Red blood cell sodium and potassium, plasma potassium, glucose and insulin responses to oral glucose load, serum urate, and plasma triglycerides were determined in a stratified subsample (n = 89) of a representative population sample (n = 1211), comprising 30 nonobese normotensive subjects with normal glucose tolerance (reference group) and 59 subjects representing each of the seven possible combinations of abnormal glucose tolerance, obesity, and hypertension. Rate of cation imbalance (red blood cell sodium ≥7.0 mEq/L, potassium <92.5 mEq/L, or plasma potassium ≥4.5 mEq/L) was 88.1% in subjects with abnormal tolerance, obesity, or hypertension, as compared with 40.0% in the reference group (p < 0.001). These subjects were also characterized by significantly greater rates of insulin response: 60- and 120-minute postload levels of 100 mU/L or more (88.1 vs 46.7%), plasma triglycerides of 80 mg/dl or more (89.8 vs 53.3%) and serum uric acid of 5.5 mg/dl or more (61.0 vs 26.7%; p < 0.001 for all). The rate of cation imbalance was significantly associated with each of these three biochemical correlates: insulin response (p < 0.01), triglycerides (p < 0.001), and urate (p < 0.001). In the total population sample, the rate of untreated hypertension increased from 18% to 35% to 55.3% (p < 0.001), with an increase in the number of biochemical correlates of cation imbalance in combination with glucose intolerance and obesity. Since insulin is a regulator of membrane cation transport, whereas abnormal glucose tolerance, obesity, and hypertension, as well as elevated serum urate and triglycerides, are correlates of hyperinsulinemia and insulin resistance, we conclude that hyperinsulinemia is implicated in the cation transport abnormalities that characterize hypertension, obesity, and glucose intolerance.