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It is an X-linked recessive disorder that results in defective glucose-6-phosphate dehydrogenase enzyme. [1] Glucose-6-phosphate dehydrogenase is an enzyme which protects red blood cells, which carry oxygen from the lungs to tissues throughout the body. A defect of the enzyme results in the premature breakdown of red blood cells.
The reaction is the second NADPH releasing reaction in the pentose phosphate pathway, the first being catalyzed by glucose-6-phosphate dehydrogenase. 3-keto-6-phosphogluconate then rapidly (in an irreversible reaction) decarboxylates to CO 2 and ribulose-5-phosphate, which is the precursor to many vital metabolic processes. [citation needed]
5' Nucleotidase (5NT) is a glycoprotein found throughout the body, in the cytoplasmic membrane, catalyzing the conversion to inorganic phosphates from nucleoside-5-phosphate. Its level is raised in conditions such as obstructive jaundice, parenchymal liver disease, liver metastases, and bone disease. [6]
G6PD converts G6P into 6-phosphoglucono-δ-lactone and is the rate-limiting enzyme of the pentose phosphate pathway. Thus, regulation of G6PD has downstream consequences for the activity of the rest of the pentose phosphate pathway. Glucose-6-phosphate dehydrogenase is stimulated by its substrate G6P.
There are two forms of glucose-6-phosphate dehydrogenase. G form is X-linked and H form, encoded by this gene, is autosomally linked. This H form shows activity with other hexose-6-phosphates, especially galactose-6-phosphate, whereas the G form is specific for glucose-6-phosphate. Both forms are present in most tissues, but H form is not found ...
6-Phosphogluconolactonase (EC 3.1.1.31, 6PGL, PGLS, systematic name 6-phospho-D-glucono-1,5-lactone lactonohydrolase) is a cytosolic enzyme found in all organisms that catalyzes the hydrolysis of 6-phosphogluconolactone to 6-phosphogluconic acid in the oxidative phase of the pentose phosphate pathway: [2] 6-phospho-D-glucono-1,5-lactone + H 2 O ...
In particular increased fructose-1,6-bisphosphate accumulation can have inhibitory effects on glucose-6-phosphate dehydrogenase, an essential enzyme of this pathway. [6] Lactate accumulation has also been noted in some patients, potentially linked to reciprocal stimulation of pyruvate kinase, a key enzyme in lactic acid fermentation. [8]
The symptoms of an episode of diabetic ketoacidosis usually evolve over a period of about 24 hours. Predominant symptoms are nausea and vomiting, pronounced thirst, excessive urine production and abdominal pain that may be severe. [13] [14] In severe DKA, breathing becomes rapid and of a deep, gasping character, called "Kussmaul breathing".