Pinkney J H, Denver A E, Foyle W J, Foster C, Yudkin J S
University College London School of Medicine, Department of Medicine, Whittington Hospital, UK.
J Hum Hypertens. 1995 Aug;9(8):685-6.
Insulin resistance and increased erythrocyte Na+/Li+ countertransport activity are well documented in subjects with essential hypertension, raising the question whether compensatory hyperinsulinaemia might be responsible for activating Na+/Li+ countertransport. We measured Na+/Li+ countertransport in 63 non-nephropathic non-insulin-dependent diabetic subjects (36 hypertensive, 27 normotensive), finding no correlation with fasting levels of insulin (r = 0.074, P = 0.28), despite using a sensitive and specific insulin assay. In contrast, in 33 of the subjects in whom insulin sensitivity was measured, Na+/Li+ countertransport correlated significantly with the whole body glucose clearance rate (r = -0.37, P = 0.036). It is concluded that increased Na+/Li+ countertransport may be a cellular marker for insulin resistance, but that hyperinsulinaemia is not likely to be the factor which mediates this relation.
胰岛素抵抗和红细胞钠/锂逆向转运活性增加在原发性高血压患者中已有充分记录,这就提出了一个问题,即代偿性高胰岛素血症是否可能是激活钠/锂逆向转运的原因。我们测量了63例非肾病非胰岛素依赖型糖尿病患者(36例高血压患者,27例血压正常者)的钠/锂逆向转运,尽管使用了灵敏且特异的胰岛素检测方法,但发现其与空腹胰岛素水平无相关性(r = 0.074,P = 0.28)。相比之下,在33例测量了胰岛素敏感性的患者中,钠/锂逆向转运与全身葡萄糖清除率显著相关(r = -0.37,P = 0.036)。结论是,钠/锂逆向转运增加可能是胰岛素抵抗的细胞标志物,但高胰岛素血症不太可能是介导这种关系的因素。