Sekiya M, Yamasaki Y, Tsujino T, Shiba Y, Kubota M, Kawamori R, Kamada T
First Department of Medicine, Osaka University School of Medicine, Japan.
Diabetes Res Clin Pract. 1995 Jul;29(1):49-56. doi: 10.1016/0168-8227(95)01115-t.
This study evaluated insulin secretion and insulin sensitivity in 17 non-obese hypertensive patients (aged 45.6 +/- 2.2 years, body mass index 24.0 +/- 0.5 kg/m2, mean +/- S.E.M.) with (n = 8) and without glucose intolerance (n = 9) and compared the results with those of 16 age-matched non-obese normotensive subjects with (n = 7) and without glucose intolerance (n = 9). The hypertensive patients without glucose intolerance showed a significantly lower insulin-mediated glucose disposal and a compensating increase in second-phase insulin secretion compared with normotensives without glucose intolerance. In hypertensives with glucose intolerance, insulin-mediated glucose disposal was significantly lower and second-phase insulin secretion was comparable to that in normotensives without glucose intolerance. After 3 months of angiotensin-converting enzyme (ACE) inhibition with oral administration of delapril, blood pressure was significantly reduced in the hypertensives with glucose intolerance (n = 9). The insulin-mediated glucose disposal significantly (P < 0.01) recovered from 6.0 +/- 0.81 to 8.0 +/- 0.71 mg/kg per min. The second-phase insulin secretion tended to be lower (but not significantly) but insulin clearance increased from 15.4 +/- 0.85 to 19.1 +/- 1.42 ml/min (P < 0.05). These data show that in hypertensive patients without glucose intolerance insulin resistance might compensatorily augment second-phase insulin secretion and lead to hyperinsulinemia. In hypertensives with glucose intolerance, insulin resistance might induce postprandial hyperglycemia, which leads to hyperinsulinemia because of second phase insulin secretion at a level similar to that of normotensives.
本研究评估了17名非肥胖高血压患者(年龄45.6±2.2岁,体重指数24.0±0.5kg/m²,均值±标准误)的胰岛素分泌和胰岛素敏感性,其中8例有糖耐量异常,9例无糖耐量异常,并将结果与16名年龄匹配的非肥胖血压正常受试者进行比较,后者7例有糖耐量异常,9例无糖耐量异常。无糖耐量异常的高血压患者与无糖耐量异常的血压正常者相比,胰岛素介导的葡萄糖处置显著降低,且第二相胰岛素分泌有代偿性增加。有糖耐量异常的高血压患者,胰岛素介导的葡萄糖处置显著降低,且第二相胰岛素分泌与无糖耐量异常的血压正常者相当。在用口服地拉普利进行血管紧张素转换酶(ACE)抑制3个月后,有糖耐量异常的高血压患者(n = 9)血压显著降低。胰岛素介导的葡萄糖处置从6.0±0.81显著恢复至8.0±0.71mg/kg每分钟(P < 0.01)。第二相胰岛素分泌有降低趋势(但不显著),但胰岛素清除率从15.4±0.85增加至19.1±1.42ml/分钟(P < 0.05)。这些数据表明,在无糖耐量异常的高血压患者中,胰岛素抵抗可能通过代偿性增加第二相胰岛素分泌而导致高胰岛素血症。在有糖耐量异常的高血压患者中,胰岛素抵抗可能诱发餐后高血糖,由于第二相胰岛素分泌水平与血压正常者相似,从而导致高胰岛素血症。