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The glycerol phosphate shuttle was first characterized as a major route of mitochondrial hydride transport in the flight muscles of blow flies. [5] [6] It was initially believed that the system would be inactive in mammals due to the predominance of lactate dehydrogenase activity over glycerol-3-phosphate dehydrogenase 1 (GPD1) [5] [7] until high GPD1 and GPD2 activity were demonstrated in ...
Glycerol 1-phosphate, sometimes called as D-glycerol 3-phosphate, is the enantiomer of glycerol 3-phosphate. Eukaryotes use the 3-phosphate, or L-configuration, for glycerolipid backbone. The 1-phosphate is specifically found in archeal lipids. [5]
The two main systems in humans are the glycerol phosphate shuttle and the malate-aspartate shuttle. The malate/a-ketoglutarate antiporter functions move electrons while the aspartate/glutamate antiporter moves amino groups. This allows the mitochondria to receive the substrates that it needs for its functionality in an efficient manner. [1]
Glycerol-3-phosphate dehydrogenase (GPDH) is an enzyme that catalyzes the reversible redox conversion of dihydroxyacetone phosphate (a.k.a. glycerone phosphate, outdated) to sn-glycerol 3-phosphate. [2] Glycerol-3-phosphate dehydrogenase serves as a major link between carbohydrate metabolism and lipid metabolism.
Compare this to the glycerol 3-phosphate shuttle, which reduces FAD + to produce FADH 2, donates electrons to the quinone pool in the electron transport chain, and is capable of generating only 2 ATPs per NADH generated in glycolysis (ultimately resulting in a net gain of 36 ATPs per glucose metabolized).
In the glycerol phosphate shuttle electrons from cytosolic NADH are transferred to dihydroxyacetone to form glycerol-3-phosphate which readily traverses the outer mitochondrial membrane. Glycerol-3-phosphate is then reoxidized to dihydroxyacetone, donating its electrons to FAD instead of NAD +. [45]
The encoded cytosolic protein and mitochondrial glycerol-3-phosphate dehydrogenase also form a glycerol phosphate shuttle that facilitates the transfer of reducing equivalents from the cytosol to mitochondria. Mutations in this gene are a cause of transient infantile hypertriglyceridemia.
When dihydroxyacetone phosphate is produced, glyceroneogenesis will branch off from gluconeogenesis. [1] With the expense of NADH, dihydroxyacetone phosphate will convert to glycerol 3-phosphate, which is the final product of glyceroneogenesis. In addition, triglyceride can be generated by re-esterifying 3 fatty acid chains on glycerol 3-phosphate.