Figure 1.

During sepsis, the production of lactate increases, and then it crosses cell membrane and enters blood circulation, which will lead to accumulation when gluconeogenesis is impaired because of the liver/kidney injury, the increase of gluconeogenesis is not sufficient to deal with elevated lactate, or microcirculation disturbance leads to the retention of lactate, finally resulting in lactic acidosis. Meanwhile, pyruvate entering TCA cycle will decrease due to increasing glycolysis, without lactate shuttle. Further, the consumption of protons will decrease, because of the decrease of transfer of MAS and transfer of pyruvate into mitochondria. (A color version of this figure is available in the online journal.)