Chinese Journal of Clinical Anatomy >
NUCB2/Nesfatin-1expression in the hypothalamus of DIO rats
Received date: 2014-01-13
Online published: 2014-12-04
Objective To explore the NUCB2/Nesfatin-1 expression level in hypothalamus of diet induced obesity（DIO）rats, and to provide experimental basis for the mechanism of nerve regulation by glucolipid metabolism. Methods To setting up high glucose and lipid rat model by high-energy feed, using immunohistochemical method to detect the hypothalamus NUCB2/Nesfatin-1 expression level. Results （1）NUCB2/Nesfatin-1 expression positive rate was 43.33% in the hypothalamus of the experimental group, which was significantly lower than that（80.00%）in the control group（P<0.05）.（2）NUCB2/Nesfatin-1 expression strength score was 2.159±0.918 in the hypothalamus in the experimental group, and was 3.683±1.250 in the control group（P<0.01）. Conclusion NUCB2/Nesfatin-1 expression level was decreased obviously in the hypothalamus of diet induced obesity rats，suggesting NUCB2/Nesfatin-1 may play an important role in regulating glucolipid metabolism.
QIN Xiao-Yun , WANG Ba-Jun , WU Shan-An , ZHANG Qiang-Jin , LIU Man-Jun , LAN Ling-Yuan , ZHANG Meng-Ya , HUANG Bei , QIN Xiao-Hua , JIA Chun-Bei . NUCB2/Nesfatin-1expression in the hypothalamus of DIO rats[J]. Chinese Journal of Clinical Anatomy, 2014 , 32(6) : 704 -707 . DOI: 10.13418/j.issn.1001-165x.2014
[1] Oh-I S，Shimizu H，Satoh T，et al. Identification of nesfatin-1 as a satiety molecule in the hypothalamus
[J]. Nature，2006，443(7112)：709-712.
[2] Reaven GM. Banting lecture 1988：Role of insulin resistance in human disease
[J]. Diabetes，1988，37(12)：1595-1607.
[3] Stern MP. Diabetes and cardiovascular. The“Common soil”hypothesis
[J]. Diabetes，1995，44(4)：369-374.
[4] 田德润，李晓东，牛东滨，等. 电针上调食源性肥胖大鼠弓状核α-MSH的表达
[J].北京大学学报（医学版），2003，35(5)：458-461.
[5] Ruchat SM，Girard M，Weisnagel SJ，et al. Association between micro-opioid receptor-1 102T>C polymorphism and intermediate type 2 diabetes phenotypes: results from the Quebec Family Study （QFS）
[J].Clin Exp Pharmacol Physiol，2008，35(9)：1018-1022.
[6] Bouret SG，Draper SJ，Simerly RB．Trophic action of leptin on hypothalamic neurons that regulate feeding
[J]．Science，2004，304(5667)：108-110．
[7] Das UN. Is metabolic syndrome X a disorder of the brain with the initiation of low-grade systemic inflammatory events during the perinatal period
[J]．J Nutr Biochem，2007，18(11)：701-713．
[8] Stengel A，Goebel M，Tache Y. Nesfatin-1: a novel inhibitory regulator of food intake and body weight
[J]. Obes Rev，2011，12(4)：261-271.
[9] Shimizu H，Oh-I S，Hashimoto K，et al. Peripheral administration of Nesfatin-1 reduces food intake in mice: the leptin-independent mechanism. Endocrinology，2009，150（2）：662-671.
[10] Su Y，Zhang J，Tang Y，et al. The novel function of nesfatin-1： antihyperglyce- mia
[J]. Biochem Biophys Res Commun，2010，391（1）：1039-1042.
[11] 王文杰，蒋正尧. Nesfatin-1对大鼠迷走复合体内葡萄糖感受神经元和胃扩张敏感神经元兴奋性的作用
[J].齐鲁医学杂志，2010，25（3）：225-227.
[12] Yang M，Zhang Z，Wang C，et al. Nesfatin-1 action in the brain increases insulin sensitivity through Akt/AMPK/TORC2 pathway in diet-induced insulin resistance
[J]. Diabetes，2012，61（8）：1959-1968.
[13] 叶菲，朱伟，杨刚毅，等. 脑室内灌注重组蛋白Nesfatin-1（1-82）对大鼠糖脂代谢和相关酶的影响
[J].中国糖尿病杂志，2013，21（6）：540-543.
/
| 〈 |
|
〉 |
