Tong Y C, Wang C J, Cheng J T
Department of Urology, National Cheng Kung University Medical College, Tainan, Taiwan.
Neurosci Lett. 1997 Sep 19;233(2-3):93-6. doi: 10.1016/s0304-3940(97)00636-8.
Glucose homeostasis was studied in the spontaneously hypertensive rat (SHR). The fasting plasma glucose levels were similar in the SHR and normotensive Wistar-Kyoto (WKY) rat (102.7+/-2.4 vs. 107.4+/-4.2 mg/dl, P > 0.01). One hour after glucose challenge, the plasma glucose level was slightly but insignificantly increased in both SHR and WKY rat (117+/-2.5 vs. 114.3+/-3.2 mg/dl, P > 0.01). After N(G)nitro-L-arginine methyl ester (L-NAME) 20 mg/kg per day was administered intraperitoneally (i.p.) for 4 days, the plasma glucose level was significantly increased in the rats (SHR 167.3+/-4.9; WKY rat 136.0+/-4.8 mg/dl); the increase was significantly more pronounced in the SHR. The fasting insulin levels were similar in the SHR and WKY rats (2.3+/-0.4 vs. 2.0+/-0.3 ng/ml, P > 0.01). One hour after glucose challenge, the insulin level was significantly increased in the WKY rat (4.8+/-0.7 ng/ml) but not in the SHR (2.2+/-0.4 ng/ml). With L-NAME treatment, plasma insulin increase was noted in the WKY rat but not SHR (4.6+/-0.6 vs. 2.6+/-0.4 ng/ml, n = 8, P < 0.01). One hour after insulin 1 IU/kg was injected intramuscularly (i.m.), the plasma glucose level was significantly decreased in both the SHR (from 115.0+/-6.5 to 48.6+/-3.6 mg/dl, n = 8) and WKY rat (from 108.3+/-3.8 to 52.6+/-4.2 mg/dl, n = 8). No significant difference was noted between the decrease of the two groups (P > 0.01). The present findings suggested that NO plays a role in the glucose homeostasis of rats. NO-synthase blockade resulted in an increase of plasma glucose level. The SHR maintains normal glucose level and tolerance in spite of a defective insulin release response. This is probably due the compensatory effect of a more prominent NO-dependent glucose homeostatic function.
在自发性高血压大鼠（SHR）中研究了葡萄糖稳态。SHR和血压正常的Wistar-Kyoto（WKY）大鼠的空腹血糖水平相似（102.7±2.4对107.4±4.2mg/dl，P>0.01）。葡萄糖激发后1小时，SHR和WKY大鼠的血糖水平均略有升高，但无统计学意义（117±2.5对114.3±3.2mg/dl，P>0.01）。每天腹腔注射（i.p.）20mg/kg的N（G）-硝基-L-精氨酸甲酯（L-NAME），持续4天，大鼠的血糖水平显著升高（SHR为167.3±4.9；WKY大鼠为136.0±4.8mg/dl）；SHR中的升高更为显著。SHR和WKY大鼠的空腹胰岛素水平相似（2.3±0.4对2.0±0.3ng/ml，P>0.01）。葡萄糖激发后1小时，WKY大鼠的胰岛素水平显著升高（4.8±0.7ng/ml），而SHR中未升高（2.2±0.4ng/ml）。经L-NAME治疗后，WKY大鼠血浆胰岛素升高，而SHR未升高（4.6±0.6对2.6±0.4ng/ml，n=8，P<0.01）。肌肉注射（i.m.）1IU/kg胰岛素1小时后，SHR（从115.0±6.5降至48.6±3.6mg/dl，n=8）和WKY大鼠（从108.3±3.8降至52.6±4.2mg/dl，n=8）的血糖水平均显著降低。两组降低幅度之间无显著差异（P>0.01）。目前的研究结果表明，NO在大鼠的葡萄糖稳态中起作用。一氧化氮合酶阻断导致血浆葡萄糖水平升高。尽管胰岛素释放反应存在缺陷，但SHR仍维持正常的血糖水平和耐受性。这可能是由于更突出的NO依赖性葡萄糖稳态功能的代偿作用。
