Liu F, Celi P, Cottrell J J, Chauhan S S, Leury B J, Dunshea F R
Faculty of Veterinary and Agricultural Sciences, The University of Melbourne, Parkville, VIC, Australia.
DSM Nutritional Products, Columbia, MD, USA.
J Anim Physiol Anim Nutr (Berl). 2018 Feb;102(1):276-285. doi: 10.1111/jpn.12689. Epub 2017 Mar 16.
Heat stress (HS) disrupts redox balance and insulin-related metabolism. Supplementation with supranutritional amounts of selenium (Se) may enhance glutathione peroxidase (GPX) activity and reduce oxidative stress, but may trigger insulin resistance. Therefore, the aim of this experiment was to investigate the effects of a short-term high Se supplementation on physiology, oxidative stress and insulin-related metabolism in heat-stressed pigs. Twenty-four gilts were fed either a control (0.20 ppm Se) or a high Se (1.0 ppm Se yeast, HiSe) diet for 2 weeks. Pigs were then housed in thermoneutral (20°C) or HS (35°C) conditions for 8 days. Blood samples were collected to study blood Se and oxidative stress markers. An oral glucose tolerance test (OGTT) was conducted on day 8 of thermal exposure. The HS conditions increased rectal temperature and respiration rate (both p < .001). The HiSe diet increased blood Se by 12% (p < .05) and ameliorated the increase in rectal temperature (p < .05). Heat stress increased oxidative stress as evidenced by a 48% increase in plasma advanced oxidized protein products (AOPPs; p < .05), which may be associated with the reductions in plasma biological antioxidant potential (BAP) and erythrocyte GPX activity (both p < .05). The HiSe diet did not alleviate the reduction in plasma BAP or increase in AOPPs observed during HS, although it tended to increase erythrocyte GPX activity by 13% (p = .068). Without affecting insulin, HS attenuated lipid mobilization, as evidenced by a lower fasting NEFA concentration (p < .05), which was not mitigated by the HiSe diet. The HiSe diet increased insulin AUC, suggesting it potentiated insulin resistance, although this only occurred under TN conditions (p = .066). In summary, HS induced oxidative stress and attenuated lipid mobilization in pigs. The short-term supranutritional Se supplementation alleviated hyperthermia, but did not protect against oxidative stress in heat-stressed pigs.
热应激（HS）会破坏氧化还原平衡和胰岛素相关代谢。补充超营养量的硒（Se）可能会增强谷胱甘肽过氧化物酶（GPX）活性并降低氧化应激，但可能会引发胰岛素抵抗。因此，本实验的目的是研究短期高硒补充对热应激猪的生理、氧化应激和胰岛素相关代谢的影响。将24头后备母猪分别饲喂对照（0.20 ppm硒）或高硒（1.0 ppm硒酵母，HiSe）日粮2周。然后将猪置于中性温度（20°C）或热应激（35°C）条件下8天。采集血样以研究血硒和氧化应激标志物。在热暴露第8天进行口服葡萄糖耐量试验（OGTT）。热应激条件下直肠温度和呼吸频率均升高（均为p < .001）。HiSe日粮使血硒升高了12%（p < .05），并改善了直肠温度的升高（p < .05）。热应激增加了氧化应激，血浆晚期氧化蛋白产物（AOPPs）增加48%证明了这一点（p < .05），这可能与血浆生物抗氧化能力（BAP）和红细胞GPX活性降低有关（均为p < .05）。HiSe日粮并未减轻热应激期间观察到的血浆BAP降低或AOPPs升高，尽管它使红细胞GPX活性有升高13%的趋势（p = .068）。热应激在不影响胰岛素的情况下减弱了脂质动员，空腹非酯化脂肪酸（NEFA）浓度较低证明了这一点（p < .05），HiSe日粮并未缓解这一情况。HiSe日粮增加了胰岛素曲线下面积（AUC），表明它增强了胰岛素抵抗，尽管这仅在中性温度条件下发生（p = .066）。总之，热应激在猪中诱导了氧化应激并减弱了脂质动员。短期超营养量的硒补充减轻了高热，但并未保护热应激猪免受氧化应激。
