W. Pories1, T. E. Jones1, J. Houmard1, C. J. Tanner1, D. Zeng1, K. Zou3, P. M. Coen2, B. H. Goodpaster4, W. E. Kraus2, J. Yang1, G. L. Dohm1, W. Pories1 1East Carolina University,Brody School Of Medicine,Greenville, NC, USA 2Duke,Metabolism,Durham, NC, USA 3Boston University,Biochemistry,Boston, MA, USA 4Sanford Bunham Prebys Medical Discovery Institute,Orlando, FL, USA
Introduction:
Blood lactate, an indicator of metabolic failure in critical care, indicates dependence on the anaerobic partitioning of glucose, reflected by increased lactate production. In this study, we explored basal lactate levels in normal individuals and preoperative patients with the metabolic syndrome, before and after correction of glucose metabolism, with surgery and with exercise.
Methods: Fasting lactate levels and insulin sensitivity were determined during IVGTT in non-obese subjects and patients with metabolic disease prior to Roux-en-Y gastric bypass as well as 1 week, 1-3 months, 7-9 months and more than 12 months following RYGB. Subjects with the metabolic syndrome were also studied at baseline and after 9 months of exercise.
Results: Subjects with the metabolic syndrome have higher lactate (1.67 +/- 0.11 mM) than non-obese controls (1.06 +/- 0.05 mM, P< .001) and respond to a glucose/insulin challenge with higher lactates. Lactate concentrations, including basal levels, were significantly reduced a week after RYGB and remained at levels like non-obese for more than a year. The greatest improvement in fasting lactate occurred in those who were most metabolically impaired (highest lactate). Fasting lactate was also reduced by exercise in metabolically impaired subjects (by 0.21 mM, p = 0.028) (Figure 1).
Conclusion: Elevated blood lactate levels reflect metabolic impairment, correctible in the severely obese with the gastric bypass and/or exercise. These data suggest that the metabolic syndrome is caused by a signal, perhaps from the foregut, which limits entry of pyruvate into the TCA cycle.