Govt Exams
GLUT4 is the insulin-responsive glucose transporter present in skeletal muscle and adipose tissue. Insulin signaling causes GLUT4 translocation to the cell membrane, increasing glucose uptake.
Phosphofructokinase-1 (PFK-1) is the rate-limiting enzyme of glycolysis. It is inhibited by ATP and citrate (signals of sufficient energy) and activated by AMP and ADP (signals of energy depletion).
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.
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.
The oxidative phase of PPP generates 2 NADPH per glucose-6-phosphate, essential for fatty acid synthesis, cholesterol synthesis, and antioxidant defense (glutathione reduction). This is particularly important in adipose tissue, liver, and RBCs.
Cellulose contains β(1→4) glycosidic bonds linking glucose units, making it indigestible to humans (no cellulase enzyme). Starch contains α(1→4) bonds, which are digestible.