Entrance Exams
Govt. Exams
Essential fructosuria results from fructokinase deficiency. It is benign because fructose is simply excreted in urine without accumulating in tissues or causing metabolic harm.
Through the non-oxidative phase of the pentose phosphate pathway, sugars are rearranged to produce fructose-6-phosphate and glyceraldehyde-3-phosphate, which directly enter glycolysis.
Glucuronic acid, derived from glucose, is a key component of glycosaminoglycans like heparin, hyaluronic acid, and chondroitin sulfate, providing their acidic properties.
Ethanol metabolism consumes NAD+, reducing the NAD+/NADH ratio. This inhibits NAD+-dependent dehydrogenases including those in gluconeogenesis and lactate oxidation, leading to lactate accumulation.
The Cori cycle describes lactate produced in muscles during anaerobic glycolysis being transported to the liver where it is converted back to glucose via gluconeogenesis, which is then returned to muscles.
Fructokinase phosphorylates fructose to fructose-1-phosphate in the liver. This bypasses the rate-limiting phosphofructokinase step, making fructose metabolism less regulated.
Sucrose (α-glucose + β-fructose) is a non-reducing sugar because both anomeric carbons are involved in the 1,2-glycosidic linkage, making it unable to reduce Benedict's reagent.
Complete oxidation of glucose yields approximately 30-32 ATP molecules when accounting for the cost of transporting NADH across the mitochondrial membrane (P/O ratio of 2.5 for NADH and 1.5 for FADH2).
Phosphoglucose isomerase catalyzes the reversible isomerization of glucose-6-phosphate to fructose-6-phosphate, the second step of glycolysis.
Type 2 diabetes is characterized by insulin resistance (defective glucose uptake and utilization) and progressive β-cell dysfunction. Impaired fasting glucose (100-125 mg/dL) is a prediabetic state. Fasting glucose ≥126 mg/dL on 2 occasions is diagnostic for diabetes.