A patient is found to excrete large amounts of fructose in his urine but his dietary fructose can still participate in glycogen synthesis. The latter is due to the activity of -
A) Hexokinase
B) Fructokinase
C) Aldolase B
D) UDP-Hexose 4-epimerase
E) Aldose Reductase
A patient is found to excrete large amounts of fructose in his urine but his dietary fructose can still participate in glycogen synthesis. The latter is due to the activity of -
A) Hexokinase
B) Fructokinase
C) Aldolase B
D) UDP-Hexose 4-epimerase
E) Aldose Reductase
A patient is found to excrete large amounts of fructose in his urine but his dietary fructose can still participate in glycogen synthesis. The latter is due to the activity of -
A) Hexokinase
B) Fructokinase
C) Aldolase B
D) UDP-Hexose 4-epimerase
E) Aldose Reductase
A patient is found to excrete large amounts of fructose in his urine but his dietary fructose can still participate in glycogen synthesis. The latter is due to the activity of -
A) Hexokinase
B) Fructokinase
C) Aldolase B
D) UDP-Hexose 4-epimerase
E) Aldose Reductase
not sure if it is fructokinase or hexokinase,i am assuming its location dependent.
as the fructose is uptaken by the intestine,via blood when fructose enters liver or kidney fructose is phosphorylated and trapped by the FRUCTOKINASE and participate in glycogensis,but when it enters other tissues say skeletal muscle HEXOKINASE phosphorylates the fructose and participate in glycogen synthesis.
This was a little tricky question but here is the explanation for it -
The clinical vignette states that the patient secretes large amounts of fructose in his urine. This leads to a conclusion that the patient has some defect in the fructose metabolic pathway leading to fructosuria. However, his dietary fructose can still participate in glycogen synthesis.
Fructokinase deficiency causes essential fructosuria, an asympotmatic disorder since the fructose is absorbed in the gut and excreted unchanged in the urine. In a normal liver, a SMALL Amount of fructose is phosphorylated to F6P which is a glycolytic intermediate. With fructokinase deficiency, the metabolism of fructose to F6P by the enzyme hexokinase is the principle method of metabolism of dietary fructose. (look at the diagram and follow along). However, this pathway of hexokinase is not significant in normal individuals but only in fructokinase deficient patients it becomes the major metabolic pathway of fructose.
Aldolase B can use F1P and F1,6BP as substrates but it is not directly involved in glycogen synthetic pathway.
Aldose reductase is the enzyme that converts glucose to sorbitol (can cause cataracts in diabetics due to high levels of glucose).
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