脂肪组织特异性反应揭示了脂肪生成在猪热应激适应过程中的重要作用。
Adipose tissue-specific responses reveal an important role of lipogenesis during heat stress adaptation in pigs.
机构信息
Department of Animal Sciences, Purdue University, West Lafayette, IN.
出版信息
J Anim Sci. 2018 Apr 3;96(3):975-989. doi: 10.1093/jas/sky022.
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. In mesenteric 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 downregulated (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 lipid storage. This indicates that adipose tissue might play an important role in heat stress adaptation.
环境温度升高会导致猪产生热应激，从而降低动物的生产性能。为了更好地了解猪在热应激下的组织反应，我们进行了一项研究，将猪分为四组进行处理：急性（24 小时）热应激（AHS）组，温度为 35°C±1°C；慢性（7 天）热应激组（HS），温度为 35°C±1°C 或 20°C±1°C，自由采食（Con）或与 HS 猪的采食量（FI）相匹配的限饲（PF）。与 Con 组相比，HS 和 AHS 组的 FI 分别下降了约 36%和 64%（P＜0.01）。与 HS 和 Con 组相比，AHS 组的游离脂肪酸（FFA）浓度升高（P=0.031）。与 Con 组相比，PF 组的血清胰岛素浓度降低（P=0.045）。与 Con 和 PF 组相比，HS 组的血尿素氮（BUN）浓度升高（P=0.008），但与 HS 组相比，AHS 组的 BUN 浓度降低（P＜0.021）。在皮下脂肪组织中，HS 组的 PCK1 mRNA 和蛋白丰度高于 Con 和 PF 组（P＜0.05），HS 组也高于 AHS 组（P＜0.05）。然而，尽管 AHS 组的 GK mRNA 表达低于 HS 组（P=0.003），但 Con、PF 和 HS 组之间的 GK mRNA 没有差异。脂肪组织内质网应激标志物 CCAT/增强子结合同源蛋白（CHOP）的蛋白丰度在 PF 组高于 Con 组（P＜0.05），在 HS 组高于 AHS 组。在肠系膜脂肪组织中，HS 组的 PCK1 mRNA 丰度高于 Con 和 PF 组（P＜0.001）。此外，AHS 组的 PCK1 表达低于 HS 组（P=0.033）。与其他处理组相比，PF 猪肝脏中的 PCK1 表达下调（P＜0.05），但肝脏和肌肉组织中其他大多数测量的基因不受处理的影响。这些结果证实，热应激会引起强烈的脂肪组织反应，有利于增加脂肪储存。这表明脂肪组织可能在热应激适应中发挥重要作用。
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