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第145期：脂肪组织应答反应揭示了脂肪生成在猪适应热应激过程中的重要作用 J. Anim. Sci. 2018.96:975–989 原文链接：https://academic.oup.com/jas/article/96/3/975/4958984 DOI: 10.1093/jas/sky022 脂肪组织应答反应揭示了脂肪生成在猪适应热应激过程中的重要作用 H. Qu, and K. M. Ajuwon 翻译： 王帅 校对： 上海亘泰实业集团 外界温度升高会引起猪热应激，降低动物生产性能。本试验的研究目的是探究猪热应激时产生的组织应答反应。
与对照组相比，慢性热应激和急性热应激造成采食量分别降低36%和64%。与慢性热应激组相比，急性热应激组生长猪血浆中游离脂肪酸浓度显著增加（P = 0.031）。配对饲喂组生长猪血浆中的胰岛素含量显著低于对照组（P =0.045）。与对照组相比，慢性热应激组生长猪血浆尿素氮含量显著提高（P = 0.008），而急性热应激组生长猪血浆尿素氮含量显著低于慢性热应激组（P < 0.021）。慢性热应激组生长猪皮下脂肪组织中PCK1的mRNA和蛋白表达水平显著高于对照组和配对饲喂组（P < 0.05），同时也显著高于急性热应激组（P < 0.05）。尽管急性热应激组生长猪皮下脂肪组织中GK的mRNA表达水平低于慢性热应急组（P = 0.003），但GK的mRNA表达水平在对照组、配对饲喂组和慢性应急组之间差异不显著。配对饲喂组生长猪皮下脂肪组织中的内质网应激标记物-增强子结合同源蛋白的蛋白表达水平显著高于对照组（P < 0.05），慢性热应激组中增强子结合同源蛋白的蛋白表达水平高于急性热应激组（P = 0.033）。慢性热应激组肠系膜组织中PCK1的mRNA表达水平显著高于对照组和配对饲喂组（P < 0.001），急性热应激组中PCK1的mRNA表达水平显著低于慢性热应激组（P = 0.039）。配对饲喂组生长猪肝脏中PCK1的表达水平显著低于其他处理组（P < 0.05），而肝脏和肌肉组织中其他检测指标在各处理组之间差异不显著。 试验结果证明，热应激能够诱导强烈的脂肪组织反应，有利于增加脂肪储存，表明了脂肪组织可能在猪适应热应激过程中起着重要作用。 关键词：脂肪组织、增强子结合同源蛋白、热应激、磷酸烯醇丙酮酸羧激酶、猪 Adipose tissue-specific responses reveal an important role of lipogenesis during heat stress adaptation in pigs H. Qu, and K. M. Ajuwon Elevated ambient temperature causes heat stress in pigs, resulting in reduced animal performance. To better understand tissue responses to heat stress in pigs, we conducted a study in which pigs were subjected to four treatments: acute (24 h) heat stress (AHS) at 35 °C ± 1 ambient temperature, chronic (7 d) heat stress at 35 °C ± 1 (HS) or normal ambient temperature (20 °C± 1) for 7 d with ad-libitum feeding (Con) or with pair-feeding to the feed intake (FI) of the HS pigs (PF). Heat stress decreased FI by approximately 36% and 64% in HS and AHS treatments respectively, compared with Con (P < 0.01). Concentration of free fatty acids (FFA) was elevated in AHS compared to HS (P = 0.031). Serum insulin concentration was lower in PF than Con (P = 0.045). Blood urea nitrogen (BUN) concentration was elevated in HS compared with Con and PF (P = 0.008), but lower (P < 0.021) in AHS compared to HS. In the subcutaneous adipose tissue, the mRNA and protein abundance of PCK1 were higher (P < 0.05) in the HS treatment than Con and PF, and also higher (P < 0.05) in HS than AHS. However, there was no difference in GK mRNA between Con, PF, and HS, although its expression was lower(P = 0.003) in AHS vs. HS. Protein abundance of the ER stress marker, CCAT/enhancer-binding homologous protein (CHOP), was higher in PF than Con (P< 0.05), and higher (P = 0.033) in HS than AHS in subcutaneous fat. Inmesenteric fat, PCK1 mRNA was higher (P < 0.001) in the HS than Con and PF treatments. Additionally, expression of PCK1 was lower (P = 0.039) in AHS vs. HS. Expression of PCK1 was down regulated (P < 0.05) in the liver of PF pigs compared to other treatments, but most other genes measured were not affected by treatment in the liver and muscle tissues. These results confirm that heat stress induces a robust adipose tissue response in favor of increased lipids torage. This indicates that adipose tissue might play an important role in heat stress adaptation. Key words: adipose tissue, CHOP, heat stress, PCK1 or PEPCK, pig 
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