脂肪組織應(yīng)答反應(yīng)揭示了脂肪生成在豬適應(yīng)熱應(yīng)激過程中的重要作用

2018-8-1 10:27| 發(fā)布者: 畜牧編輯| 查看: 8943| 評(píng)論: 1|原作者: 畜牧編輯

　　第145期：脂肪組織應(yīng)答反應(yīng)揭示了脂肪生成在豬適應(yīng)熱應(yīng)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(yīng)答反應(yīng)揭示了脂肪生成在豬適應(yīng)熱應(yīng)激過程中的重要作用
　　H. Qu, and K. M. Ajuwon
　　翻譯：王帥校對(duì)：上海亙泰實(shí)業(yè)集團(tuán)
　　外界溫度升高會(huì)引起豬熱應(yīng)激，降低動(dòng)物生產(chǎn)性能。本試驗(yàn)的研究目的是探究豬熱應(yīng)激時(shí)產(chǎn)生的組織應(yīng)答反應(yīng)。

　　將生長(zhǎng)豬隨機(jī)分為4個(gè)處理組：急性熱應(yīng)激組，35 ± 1 oC處理24 h；慢性熱應(yīng)激組，35 ± 1 oC處理7天；對(duì)照組，20 ± 1 oC處理7天；配對(duì)飼喂組，溫度處理同對(duì)照組，按照慢性熱應(yīng)激組的采食量給予飼料。除配對(duì)飼喂組外，其他處理組均自由采食。

　　與對(duì)照組相比，慢性熱應(yīng)激和急性熱應(yīng)激造成采食量分別降低36%和64%。與慢性熱應(yīng)激組相比，急性熱應(yīng)激組生長(zhǎng)豬血漿中游離脂肪酸濃度顯著增加（P = 0.031）。配對(duì)飼喂組生長(zhǎng)豬血漿中的胰島素含量顯著低于對(duì)照組（P =0.045）。與對(duì)照組相比，慢性熱應(yīng)激組生長(zhǎng)豬血漿尿素氮含量顯著提高（P = 0.008），而急性熱應(yīng)激組生長(zhǎng)豬血漿尿素氮含量顯著低于慢性熱應(yīng)激組（P < 0.021）。慢性熱應(yīng)激組生長(zhǎng)豬皮下脂肪組織中PCK1的mRNA和蛋白表達(dá)水平顯著高于對(duì)照組和配對(duì)飼喂組（P < 0.05），同時(shí)也顯著高于急性熱應(yīng)激組（P < 0.05）。盡管急性熱應(yīng)激組生長(zhǎng)豬皮下脂肪組織中GK的mRNA表達(dá)水平低于慢性熱應(yīng)急組（P = 0.003），但GK的mRNA表達(dá)水平在對(duì)照組、配對(duì)飼喂組和慢性應(yīng)急組之間差異不顯著。配對(duì)飼喂組生長(zhǎng)豬皮下脂肪組織中的內(nèi)質(zhì)網(wǎng)應(yīng)激標(biāo)記物-增強(qiáng)子結(jié)合同源蛋白的蛋白表達(dá)水平顯著高于對(duì)照組（P < 0.05），慢性熱應(yīng)激組中增強(qiáng)子結(jié)合同源蛋白的蛋白表達(dá)水平高于急性熱應(yīng)激組（P = 0.033）。慢性熱應(yīng)激組腸系膜組織中PCK1的mRNA表達(dá)水平顯著高于對(duì)照組和配對(duì)飼喂組（P < 0.001），急性熱應(yīng)激組中PCK1的mRNA表達(dá)水平顯著低于慢性熱應(yīng)激組（P = 0.039）。配對(duì)飼喂組生長(zhǎng)豬肝臟中PCK1的表達(dá)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(cè)指標(biāo)在各處理組之間差異不顯著。

　　試驗(yàn)結(jié)果證明，熱應(yīng)激能夠誘導(dǎo)強(qiáng)烈的脂肪組織反應(yīng)，有利于增加脂肪儲(chǔ)存，表明了脂肪組織可能在豬適應(yīng)熱應(yīng)激過程中起著重要作用。

　　關(guān)鍵詞：脂肪組織、增強(qiáng)子結(jié)合同源蛋白、熱應(yīng)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