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Galactose metabolism and Explanation of the Manifestations of Galactosemia
Before tackling the explanation of themanifestations of galactosemia, we must first discuss the galactose pathway. This is the galactose pathway. There are 3 major enzymes involved in the metabolism of galactose, and they are: (1) the galactokinase; (2) the galactose1phosphate uridyltransferase and; (3) the UDPgalactose4'epimerase. The first reaction is the conversion of galactose to galactose1phosphate.
Galactose is phosphorylated by the enzyme galactokinase (GALK) at the expense of 1 molecule of ATP, thereby producing galactose1phosphate and a molecule of ADP. Next, is the uridylation of galactose1phosphate toUDPgalactose catalyzed by the enzyme GALT This involves the release of glucose1phosphate, which is then readily metabolized toglucose6phosphate, for entry to the glycolytic pathway. Lastly, UDPgalactose undergoes epimerization to form UDPglucose. This is catalyzed by the enzymeUDPgalactose4'epimerase (GALE)
This reaction is reversible, so that UDPgalactose and UDPglucose are freely interconvertible. This, in fact, permits the biosynthesis of galactose from glucose, even when galactose is excluded from the diet. A deficiency in galactose1phosphate uridyl transferase (GALT) will block the formation of UDPgalactose. This will result *to the accumulation of galactose1phophate, and eventually, of galactose as well. As galactose builds up in the circulation, it can enter the lens of the eye. There, part of it is converted to galactitol (or dulcitol) by aldose reductase. Galactitol produces osmotic effects, including swelling of lens fibers that may result in cataracts.
The same process has been hypothesized to produce swelling of neurons, and subsequently, pseudotumor cerebri. The accumulation of galactose1phosphate in the liver depletes inorganic phosphate source,and so, leads to liver damage. When GALT is deficient, there would be no UDPgalactose formed. Hence, UDPglucose will be greatly decreased. It is UDPglucose, that is converted to UDPglucoronic acid, which is needed for the conjugation of bilirubin. When UDPglucose is decreased, UDPglucoronic acid will also decrease.
And only a minute fraction of bilirubin would be conjugated. Thereby, increasing the amount of unconjugated bilirubin, and ultimately, causing jaundice. When GALT is deficient, the concentration ofgalactose1phosphate increases, thereby, inhibiting phosphoglucomutase. Phosophoglucomutase catalyzes the interconversion of glucose6phosphate and glucose1phosphate. Hence, there is hypoglycemia when GALT is deficient. During hypoglycemia, the body will try to compensate by gluconeogenesis.
In gluconeogenesis, new glucose is formed from precursors other than carbohydrates. Among these precursors are amino acids. Ammonia is the product of amino acid metabolism. Hence, during hypoglycemia, there would be an increase in serum ammonia. When there is a defect in energy metabolism, such as in galactosemia, the bactericidal activity of white blood cells is decreased. Hence, there is bacterial overgrowth or infection Vomiting and diarrhea are due tobacterial gas formation in the intestines.