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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-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is an enzyme that catalyzes the reversible redox conversion of dihydroxyacetone phosphate (a.k.a. glycerone phosphate, outdated) to sn-glycerol 3-phosphate.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.
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]
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.
Glycerol 3-phosphate is synthesized by reducing dihydroxyacetone phosphate (DHAP), an intermediate in glycolysis. The reduction is catalyzed by glycerol-3-phosphate dehydrogenase. DHAP and thus glycerol 3-phosphate can also be synthesized from amino acids and citric acid cycle intermediates via the glyceroneogenesis pathway. + NAD(P)H + H + → ...
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).
The head group substituent glycerol is bonded through a phosphomonoester. It is the precursor of surfactant and its presence (>0.3) in the amniotic fluid of the newborn indicates fetal lung maturity. Approximately 98% of alveolar wall surface area is due to the presence of type I cells, with type II cells producing pulmonary surfactant covering ...
Schematic demonstrating mitochondrial fatty acid beta-oxidation and effects of long-chain 3-hydroxyacyl-coenzyme A dehydrogenase deficiency, LCHAD deficiency. Mitochondrial trifunctional protein (MTP) is a protein attached to the inner mitochondrial membrane which catalyzes three out of the four steps in beta oxidation.