Background: The mechanism linking obesity with its downstream complications is poorly understood. Accumulating evidence suggests that insufficient oxidative capacity plays a central role in the development of insulin resistance and, perhaps, hypertension.
Methods: To investigate this hypothesis, we measured lactate, a marker of the gap between energy expenditure and oxidative capacity, in 40 obese subjects with the metabolic syndrome (Ob-MS), 40 obese subjects without the metabolic syndrome (Ob), and 20 lean controls (LCs). The 40 Ob-MS participants were then entered into a 12-20 week very low-calorie diet (VLCD) intervention. The change in lactate and a number of other metabolic factors including blood pressure were subsequently assessed.
Results: At baseline, median lactate levels were significantly higher in both the Ob (36.4 mg/dl) and Ob-MS (34.7 mg/dl) groups when compared to LCs (17.4 mg/dl; P < 0.001). After the VLCD intervention, Ob-MS subjects lost 14.7 kg on average, corresponding to a 5.0 kg/m(2) decrease in body mass index (BMI). Lactate levels fell from 41.3 to 28.7 mg/dl, a 31% reduction (P = 0.006). Even after adjustment for BMI change, change in lactate was strongly associated with change in diastolic blood pressure (DBP) (P = 0.007) and mean arterial pressure (P = 0.014), but not with systolic blood pressure (SBP) (P = 0.20) or other obesity-related traits.
Conclusions: Baseline and longitudinal associations between lactate and DBP suggest that insufficient oxidative capacity may play a role in obesity-related hypertension.