboxylase), mitophagy (autophagy-related gene 12:5, BCL2-interacting protein 3, P62, and LC3 II/I), and mitochondria biogenesis/content (mitochondrial transcription factor A and OXPHOS-Complex II) were significantly increased in female versus male offspring.
Although maternal physical activity did not attenuate maternal WD-induced hepatic steatosis as has been previously reported in older adult offspring, it did significantly increase hepatic markers of mitochondrial biogenesis and mitophagy. Furthermore, female offspring had elevated hepatic markers of mitochondrial health, possibly explaining why female rats are protected against maternal WD-induced hepatic steatosis. Future studies are warranted to shed light on the time line of hepatic steatosis development under the influence of maternal physical activity.
孕期母体运动和体育活动可以预防母体高脂肪饮食引起的子代肝脂肪变性。然而，目前尚不清楚这些保护作用是否在年轻子代中出现。在这项研究中，我们研究了母体体育活动是否会减轻年轻成年大鼠的母体西式饮食（WD）诱导的肝脂肪变性。
将 7-8 周龄的雌性 Wistar 大鼠随机分为 WD（42%脂肪，27%蔗糖）或正常 chow 饮食（ND），并进一步随机分为运动（RUN）或静止（SED）条件，共分为四组。产后，母鼠恢复到 ND/SED 条件。断奶后，子代在 ND/SED 条件下维持 18 周。
母体 WD 喂养引起的雄性子代体重增加在 WD/RUN 子代中减轻（P < 0.05）。母体 WD 喂养显著增加了雄性（但不包括雌性）子代的肝脂肪变性，但母体 RUN 并未减轻。然而，母体 RUN 增加了（P < 0.05）所有子代的肝线粒体生物发生和线粒体自噬的标志物（线粒体转录因子 A、过氧化物酶体增殖物激活受体 γ 和核因子 E2 相关因子 2）和 WD/RUN 子代的线粒体自噬标志物 BCL2 相互作用蛋白 3。有趣的是，肝内从头合成脂质的标志物（脂肪酸合酶和乙酰辅酶 A 羧化酶）、线粒体自噬（自噬相关基因 12:5、BCL2 相互作用蛋白 3、P62 和 LC3 II/I）和线粒体生物发生/含量（线粒体转录因子 A 和 OXPHOS-Complex II）在雌性子代中明显高于雄性子代。
尽管母体体育活动并未像先前在老年子代中报道的那样减轻母体 WD 诱导的肝脂肪变性，但它确实显著增加了肝线粒体生物发生和自噬的标志物。此外，雌性子代肝线粒体健康的标志物升高，这可能解释了为什么雌性大鼠能抵抗母体 WD 诱导的肝脂肪变性。未来的研究有必要阐明母体体育活动对肝脂肪变性发展的时间线。
