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Phenylketonuria (PKU) is a protein metabolism disorder characterized by high blood levels of the amino acid phenylalanine. This results from a mutation in the gene responsible for phenylalanine hydroxylase, an enzyme that converts phenylalanine into tyrosine. When this enzyme is deficient, phenylalanine builds up in the blood, leading to symptoms such as vomiting, rashes, seizures, growth deficiency, and severe mental retardation. An early diagnosis and a diet restricting phenylalanine intake...
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Related Experiment Video

Updated: Oct 21, 2025

Measuring Lactase Enzymatic Activity in the Teaching Lab
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[Hyperlactataemia].

Ronan Mg Berg1, Troels E Jeppesen, Milan Mohammad

  • 1ronan@sund.ku.dk.

Ugeskrift for Laeger
|September 3, 2021
PubMed
Summary
This summary is machine-generated.

Blood lactate levels do not directly indicate lactic acid production. Elevated blood lactate can occur without increased production, suggesting "lactic acidosis" is a misnomer. The term "hyperlactataemia-associated metabolic acidosis" is proposed instead.

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Area of Science:

  • Biochemistry
  • Physiology
  • Medical Terminology

Background:

  • The common assumption that blood lactate directly reflects tissue lactic acid production is scientifically inaccurate.
  • Lactate plays a role in intracellular pH buffering by transporting protons (H+) to the extracellular space.
  • Elevated blood lactate can occur independently of increased lactate production.

Purpose of the Study:

  • To challenge the conventional understanding of blood lactate's role in metabolic acidosis.
  • To clarify the physiological mechanisms behind elevated blood lactate.
  • To propose a more accurate term for metabolic acidosis associated with high lactate levels.

Main Methods:

  • Review of existing biochemical and physiological literature on lactate metabolism and acid-base balance.
  • Analysis of the relationship between lactate production, intracellular pH, and extracellular buffering.
  • Critique of the term "lactic acidosis" based on mechanistic understanding.

Main Results:

  • Lactate is formed from pyruvate and acts as a buffer, not solely a product of anaerobic glycolysis.
  • Elevated blood lactate (hyperlactataemia) can result from buffering mechanisms rather than increased production.
  • The term "lactic acidosis" incorrectly implies lactate production as the primary cause of acidosis.

Conclusions:

  • The term "lactic acidosis" is misleading and should be abandoned.
  • Metabolic acidosis associated with elevated lactate should be referred to as "hyperlactataemia-associated metabolic acidosis".
  • This revised terminology more accurately reflects the underlying pathophysiology.