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第145期：脂肪組織應答反應揭示了脂肪生成在豬適應熱應激過程中的重要作用 J. Anim. Sci. 2018.96:975–989 原文鏈接：https://academic.oup.com/jas/article/96/3/975/4958984 DOI: 10.1093/jas/sky022 脂肪組織應答反應揭示了脂肪生成在豬適應熱應激過程中的重要作用 H. Qu, and K. M. Ajuwon 翻譯： 王帥 校對： 上海亙泰實業集團 外界溫度升高會引起豬熱應激，降低動物生產性能。本試驗的研究目的是探究豬熱應激時產生的組織應答反應。
與對照組相比，慢性熱應激和急性熱應激造成采食量分別降低36%和64%。與慢性熱應激組相比，急性熱應激組生長豬血漿中游離脂肪酸濃度顯著增加（P = 0.031）。配對飼喂組生長豬血漿中的胰島素含量顯著低于對照組（P =0.045）。與對照組相比，慢性熱應激組生長豬血漿尿素氮含量顯著提高（P = 0.008），而急性熱應激組生長豬血漿尿素氮含量顯著低于慢性熱應激組（P < 0.021）。慢性熱應激組生長豬皮下脂肪組織中PCK1的mRNA和蛋白表達水平顯著高于對照組和配對飼喂組（P < 0.05），同時也顯著高于急性熱應激組（P < 0.05）。盡管急性熱應激組生長豬皮下脂肪組織中GK的mRNA表達水平低于慢性熱應急組（P = 0.003），但GK的mRNA表達水平在對照組、配對飼喂組和慢性應急組之間差異不顯著。配對飼喂組生長豬皮下脂肪組織中的內質網應激標記物-增強子結合同源蛋白的蛋白表達水平顯著高于對照組（P < 0.05），慢性熱應激組中增強子結合同源蛋白的蛋白表達水平高于急性熱應激組（P = 0.033）。慢性熱應激組腸系膜組織中PCK1的mRNA表達水平顯著高于對照組和配對飼喂組（P < 0.001），急性熱應激組中PCK1的mRNA表達水平顯著低于慢性熱應激組（P = 0.039）。配對飼喂組生長豬肝臟中PCK1的表達水平顯著低于其他處理組（P < 0.05），而肝臟和肌肉組織中其他檢測指標在各處理組之間差異不顯著。 試驗結果證明，熱應激能夠誘導強烈的脂肪組織反應，有利于增加脂肪儲存，表明了脂肪組織可能在豬適應熱應激過程中起著重要作用。 關鍵詞：脂肪組織、增強子結合同源蛋白、熱應激、磷酸烯醇丙酮酸羧激酶、豬 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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