In organs where glucose is the major substrate for oxidation, a variable fraction of the glucose uptake can be diverted to lactate depending on the metabolic state of the tissue. In tis sues or metabolic states where pyruvate oxidation is absent or impaired, pyruvate is diverted to lactate and released so as to recycle the NAD to support glycolysis and the generation of ATP to support cellular metabolic work. In erythrocytes pyruvate always terminates in lactate. They lack mitochondria and thus cannot oxidize pyruvate. This is true of some skeletal muscle, particularly the white fibers. During states of high-work output they mobilize muscle glycogen stores. Because they lack glucose-6-phosphatase the glucose-6-phosphate mobilized from glycogen traverses down the glycolytic pathway and combined with the relatively low rates of pyruvate oxidation due to lower mitochondrial oxidative capacity, lactate is released. The need for ATP formation may exceed the rate at which oxygen is delivered. In those tissues they rely on anaerobic glycolysis to support metabolism (eg, tumors, retina and renal medulla, skin). Lactate production is also increased in septic shock secondary to both impaired oxygen delivery and shifts on metabolic capacity due to cellular injury. Other tissues like the brain that normally derive much of their energy from glucose oxidation produce some lactate (3-5% of total glycolytic flux) because of the high glycolytic rates. The liver, kidneys, oxidative skeletal muscle, and heart have very high oxidative capacity to oxidize multiple fuels. They normally take up lactate and oxidize it, but can produce it under hypoxic conditions. When lactate production is high, as in vigorous exercise, septic shock, and cancer cachexia, lactate is used in the liver for gluconeogenesis (see Chapter 19), leading to an increase in metabolic rate to provide the ATP and GTP needed. This increase may contribute to the increase in metabolic rate after cessation of vigorous exercise.

Under some states lactate can be directly transported into the mitochondria to generate pyruvate and NADH. This allows for the transfer of reducing equivalents (eg, NADH) from the cytosol into the mitochondrion for the electron transport chain in addition to the glycerophosphate and malate-aspartate  shuttles.

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مواضيع ذات صلة

Cyclic AMP Integrates The Regulation of Glycogenolysis & Glycogenesis

Glycogenolysis is not the Reverse of Glycogenesis, it is A Separate Pathway

Glycogenesis Occurs Mainly in Muscle & Liver

The Oxidation of Pyruvate to Acetyl-COA is The Irreversible Route from Glycolysis to The Citric Acid Cycle

Glycolysis is Regulated at Three Nonequilibrium Reactions

Glycolysis Constitutes The Main Pathway of Glucose Utilization

Glycolysis Can Function Under Anaerobic Conditions

Regulation of the Citric Acid Cycle Depends Primarily on a Supply of Oxidized Cofactors

The Citric Acid Cycle Takes Part in Fatty Acid Synthesis

The Citric Acid Cycle Takes Part in Gluconeogenesis, Transamination, & Deamination

Reactions of The Citric Acid Cycle Generate Reducing Equivalents & CO2

The Citric Acid Cycle Provides Substrates for The Respiratory Chain