| 王丽霞 王巧玲 逄明杰 祝海 郭菲菲 孙向荣 徐珞.糖尿病大鼠ghrelin和nesfatin-1表达动力学及其调控[J].,2015,15(10):1820-1824 |
| 糖尿病大鼠ghrelin和nesfatin-1表达动力学及其调控 |
| Dynamics Expression and Regulation of Ghrelin and Nesfatin-1in Diabetic Rats |
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| DOI： |
| 中文关键词: Ghrelin Nesfatin-1 糖尿病 胃 生长激素 |
| 英文关键词: Ghrelin Nesfatin-1 Diabetes Stomach Growth hormone |
| 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） |
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| 中文摘要: |
| 目的：探讨STZ诱导糖尿病大鼠ghrelin和nesfatin-1 动力学及分泌调节变化。方法：STZ诱导糖尿病大鼠模型；采用葡糖糖
脱氢酶分析法测量血浆葡萄糖水平；免疫放射分析检测血浆ghrelin、nesfatin-1、胰岛素、胰岛素样生长因子1(IGF-1)、生长激素
(GH)含量；采用real-time PCR 检测ghrelin mRNA 水平变化；免疫组化观察ghrelin 和nesfatin-1 免疫活性细胞数量。结果：糖尿病
大鼠体重显著降低(t=23.16，P＜0.01)，血糖水平显著升高(t=22.55，P＜0.01)，血浆胰岛素和IGF-1 水平显著降低(t=6.50，t=24.13，
P＜0.01)，但GH水平显著升高(t=3.30，P＜0.05)。糖尿病大鼠血浆总ghrelin（t=7.03，P＜0.01）和活性ghrelin(t=3.33，P＜0.05)水平
均显著升高，血浆nesfatin-1 水平则显著降低（t=6.24，P＜0.01）；糖尿病大鼠血浆总ghrelin 与GH(r=0.81，P＜0.01) 和IGF-1 水平
(r=-0.58，P＜0.01)呈显著相关性；与对照组大鼠相比，糖尿病大鼠胃总ghrelin(t=16.86，P＜0.01)和活性ghrelin(t=3.30，P＜0.05)水
平均显著降低；而胃nesfatin-1（t=7.93，P＜0.01)水平则显著升高。胃总ghrelin 水平与血浆IGF-1 水平呈明显相关性(r=0.65，P<0.
01)；与对照组大鼠相比，糖尿病大鼠胃ghrelin mRNA表达水平显著升高(t=16.8，P＜0.01)，胃底ghrelin 免疫活性细胞数量显著减
少（t=3.98，P＜0.01）；实验中给予大鼠自由饮食，糖尿病大鼠血浆总ghrelin 水平显著增加(t=7.53，P＜0.01)，nesfatin-1 水平显著降
低(t=5.46，P＜0.01)。糖尿病大鼠注射胰岛素后，可使增加的ghrelin 水平(t=1.76，P=0.11）和降低的nesfatin-1 水平接近正常(t=1.
96，P=0.06）；且胰岛素可显著反转糖尿病大鼠胃总ghrelin（t=8.54，P＜0.01）和nesfatin-1 水平（t=2.42，P＜0.05）；以及注射胰岛素
后，糖尿病大鼠胃底ghrelin 细胞显著增加，nesfatin-1 细胞明显减少（t=3.21，t=2.59，P＜0.05)。结论：Ghrelin 或nesfatin-1 参与糖尿
病大鼠能量平衡调控。 |
| 英文摘要: |
| Objective:To study the changes of ghrelin and nesfatin-1 dynamics and secretory regulation in rats with STZ-induced
diabetes.Methods:Diabetes was induced by intraperitoneal injection of streptozotocin (STZ). Serum glucose were measured by the
glucose dehydrogenase, while the levels of ghrelin, nesfatin-1, insulin, IGF-1 and GH were detected by RIA. Preproghrelin mRNA level
was tested using real-time RT-PCR and the ghrelin and nesfatin-1-immunoreactive cells were observed using immunohistochemistry.
Results:The weight of diabetic rats decreased significantly (t=23.16, P<0.01), the glucose was increased significantly (t=22.55, P<0.01),plasma insulin and IGF-1 level was decreased significantly (t=6.50, t=24.13, P<0.01), but the GH level was increased significantly (t=3.
30, P<0.05). The level of total (t=7.03, P＜0.01) and active (t=3.33, P<0.05) plasma ghrelin of the diabetic rats was increased
significantly, while the plasma nesfatin-1 level was decreased（t=6.24, P＜0.01）, compared with that of the control group. The total
plasma ghrelin level of the diabetic rats correlated significantly with their serum GH level (r=0.81, P<0.01) and with their serum IGF-1
level (r=-0.58, P<0.01). The gastric total (t=16.86, P<0.01) and active (t=3.30, P<0.05) ghrelin level of the diabetic rats was decreased
significantly, while the gastric nesfatin-1 levels was increased（t=7.93, P＜0.01) compared with that in the control group, and their gastric
total ghrelin level correlated significantly with their serum IGF-1 level (r=0.65, P<0.01). The preproghrelin mRNA expression in the
stomach was increased significantly (t=16.8, P<0.01) in the diabetic rats compared with the control and the number of
ghrelin-immunoreactive cells in the gastric fundus of the diabetic rats was decreased significantly (t=3.98, P<0.01). Giving rats free diet
in the experiments, the total plasma ghrelin level in diabetic rats was increased significantly (t=7.53, P<0.01), nesfatin-1 level significantly reduced (t=5.46, P<0.01). After insulin injections, the increasing level of ghrelin (t=1.76, P=0.11) and reducing level of
nesfatin-1 in diabetic rats was close to normal (t=1.96, P=0.06). Insulin significantly reversed the total gastric ghrelin (t=8.54, P<0.01)
and nesfatin-1 level (t=2.42, P<0.05) of diabetes rats. After injection of insulin, ghrelin cells were increased significantly, while nesfatin-1
cells were decreased significantly (t=3.21, t=2.59, P<0.05) in stomach fundus of diabetic rats.Conclusion:Ghrelin or nesfatin-1 may
participate in the regulation of energy balance in diabetic rats. |
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