Sodium-lithium countertransport activity is decreased after weight loss in healthy obese men

Abstract

Maximal red blood cell (RBC) sodium-lithium countertransport activity has been consistently releted to essential hypertension and may be a marker for risk of developing hypertension. Although there is strong evidence for genetic control of sodium-lithium countertransport, increasing evidence suggests that obesity and insulin-glucose metabolism are related to countertransport activity. This study was performed to determine whether countertransport activity decreases with weight loss in healthy obese adults. Forty-five healthy, white, obese adults were studied at baseline and after 6 months of behavioral dietary intervention. Weight loss was 11.5 kg (25.4 lb) in 24 men and 8.1 kg (17.8 lb) in 21 women. Sodium-lithium countertransport activity decreased 55.0 μmol Li/L RBC/h in men ( P < .001, paired t test) and 14.6 μmol Li/L RBC/h in women (NS). Change in countertransport activity was correlated with change in body mass index (BMI) in men ( r = .52, P < .01) and women ( r = .27, NS) and was also strongly correlated with change in fasting glucose levels in both men and women ( r = .50 and r = .56, respectively; P < .01) and with change in fasting insulin levels in men ( r = .42, P = .04). Change in countertransport activity was not significantly related to change in physical exercise or serum lipid levels. There was a large decrease in systolic blood pressure in men (10.0 mm Hg, P < .001) and a smaller decrease in women (4.1 mm Hg, P < .05). These changes were significantly correlated with change in weight, but not with change in countertransport or baseline countertransport activity. Countertransport activity decreased with weight loss in obese men, possibly mediated by some aspect of insulin-glucose metabolism. We conclude that both genetic and nongenetic factors are important in the regulation of sodium-lithium countertransport activity and blood pressure.