A. O-α-D-glucopyranosyl-(1->6)-α -D- fructofuranoside
B. O-β-D-glucopyranosyl-(1->6)-α -D- fructofuranoside
C. O-α-D-glucopyranosyl-(1->2)-β -D-fructofuranoside
D. O-α-D-glucopyranosyl-(1->2)-α -D-fructofuranoside
E. None of the above.
The correct answer is C- O-α D-glucopyranosyl-(1->2)-β -D-fructofuranoside. The onset of symptoms after ingestion of juice (fructose or fructose containing diet) is a sign of hereditary fructose Intolerance’.
Hereditary fructose intolerance is caused by deficiency of Aldolase B, the enzyme required for the metabolism of fructose. These patients are healthy and asymptomatic until fructose or sucrose (table sugar) is ingested (usually from fruit, sweetened cereal, or sucrose-containing formula). Elimination of dietary fructose is both a compulsory and therapeutic step.
In patients who are ill, elimination may also serve as a diagnostic test because all symptoms should completely resolve. With this treatment, as the patient matures, symptoms become milder, even after fructose ingestion, and the long-term prognosis is good.
Table sugar (sucrose) is a source of fructose and in Sucrose, the anomeric carbon atoms of a glucose unit and a fructose unit are joined; the configuration of this glycosidic linkage is α-for glucose and β-for fructose (figure).
Figure- Structure of sucrose
Sucrose can be cleaved into its component monosaccharides by the enzyme sucrase.
An overview of properties of sucrose
- Sucrose has no free reactive group because the anomeric carbons of both monosaccharides units are involved in the glycosidic bond. Therefore, sucrose neither shows reducing nor mutarotation characters.
- Sucrose is called invert sugar because the optical activity of sucrose (dextrorotatory) is inverted after hydrolysis (by an acid or an enzyme (invertase or sucrase) into an equimolar mixture of its two components glucose (+52.5) and fructose (-92.5) and the optical activity of the mixture becomes levorotatory.
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