Effects of prenatal caffeine exposure on glucose homeostasis of adult offspring rats
Effects of prenatal caffeine exposure on glucose homeostasis of adult offspring rats
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产前咖啡因暴露对成年子代大鼠葡萄糖稳态的影响
DOI：
10.1007/s00114-017-1510-4
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发表时间：
2017-10
影响因子：
1.8
通讯作者：
Wang Hui
中科院分区：
文献类型：
--
作者：
Kou Hao;Wang Gui hua;Pei Lin guo;Zhang Li;Shi Chai;Guo Yu;Wu Dong fang;Wang Hui
流行病学证据表明，产前咖啡因暴露（PCE）可导致胎儿宫内发育迟缓（IUGR）。IUGR子代在成熟后还存在糖耐量异常和2型糖尿病。我们以前已经证明，PCE诱导IUGR和增加成年代谢综合征的易感性大鼠。本研究旨在进一步研究PCE对成年子代大鼠葡萄糖稳态的影响。妊娠大鼠从妊娠第11天至第20天给予咖啡因（120 mg/kg/天，灌胃）。PCE仔鼠出生后呈部分追赶型生长，表现为增重率增加。PCE对成年子代的基础血糖和胰岛素表型无显著影响，但可增加雌性子代的糖耐量、葡萄糖刺激的胰岛素分泌和β细胞对葡萄糖的敏感性。雄性和雌性PCE后代的胰岛素敏感性均增强，同时β细胞比例和质量降低。Western blotting结果显示，PCE女性的肝脏胰岛素信号元件，包括胰岛素受体（INSR），胰岛素受体底物1（IRS-1）和丝氨酸-苏氨酸蛋白激酶（Akt）的磷酸化的蛋白质表达的显着增强，也被加强。总之，我们证明PCE降低了成年后代大鼠的胰腺β质量，但增加了葡萄糖耐量，尤其是雌性大鼠。β细胞对葡萄糖反应性的适应性代偿性增强和主要由肝脏胰岛素信号上调介导的胰岛素敏感性升高可能协同促进葡萄糖耐量增加。
Epidemiological evidences show that prenatal caffeine exposure (PCE) could induce intrauterine growth retardation (IUGR). The IUGR offspring also present glucose intolerance and type 2 diabetes mellitus after maturity. We have previously demonstrated that PCE induced IUGR and increased susceptibility to adult metabolic syndrome in rats. This study aimed to further investigate the effects of PCE on glucose homeostasis in adult offspring rats. Pregnant rats were administered caffeine (120 mg/kg/day, intragastrically) from gestational days 11 to 20. PCE offspring presented partial catch-up growth pattern after birth, characterizing by the increased body weight gain rates. Meanwhile, PCE had no significant influences on the basal blood glucose and insulin phenotypes of adult offspring but increased the glucose tolerance, glucose-stimulated insulin section and β cell sensitivity to glucose in female progeny. The insulin sensitivity of both male and female PCE offspring were enhanced accompanied with reduced β cell fraction and mass. Western blotting results revealed that significant augmentation in protein expression of hepatic insulin signaling elements of PCE females, including insulin receptor (INSR), insulin receptor substrate 1 (IRS-1) and the phosphorylation of serine–threonine protein kinase (Akt), was also potentiated. In conclusion, we demonstrated that PCE reduced the pancreatic β mass but increased the glucose tolerance in adult offspring rats, especially for females. The adaptive compensatory enhancement of β cell responsiveness to glucose and elevated insulin sensitivity mainly mediated by upregulated hepatic insulin signaling might coordinately contribute to the increased glucose tolerance.
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影响因子：
3.8
作者：
Dan Xu;Yimeng Wu;Fulin Liu;Yanzhuo Liu;L. Shen;You-ying Lei;J. Liu;Jie Ping;Jun Qin
通讯作者：
Dan Xu;Yimeng Wu;Fulin Liu;Yanzhuo Liu;L. Shen;You-ying Lei;J. Liu;Jie Ping;Jun Qin
DOI：
10.1016/s0084-3954(07)70241-5
发表时间：
2006
期刊：
Yearbook of Pediatrics
影响因子：
--
作者：
J. Stockman
通讯作者：
J. Stockman
DOI：
10.1016/j.metabol.2005.05.005
发表时间：
2005-10
期刊：
Metabolism: clinical and experimental
影响因子：
--
作者：
C. Jensen;H. Storgaard;J. Holst;F. Dela;S. Madsbad;A. Vaag
通讯作者：
C. Jensen;H. Storgaard;J. Holst;F. Dela;S. Madsbad;A. Vaag
DOI：
10.1016/b978-0-443-06930-7.50031-1
发表时间：
2001-01
影响因子：
3.8
作者：
通讯作者：
--
DOI：
10.1016/b978-0-323-06545-0.00023-6
发表时间：
2011
期刊：
--
影响因子：
--
作者：
R. Kliegman
通讯作者：
R. Kliegman