Zhou Weixin, Miao Zhonghua, Cheng Ruyue, Luo Yating, Shen Xi, Li Ming, He Fang
West China School of Public Health and West China Fourth Hospital, Sichuan University, Chengdu 610041, China.
Wei Sheng Yan Jiu. 2020 Jan;49(1):92-97. doi: 10.19813/j.cnki.weishengyanjiu.2020.01.016.
This study aimed to explore whether exposure to ceftriaxone during early life could influences glucose and lipid metabolism of high fat diet-induced mice.
Total 48 of female BALB/c aged 2 week old were randomly divided into control group(treated with saline), antibiotic group(treated with100 mg/kg ceftriaxone), high-fat diet group(treated with saline) and combined action group(treated with 100 mg/kg ceftriaxone)(n=12), respectively to stop gavage 2 weeks later. Then high-fat diet group and combined action group were fed with high-fat diet for 12 weeks. Fasting blood glucose(FBG) and oral glucose tolerance test were conducted in the last week. Serum total cholesterol(TC), triglyceride(TG), high-density lipoprotein cholesterol(HDL-C), low-density lipoprotein cholesterol(LDL-C), fasting insulin, leptin and TG, TC in liver were also measured. Furthermore, homeostasis model assessment of insulin resistance(HOMA-IR) was calculated from FBG and insulin.
Compared with normal chow diet, high-fat diet impaired oral glucose tolerance and increased the levels of abdominal adipose tissue, FBG, HOMA-IR, lips in serum and liver and leptin(P<0. 05). The oral administration of ceftriaxone in early life impaired oral glucose tolerance and increased the levels of abdominal adipose tissue, FBG and TG in liver(P<0. 05). In addition, early ceftriaxone intervention could enhance the impaired glucose tolerance, the increasing FBG, insulin resistance and liver lipids associated with high-fat diet(P<0. 05).
Early ceftriaxone intervention not only significantly increases the level of abdominal adipose tissue, FBG, insulin resistance and liver lipids, but also enhances glycolipid metabolic disorders induced by high-fat diet. These result suggest that the exposure to antibiotics in the early life might increase the sensitivity of host animal to high fat diet induced abnormal glycolipid metabolism late.
本研究旨在探讨生命早期接触头孢曲松是否会影响高脂饮食诱导小鼠的糖脂代谢。
将48只2周龄雌性BALB/c小鼠随机分为对照组（用生理盐水处理）、抗生素组（用100mg/kg头孢曲松处理）、高脂饮食组（用生理盐水处理）和联合作用组（用100mg/kg头孢曲松处理）（n = 12），2周后停止灌胃。然后高脂饮食组和联合作用组给予高脂饮食12周。在最后一周进行空腹血糖（FBG）和口服葡萄糖耐量试验。还测量了血清总胆固醇（TC）、甘油三酯（TG）、高密度脂蛋白胆固醇（HDL-C）、低密度脂蛋白胆固醇（LDL-C）、空腹胰岛素、瘦素以及肝脏中的TG、TC。此外，根据FBG和胰岛素计算胰岛素抵抗稳态模型评估（HOMA-IR）。
与正常饮食相比，高脂饮食损害了口服葡萄糖耐量，增加了腹部脂肪组织、FBG、HOMA-IR、血清和肝脏中的脂质以及瘦素水平（P<0.05）。生命早期口服头孢曲松损害了口服葡萄糖耐量，增加了腹部脂肪组织、FBG和肝脏中TG的水平（P<0.05）。此外，早期头孢曲松干预可加重与高脂饮食相关的葡萄糖耐量受损、FBG升高、胰岛素抵抗和肝脏脂质增加（P<0.05）。
早期头孢曲松干预不仅显著增加腹部脂肪组织、FBG、胰岛素抵抗和肝脏脂质水平，还加重了高脂饮食诱导的糖脂代谢紊乱。这些结果表明，生命早期接触抗生素可能会增加宿主动物对高脂饮食诱导的后期异常糖脂代谢的敏感性。
