Bai Shiping, Pan Shuqin, Zhang Keying, Ding Xuemei, Wang Jianping, Zeng Qiufeng, Xuan Yue, Su Zuowei
Animal Nutrition Institute, Sichuan Agricultural University, Chengdu 611130, Sichuan, China.
Animal Nutrition Institute, Sichuan Agricultural University, Chengdu 611130, Sichuan, China.
Environ Toxicol Pharmacol. 2017 Jan;49:163-171. doi: 10.1016/j.etap.2016.12.012. Epub 2016 Dec 26.
To investigate the toxic effects of dietary overload lithium on the adipogenesis in adipose tissue of chicken and the role of hypothalamic neuropeptide Y (NPY) in this process, one-day-old male chicks were fed with the basal diet added with 0 (control) or 100mg lithium/kg diet from lithium chloride (overload lithium) for 35days. Abdominal adipose tissue and hypothalamus were collected at day 6, 14, and 35. As a percentage of body weight, abdominal fat decreased (p<0.001) at day 6, 14, and 35, and feed intake and body weight gain decreased during day 7-14, and day 15-35 in overload lithium treated broilers as compared to control. Adipocyte diameter and DNA content in abdominal adipose tissue were significantly lower in overload-lithium treatment than control at day 35, although no significant differences were observed at day 6 and 14. Dietary overload lithium decreased (p<0.01) transcriptional expression of preadipocyte proliferation makers ki-67 (KI67), microtubule-associated protein homolog (TPX2), and topoisomerase 2-alpha (TOP2A), and preadipocyte differentiation transcriptional factors peroxisome proliferator-activated receptor-γ (PPARγ), and CCAAT/enhancer binding protein (C/EBP) α mRNA abundance in abdominal adipose tissue. In hypothalamus, dietary overload lithium influenced (p<0.001) NPY, and NPY receptor (NPYR) 6 mRNA abundance at day 6 and 14, but not at day 35. In conclusion, dietary overload lithium decreased the adipogenesis in abdominal adipose tissue of chicken, which was accompanied by depressing transcriptional expression of adipogenesis-associated factors. Hypothalamic NPY had a potential role in the adipogenesis in abdominal adipose tissue of broilers with a short-term overload lithium treatment.
为研究日粮中过量锂对鸡脂肪组织脂肪生成的毒性作用以及下丘脑神经肽Y（NPY）在此过程中的作用，将1日龄雄性雏鸡用添加0（对照）或100mg/kg日粮的氯化锂（过量锂）基础日粮喂养35天。在第6、14和35天收集腹部脂肪组织和下丘脑。与对照相比，过量锂处理的肉鸡在第6、14和35天腹部脂肪占体重的百分比降低（p<0.001），并且在第7 - 14天和第15 - 35天采食量和体重增加减少。在第35天，过量锂处理组腹部脂肪组织中的脂肪细胞直径和DNA含量显著低于对照组，尽管在第6天和第14天未观察到显著差异。日粮中过量锂降低了（p<0.01）腹部脂肪组织中前脂肪细胞增殖标志物ki - 67（KI67）、微管相关蛋白同源物（TPX2）和拓扑异构酶2 - α（TOP2A）的转录表达，以及前脂肪细胞分化转录因子过氧化物酶体增殖物激活受体 - γ（PPARγ）和CCAAT/增强子结合蛋白（C/EBP）α mRNA丰度。在下丘脑中，日粮中过量锂在第6天和第14天影响（p<0.001）NPY和NPY受体（NPYR）6 mRNA丰度，但在第35天无影响。总之，日粮中过量锂降低了鸡腹部脂肪组织的脂肪生成，这伴随着脂肪生成相关因子转录表达的抑制。下丘脑NPY在短期过量锂处理的肉鸡腹部脂肪组织脂肪生成中具有潜在作用。
