Department of Animal Science, University of Tennessee, Knoxville, Tennessee, USA.
BMC Genomics. 2012 Aug 31;13:441. doi: 10.1186/1471-2164-13-441.
Domestic broiler chickens rapidly accumulate adipose tissue due to intensive genetic selection for rapid growth and are naturally hyperglycemic and insulin resistant, making them an attractive addition to the suite of rodent models used for studies of obesity and type 2 diabetes in humans. Furthermore, chicken adipose tissue is considered as poorly sensitive to insulin and lipolysis is under glucagon control. Excessive fat accumulation is also an economic and environmental concern for the broiler industry due to the loss of feed efficiency and excessive nitrogen wasting, as well as a negative trait for consumers who are increasingly conscious of dietary fat intake. Understanding the control of avian adipose tissue metabolism would both enhance the utility of chicken as a model organism for human obesity and insulin resistance and highlight new approaches to reduce fat deposition in commercial chickens.
We combined transcriptomics and metabolomics to characterize the response of chicken adipose tissue to two energy manipulations, fasting and insulin deprivation in the fed state. Sixteen to 17 day-old commercial broiler chickens (ISA915) were fed ad libitum, fasted for five hours, or fed but deprived of insulin by injections of anti-insulin serum. Pair-wise contrasts of expression data identified a total of 2016 genes that were differentially expressed after correction for multiple testing, with the vast majority of differences due to fasting (1780 genes). Gene Ontology and KEGG pathway analyses indicated that a short term fast impacted expression of genes in a broad selection of pathways related to metabolism, signaling and adipogenesis. The effects of insulin neutralization largely overlapped with the response to fasting, but with more modest effects on adipose tissue metabolism. Tissue metabolomics indicated unique effects of insulin on amino acid metabolism.
Collectively, these data provide a foundation for further study into the molecular basis for adipose expansion in commercial poultry and identify potential pathways through which fat accretion may be attenuated in the future through genetic selection or management practices. They also highlight chicken as a useful model organism in which to study the dynamic relationship between food intake, metabolism, and adipose tissue biology.
由于对快速生长的强烈遗传选择,国内肉鸡迅速积累脂肪组织,且天然高血糖和胰岛素抵抗,这使它们成为肥胖和 2 型糖尿病人类研究中啮齿动物模型的有力补充。此外,由于饲料效率降低和氮浪费过多,以及消费者对饮食脂肪摄入越来越关注,鸡的脂肪组织被认为对胰岛素的敏感性较差,脂肪分解受胰高血糖素的控制。脂肪过度积累也是肉鸡产业的一个经济和环境问题。
我们结合转录组学和代谢组学来描述鸡脂肪组织对两种能量处理(禁食和喂食状态下的胰岛素剥夺)的反应。16-17 日龄商业肉鸡(ISA915)自由采食,禁食 5 小时,或喂食但注射抗胰岛素血清以剥夺胰岛素。表达数据的两两对比在经过多次测试校正后共鉴定出 2016 个差异表达基因,绝大多数差异是由于禁食(1780 个基因)引起的。GO 和 KEGG 通路分析表明,短期禁食会影响与代谢、信号和脂肪生成相关的广泛选择途径中的基因表达。胰岛素中和的作用在很大程度上与禁食的反应重叠,但对脂肪组织代谢的影响较小。组织代谢组学表明胰岛素对氨基酸代谢有独特的影响。
总的来说,这些数据为进一步研究商业家禽脂肪扩张的分子基础提供了基础,并确定了通过遗传选择或管理实践减轻脂肪积累的潜在途径。它们还强调了鸡作为研究食物摄入、代谢和脂肪组织生物学之间动态关系的有用模型生物。