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|本期目录/Table of Contents|

糖脂消对胰岛素抵抗高血压大鼠胰岛素敏感性的影响

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2010年第3期
页码:
351-353
栏目:
基础研究
出版日期:
2010-04-06

文章信息/Info

Title:
Effects of tangzhixiao on insulin sensitivity in insulin-resistant hypertensive rats
作者:
赵旭燕1; 李玉明2; 杨宁2; 石蕊2
1.武警总医院心内科，北京 100039；2.武警医学院附属医院心内科，天津 300162
Author(s):
ZHAO Xu-yan1;  LI Yu-ming2;  YANG Ning2;  SHI Rui2
1.Department of Cardiology, General Hospital of Chinese People’s Armed Police Force, Beijing,100039 China; 2.Department of Cardiology, Affiliated Hospital, Medical College of Chinese People's Armed Police Force, Tianjin, 300162, China
关键词:
胰岛素抵抗; 瘦素; 糖脂消; 大鼠
Keywords:
insulin resistance;  leptin;  rat model;  tangzhixiao
分类号:
R977.15
DOI:
-
文献标识码:
A
摘要:
目的: 观察不同剂量的糖脂消对胰岛素抵抗高血压大鼠胰岛素敏感性的影响并探讨其作用机制。方法: 用高果糖饲料喂养雄性SD大鼠建立胰岛素抵抗大鼠模型，随机分为3组（每组各13只），即模型对照组、低剂量和高剂量的糖脂消组，分别喂高果糖、高果糖加不同剂量(15 g/L和60 g/L)的糖脂消。4周后，采用葡萄糖氧化酶法检测空腹血糖（FBG），用放免法测定空腹胰岛素（FINS）和瘦素（LP），用稳态模型（HOMA）评估法检测胰岛素抵抗（IR）。结果: 高果糖组大鼠的LP与FINS和IR呈显著的正相关（r=0.67,P<0.05;r=0.68,P<0.05）。随着糖脂消剂量的增加，LP、FINS和IR的水平逐渐下降，但仅高剂量糖脂消组与模型对照组的差异有统计学意义(均P<0.05)。结论: 糖脂消能明显改善IR，其部分机制可能与降低LP和FINS有关。
Abstract:
AIM: To observe the effects of different doses of tangzhixiao on insulin sensitivity in high fructose-fed rats and to explore its mechanism. METHODS: Insulin-resistant (IR) models established in male Sprague Dawley rats were randomly divided into three groups. Rats were given a high-fructose diet or high-fructose diet containing two doses of tangzhixiao. Fasting blood glucose (FBG), fasting insulin (FINS) and LP were measured after 4 weeks. The HOMA model was used to evaluate IR. RESULTS: In rats fed with high fructose, LP was positively related to FINS and HOMA-IR. FINS, LP and HOMA-IR of different doses of the tangzhixiao group decreased compared with those in the control group, but significant changes were found only in high-dose tangzhixiao group (all P<0.05). CONCLUSION: Tangzhixiao greatly prevents IR, possibly by decreasing leptin levels.

参考文献/References

［1］Mikhail N. The metabolic syndrome: insulin resistance［J］. Curr Hypertens Rep, 2009, 11(2):156-158.

［2］Hwang IS, Ho H, Hoffman B, et al. Fructose-induced insulin resistance and hypertension in rats［J］. Hypertension, 1987, 10(5):512-516.

［3］ Gutierrez DA, Puglisi MJ, Hasty AH. Impact of increased adipose tissue mass on inflammation, insulin resistance, and dyslipidemia［J］. Curr Diab Rep, 2009, 9(1):26-32.

［4］ D’Anna R, Baviera G, Cannata ML, et al. Midtrimester amniotic fluid leptin and insulin levels and subsequent gestational diabetes［J］. Gynecol Obstet Invest, 2007, 64(2):65-68.

［5］ Pehlivanov B, Mitkov M. Serum leptin levels correlate with clinical and biochemical indices of insulin resistance in women with polycystic ovary syndrome［J］. Eur J Contracept Reprod Health Care, 2009, 14(2):153-159.

［6］ Kraus D, Fasshauer M, Ott V, et al. Leptin secretion and negative autocrine crosstalk with insulin in brown adipocytes［J］. Endocrinol, 2002, 175(1):185-191.

［7］ Eckle RH, Grundy SM, Zimmet PZ. The metabolic syndrome［J］. Lancet, 2005, 365(9468):1415-1428..

备注/Memo

备注/Memo:
收稿日期：2009-05-27.作者简介：赵旭燕，主治医师，硕士生 Email:zhaoxuyan76@126.com
更新日期/Last Update: 2010-04-09