文章摘要
张玮 王巧玲 逄明杰 祝海 郭菲菲 孙向荣 公衍玲 徐珞.下丘脑Nesfatin-1/NUCB2对糖尿病小鼠摄食的影响[J].,2015,15(8):1440-1443
下丘脑Nesfatin-1/NUCB2对糖尿病小鼠摄食的影响
The Effects of Hypothalamic Nesfatin-1/NUCB2 on Feeding in Diabetes Mice
  
DOI:
中文关键词: 摄食过多  Nesfatin-1/ NUCB2  下丘脑  糖尿病  小鼠
英文关键词: Hyperphagic feeding  Nesfatin-1/nucleobindin-2  Hypothalamus  Diabetes  Mice
基金项目:国家自然科学基金项目(31071014;81100260;81270460;81300281;81470815); 青岛市科技局项目(13-1-4-170-jch,11-2-3-3-(2)-nsh;14-2-3-3-nsh)
作者单位
张玮 王巧玲 逄明杰 祝海 郭菲菲 孙向荣 公衍玲 徐珞 青岛大学医学院病理生理学教研室菏泽鄄城县人民医院青岛市立医院青岛科技大学化工学院 
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中文摘要:
      目的:探讨下丘脑神经肽NUCB2与Tsumura Suzuki(TS)多基因突变2 型糖尿病(T2DM)小鼠摄食过多的关系。方法:将动 物分为Tsumura Suzuki 糖尿病(TSD)小鼠、正常小鼠;监视器监测小鼠摄食量;分析血生化指标;定量RT-PCR 分析摄食相关神经 肽mRNA 表达水平;放射免疫分析法检测nesfatin-1 蛋白水平。结果:与年龄匹配的TSN 小鼠相比,TSD 小鼠在1 月龄就存在体 重增加(P<0.05)和高瘦素血症(P<0.05),3-12 月龄出现贪食(P<0.05)、高血糖(P<0.05)、高血脂(P<0.05)和高胰岛素血症(P<0. 05),且3-12 月龄时厌食肽nesfatin-1 前体核连蛋白2(NUCB2)mRNA 和nesfatin-1 蛋白水平均显著降低(P<0.05~0.01);TSD 小 鼠下丘脑甘丙肽、黑色素浓集素、神经肽Y 及前黑素细胞皮质素原mRNA水平也有显著改变(P<0.05)。结论:下丘脑NUCB2 介 导信号通路破坏可能导致TSD 小鼠摄食过多。
英文摘要:
      Objective:To discuss the relationship between hypothalamic neuropeptide NUCB2 and hyperphagic feeding in Tsumura Suzuki Diabetes (TSD) mice, a model of type 2 diabetes with polygenic abnormalities.Methods:Animals can be divided into Male Tsumura Suzuki Diabetes (TSD) mice, Tsumura Suzuki normal (TSN) mice. Food intake in mice was monitored and blood chemistry was analyzed. Quantitative real-time polymerase chain reaction (PCR) assay was used to measure the expression level of feeding-related neuropeptide mRNA; radiation immunoassay was used to detect the protein level of nesfatin-1.Results:TSD mice showed an increase in body weight (P<0.05) and hyperleptinemia (P<0.05) from 1 month of age and hyperphagic feeding (P<0.05), hyperglycemia (P<0.05), hyperlipidemia (P<0.05) and hyperinsulinemia (P<0.05) from 3 to 12 months of age compared with age-matched non-diabetic control TSN mice. The mRNA and protein levels of nucleobindin-2 (NUCB2), the precursor of the anorexigenic neuropeptide nesfatin-1, was significantly decreased (P<0.05~0.01) in the hypothalamus of TSD mice compared with that in TSN mice from 3 to 12 months of age. The mRNA levels of galanin, melanin-concentrating hormone, neuropeptide Y, and pro-opiomelanocortin were significantly changed (P<0.05) in the hypothalamus in TSD mice at several time points.Conclusion:The results suggest that the disrupted control of hypothalamic NUCB2-mediated signaling may contribute to hyperphagic feeding in TSD mice.
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