Lactate, glucose and energy metabolism in the ischemic brain (Review)

Abstract

For many decades, lactate was considered to be an end product of anaerobic glycolysis in mammalian tissues with no other function in metabolism. As determination of lactate level became a routine in hospital blood work, fluctuations in its levels were associated with situations other than oxygen lack. It was just a matter of time before elevated lactate blood levels emerged as a 'red flag' for potential malaise and frequently was blamed as the of it. Lactate and its accompanying acidosis are still considered today to be major contributors to selective neuronal damage in cerebral ischemia despite the emergence of alternative, more compelling postulates as to the causes of this damage. The attitude, especially among clinicians, has been difficult to change despite recent findings that strongly indicate lactate to be a possible beneficial intermediate in brain energy metabolism. This review revisits briefly the annals that brought about the lingering negative attitude toward lactate and expands on the more recent findings and debates that have illuminated this monocarboxylate in a different, more positive light.