Zhao J, Sha H, Zhou S, Tong X, Zhuang F Y, Gregersen H
China-Japan Friendship Hospital, Beijing, PR China.
Dig Liver Dis. 2002 Oct;34(10):707-16. doi: 10.1016/s1590-8658(02)80022-6.
Biomechanical properties in terms of residual strains in diabetic small intestine have not been studied. Furthermore, no data have been reported on affect of gliclazide on gastrointestinal complications of diabetes.
To determine remodelling of zero-stress state of small intestine in streptozotocin-induced diabetic rats and effect of gliclazide treatment.
Morphological properties and residual strains were studied in duodenum, jejunum and ileum obtained from diabetic rats, gliclazide-treated diabetic rats and normal rats (n = 8 each group).
Diabetes was induced by single intraperitoneal injection of 65 mg/kg streptozotocin. Gliclazide (10 mg kg(-1) day(-1) was injected directly into stomach lumen by intragastric gavage twice daily. Experimental period was 35 days. To approach no-load state; intestinal segments were surgically excised and cut transversely into short ring-shaped segments. Each ring was cut radially to obtain geometry of zero-stress state. Circumferential length, the wall thickness and opening angle were measured from digital images of each specimen and residual strains were computed.
Blood glucose level of diabetic group (approximately 20 mmol/l) was consistently higher than that in normal group (approximately 4 mmol/l) after induction of diabetes (p < 0.001). Gliclazide lowered average blood glucose level to between 10 and 15 mmol/l (p < 0.001). Plasma insulin levels of both diabetic groups (average between 10 and 15 pmol/l) were significantly lower than those in normal group (average approximately 18 pmol/l, p < 0.05). Wet weight per unit length and wall thickness of duodenum, jejunum and ileum were significantly higher in Diabetes group than those in Normal group (p < 0.05). Opening angle and absolute value of residual strain were significantly smaller in duodenum and larger in jejunum and ileum in Diabetes group than in Normal group (p < 0.001). Gliclazide treatment partly restored these changes (p < 0.05).
Diabetes induced morphometric and biomechanical remodelling in intestine. Gliclazide partly restored these changes.
糖尿病小肠残余应变方面的生物力学特性尚未得到研究。此外，关于格列齐特对糖尿病胃肠道并发症的影响尚无数据报道。
确定链脲佐菌素诱导的糖尿病大鼠小肠零应力状态的重塑情况以及格列齐特治疗的效果。
对从糖尿病大鼠、格列齐特治疗的糖尿病大鼠和正常大鼠（每组n = 8）获取的十二指肠、空肠和回肠的形态学特性及残余应变进行研究。
通过单次腹腔注射65 mg/kg链脲佐菌素诱导糖尿病。格列齐特（10 mg kg⁻¹ 天⁻¹）通过胃内灌胃每日两次直接注入胃腔。实验期为35天。为达到无负荷状态；手术切除肠段并横向切成短环形段。每个环径向切开以获得零应力状态的几何形状。从每个标本的数字图像测量圆周长度、壁厚和开口角度，并计算残余应变。
糖尿病诱导后，糖尿病组的血糖水平（约20 mmol/l）始终高于正常组（约4 mmol/l，p < 0.001）。格列齐特将平均血糖水平降至10至15 mmol/l之间（p < 0.001）。两个糖尿病组的血浆胰岛素水平（平均在10至15 pmol/l之间）均显著低于正常组（平均约18 pmol/l，p < 0.05）。糖尿病组十二指肠、空肠和回肠的单位长度湿重和壁厚显著高于正常组（p < 0.05）。糖尿病组十二指肠开口角度和残余应变绝对值显著小于正常组，空肠和回肠则大于正常组（p < 0.001）。格列齐特治疗部分恢复了这些变化（p < 0.05）。
糖尿病诱导肠道形态和生物力学重塑。格列齐特部分恢复了这些变化。
