Sulaiman Usman, Vaughan Reagan S, Siegel Paul, Liu Dongmin, Gilbert Elizabeth Ruth, Cline Mark Andrew
School of Animal Sciences, Virginia Polytechnic Institute and State University, Blacksburg, VA, United States.
Department of Human Nutrition, Foods and Exercise, Virginia Polytechnic Institute and State University, Blacksburg, VA, United States.
Front Physiol. 2024 Sep 2;15:1445569. doi: 10.3389/fphys.2024.1445569. eCollection 2024.
Exposure to elevated temperatures during incubation is known to induce epigenetic changes that are associated with immunological and stress-response differences at a later age. Reports on its effects on the adipose tissue are still scarce. In this experiment, we investigated the effect of embryonic heat conditioning (EHC) on growth, adipose tissue mRNA and global DNA methylation in broiler chicks at day 4 post-hatch.
Fertile eggs were divided into two groups: control and EHC. Eggs in the control group were incubated at 37.8°C and 80% relative humidity from day 0 to day 18.5 (E0 to E18.5). The EHC eggs were subjected to an intermittent increase in temperature to 39.5°C and 80% relative humidity from E7 to E16 for 12 h (07:30-19:30) per day. On day 4 post-hatch, control and EHC chicks were subjected to 36°C using three time points: 0 (no heat challenge serving as the control), and 2 and 12 h relative to start of the heat challenge. Fifteen chicks were sampled from each group for every timepoint. Body weight was recorded before euthanasia and subcutaneous adipose tissue was collected.
Body weights were similar in control and EHC groups. Diacylglycerol O-acyltransferase 2 (DGAT2) mRNA was lower in the EHC group at time 0 relative to control. Hormone-sensitive lipase (HSL) mRNA was greater in the EHC than control group at the 0 h timepoint. Heat challenge affected adipose tissue DNA methylation, with methylation highest at 12 h into the heat challenge.
These findings highlight the dynamic molecular responses of chicks to heat stress during early post-hatch development and suggest that EHC may affect heat stress responses and adipose tissue development through mechanisms involving lipid remodeling and DNA methylation.
已知孵化期间暴露于高温会诱导表观遗传变化,这些变化与后期的免疫和应激反应差异有关。关于其对脂肪组织影响的报道仍然很少。在本实验中,我们研究了胚胎热预处理(EHC)对孵化后第4天肉鸡雏鸡生长、脂肪组织mRNA和全基因组DNA甲基化的影响。
将受精蛋分为两组:对照组和EHC组。对照组的蛋从第0天到第18.5天(E0到E18.5)在37.8°C和80%相对湿度下孵化。EHC组的蛋在E7到E16期间每天12小时(07:30 - 19:30)经历温度间歇性升高至39.5°C和80%相对湿度。在孵化后第4天,对照组和EHC组的雏鸡在三个时间点接受36°C处理:0(无热应激作为对照),以及相对于热应激开始的2小时和12小时。每个时间点从每组中抽取15只雏鸡。在安乐死之前记录体重,并收集皮下脂肪组织。
对照组和EHC组的体重相似。在时间0时,EHC组的二酰甘油O - 酰基转移酶2(DGAT2)mRNA相对于对照组较低。在0小时时间点,EHC组的激素敏感性脂肪酶(HSL)mRNA比对照组更高。热应激影响脂肪组织DNA甲基化,在热应激12小时时甲基化最高。
这些发现突出了雏鸡在孵化后早期发育过程中对热应激的动态分子反应,并表明EHC可能通过涉及脂质重塑和DNA甲基化的机制影响热应激反应和脂肪组织发育。