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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m RNA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)m RNA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m RNA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。
Objective: To investigate the relationship between hypothalamic neuropeptide NUCB2 and Tsumura Suzuki (TS) polygenic mutant in type 2 diabetes (T2DM) mice. Methods: The animals were divided into Tsumura Suzuki diabetic (TSD) mice and normal mice. The food intake of mice was monitored by the monitor. The blood biochemistry indexes were analyzed. The expression of m-RNA was detected by quantitative RT-PCR. The radioimmunoassay Nesfatin-1 protein levels were measured. RESULTS: TSD mice had weight gain (P <0.05) and hyperleptinemia (P <0.05) at 1 month of age compared with age-matched TSN mice, bulimia at 3-12 months of age (P <0.05 ), Hyperglycemia (P <0.05), hyperlipidemia (P <0.05) and hyperinsulinemia (P <0.05). The nemsfatin-1 precursor nucleoprotein 2 (NUCB2) m RNA and nesfatin-1 protein levels were significantly decreased (P <0.05 ~ 0.01); TSD mouse hypothalamus galanin, melanin concentration, neuropeptide Y and pre-melanocyte cortex progenitor m RNA levels were also significantly changed P <0.05). Conclusion: NUCB2-mediated signal pathway destruction in the hypothalamus may lead to excessive TSD ingestion in mice.