Resting metabolic rate and substrate use in obesity hypertension

There is substantial evidence that obesity is a prime risk factor for the d evelopment of hypertension. Although hyperinsulinemia and an increased acti vity of the sympathetic nervous system have been implicated in the pathogen esis of "obesity hypertension," their effects on energy metabolism have not been studied thus far. In the present study, we therefore examined resting metabolic rate (RMR) and basal substrate oxidation in subjects with obesit y and obesity-related hypertension. A total of 166 subjects were characteri zed for RMR and basal substrate use through indirect calorimetry. Blood pre ssure was measured at rest and with 24-hour ambulatory monitoring. Blood sa mples were collected for the measurement of plasma catecholamines, leptin, and the insulin response to an oral glucose load. In our study population, 116 subjects were defined as hypertensive and 91 were defined as obese. Hyp ertensive patients under beta-adrenergic blockade (n=42) had a significantl y lower RMR than did patients without beta-blockade (P<0.05) and were there fore excluded from further analyses. Univariate regression analysis reveale d a significant relationship between RMR and body fat mass, as well as body fat-free mass, in both groups. Compared with obese normotensive control su bjects (n=27), obese hypertensives (n=43) had a 9% higher RMR (P<0.05), hig her plasma catecholamine (P<0.05) and leptin (P<0.05) levels, and an increa sed insulin response to oral glucose (P<0.01). Together, these findings are compatible with the idea that chronic neurogenic and metabolic adaptations related to obesity may play a role in the development of obesity hypertens ion in susceptible individuals.