The effection of Tangnai-Kang for Insulin signal-transduction in Spontaneous Type 2 Diabetic animal KKAy mouse

WANG Fen~1; HE Hua-liang~2; JIANG Nan~2; JIA Shu-ming~2; LIU Tong-hua~

doi:10.13422/j.cnki.syfjx.2008.01.030

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The effection of Tangnai-Kang for Insulin signal-transduction in Spontaneous Type 2 Diabetic animal KKAy mouse

更新时间：2024-09-23

- The effection of Tangnai-Kang for Insulin signal-transduction in Spontaneous Type 2 Diabetic animal KKAy mouse
- Chinese Journal of Experimental Traditional Medical Formulae Issue 1, Pages: 46-49(2008)
- 作者机构：
  
  1. 北京中医药大学
  2. 武警北京总队第二医院
- 作者简介：
- 基金信息：
- DOI：10.13422/j.cnki.syfjx.2008.01.030
  CLC： R587.1
- Published：2008
- 稿件说明：
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[1]王芬,何华亮,江南,贾淑明,刘铜华.糖耐康对自发性2型糖尿病KKAy小鼠胰岛素信号转导的影响[J].中国实验方剂学杂志,2008(01):46-49.

WANG Fen~1, HE Hua-liang~2, JIANG Nan~2, et al. The effection of Tangnai-Kang for Insulin signal-transduction in Spontaneous Type 2 Diabetic animal KKAy mouse[J]. Chinese journal of experimental traditional medical formulae, 2008, (1): 46-49.
[1]王芬,何华亮,江南,贾淑明,刘铜华.糖耐康对自发性2型糖尿病KKAy小鼠胰岛素信号转导的影响[J].中国实验方剂学杂志,2008(01):46-49. DOI： 10.13422/j.cnki.syfjx.2008.01.030.

WANG Fen~1, HE Hua-liang~2, JIANG Nan~2, et al. The effection of Tangnai-Kang for Insulin signal-transduction in Spontaneous Type 2 Diabetic animal KKAy mouse[J]. Chinese journal of experimental traditional medical formulae, 2008, (1): 46-49. DOI： 10.13422/j.cnki.syfjx.2008.01.030.

摘要

目的:观察糖耐康对自发性2型糖尿病KKAy小鼠胰岛素抵抗及胰岛素信号转导途径中磷脂酰肌醇-3激酶（PI3-K）、葡萄糖转运子4（GluT4）mRNA表达的影响。方法:将SPF级KKAy小鼠40只按血糖值随机分为模型组、糖耐康高剂量组、糖耐康低剂量组、吡咯列酮组

并选C57bl/6J小鼠为正常对照组

连续灌喂给药60 d。60 d后测定空腹血糖（FPG）、空腹胰岛素（Fins）并计算胰岛素敏感指数（ISI）、总胆固醇（TC）、甘油三酯（TG）、高密度脂蛋白胆固醇（HDL-C）、低密度脂蛋白胆固醇（LDL-C）

游离脂肪酸（FFA）及肿瘤坏死因子-α（TNF-α）

并对胰岛进行病理学检查。用实时定量RT-PCR法测定小鼠骨骼肌和脂肪组织中PI3-K及GluT4的mRNA的表达。结果:糖耐康高剂量组的FPG、TNF-α水平较模型组显著降低（P<0.05）

高

低剂量组PI3-K及GluT4mRNA表达较模型组明显升高（P<0.05或P<0.01）

且糖耐康在一定程度上能够保护胰岛β细胞

延缓β细胞衰竭

对血脂及FFA有降低趋势。结论:通过提高胰岛素信号转导受体后途径中PI3-K的表达

从而改善GluT4的转位是糖耐康改善胰岛素抵抗状态的可能作用机制之一。

Abstract

Objective:To study the effection of Tangnai-Kang conction for insulin resistance and expression of Phosphatidylinositol 3 Kinase、Glucose Transport 4 messenger ribonucleic acid（mRNA）.Methods:Specific pathogen free（SPF） KKAy mice 40 were divided randomly according to plasma glucose level into Models

TNK-low dosage

TNK-high dosage

Pioglitazone and normal C57BL/6J mice（normal control group）.60 days later

all animals were tested Fasting plasma glucose（PFG）

Fasting insulin level for caculating Insulin Sensitivity Index（ISI）

Total Cholesterol（TC）

Total triacylglycerol（TG）

High-density Lipoprotein Cholesterol（HDL-C）

Low-density Lipoprotein Cholesterol（LDL-C）

Floating fatty acid（FFA）

Tumor necrosis factor-α（TNF-α） and pathological examination for the islet.The muscle and adipose expressio of PI-3K and GluT4 mRNA by reverse transcriptase PCR（RT-PCR） were determined.Results:Compared with Model groups

FPG、TNF-α levels were decreased significantly for TNK-high dosage（P<0.05）

the expression of PI-3K and GluT4 mRNA were all up-regulated（P<0.05 or P<0.01）

the recipe could protect β-cells in some degree and postponting β-cells failure in islet

displayed decreasing tendency to plasma lipocy and FFA levels.Conclusions:One of the mechanism of Tangnai-Kang improving insulin resistance might be up-regulated the expression of PI-3K mRNA in post-receptor of insulin signal-transduction roads

thereby increased GluT4 translocation.

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Related Author

WANG Fen1

HE Hua-liang2

JIANG Nan2

JIA Shu-ming2

LIU Tong-hua1

LI Liqin

ZENG Zixuan

TANG Ye

Related Institution

Key Laboratory of Modern Chinese Medicine Formulations of Jiangxi University of Chinese Medicine， Ministry of Education

School of Pharmacy， Jiangxi University of Chinese Medicine

National Key Laboratory of Creation of Modern Chinese Medicine with Classical Formulas

Dongfang Hospital， Beijing University of Chinese Medicine

Key Laboratory of Health Preservation and Rehabilitation， Ministry of Education， Beijing University of Chinese Medicine

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