Biochem

Lacotse intolerance is experienced by a large portion of adults, when they lose the enzyme, lactase that is nessesary for the body to digest lactose. However, this doesn't mean that the body loses the ability to digest lactose, rather lactobacilli in the intestins are capable of digesting lactose. However, as a biproduct of lactose digestion they genrate gas and other discomfort experienced.

Fructose enters glycolysis in the liver. It is first phosphorilated by fructokinase and ATP to produce Fructose-1-phosphate. This is a determaning step as it cannot be reversed. Next F-1-P is converted with Fructose-1-phosphate aldolase to yeild Glyceraldehde + Dihydroxyacetone phosphate. Glyceraldehyde is converted into Glyceraldehyde-3-phospate by Triose Kinase. Dihydroxyacetone phosphate can also be converted into G-3-P.

Galactose undergoes 4 steps,

• 1) Galactose is phosphorilated by galactokinase into Galactose-1-phosphate.
• 2) G-1-P combines with UDP-glucose (w/ a uridine residue) by Galactose-1-phosphate uridyl transferace to produces UDP-galactose + uridine and a Glucose-1-phosphate.
• 3)UDP-galactose + uridine is then converted by UDP-galactose 4-epimerase into UDP-glucose. UDP-Glucose+uridien can then cype back to step to.
• 4)Glucose-1-phosphat is "mutated" by phosphoglucomutase to form Glucose-6-phosphate.

• It is caused when any of the enzymes involved in galatose entry is defective.
• 1)In galactokinase deficiancy galactosemia, the build up of galactose concentration in the blood an urine. affected individuals develope cataracts in infancy, when the galactose metabolite galactitol builds up in the lens. Diet restrictions can lessen the severity.
• 2) In transferase-deficiancy galactosemia, is more seriouse and is characterized by poor growth in childhood, speach abnormality, mental deficiency and liver damage. Even whin galactose is withheld from the diet it can still be fatal.
• 3)Epimerase-deficiency galactosemia leads to similar symptoms, but is less severe when dietary galactose is controled.