Association of lactate with blood pressure before and after rapid weight loss

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.

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.

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.

Baseline and longitudinal associations between lactate and DBP suggest that insufficient oxidative capacity may play a role in obesity-related hypertension.