Carbohydrate Metabolism MCQs

ASPARTATE → (ASPARTATE TRANSAMINASE, AST/GOT) → OXALOACETATE + GLUTAMATE. Reaction: aspartate + alpha-KG → OAA + glutamate. OAA = KEY GLUCONEOGENIC INTERMEDIATE → (PEPCK) → PEP → upstream gluconeogenesis. ASPARTATE provides a DIRECT route to OAA: bypasses the pyruvate carboxylase step (unlike alanine which must go pyruvate → OAA via pyruvate carboxylase). ASPARTATE ALSO functions in: UREA CYCLE (carries nitrogen as aspartate → argininosuccinate), MALATE-ASPARTATE SHUTTLE (transfers reducing equivalents), PURINE SYNTHESIS. Clinically: ELEVATED SERUM AST = hepatocyte damage (AST abundant in hepatocyte mitochondria and cytoplasm).\ \ 📹 [VIDEO LINK]

ASPARTATE TRANSAMINASE (AST, GOT): aspartate + alpha-ketoglutarate ⇌ OAA + GLUTAMATE. This REVERSIBLE TRANSAMINATION converts aspartate → OAA (gluconeogenic precursor). Requires PLP (vitamin B6). CLINICAL SIGNIFICANCE: ELEVATED SERUM AST in: MI (cardiac mitochondrial AST released), LIVER DISEASE (hepatocyte damage), HAEMOLYSIS. AST:ALT > 2 = ALCOHOLIC HEPATITIS (mitochondrial damage preferentially releases mitochondrial AST). Compare: PYRUVATE CARBOXYLASE = converts pyruvate → OAA (different reaction, requires biotin + ATP, mitochondrial). Both produce OAA for gluconeogenesis but from DIFFERENT SUBSTRATES (aspartate vs pyruvate).\ \ 📹 [VIDEO LINK]

INSULIN-INDUCED HYPOGLYCAEMIA → GLUCAGON (IM or SC) = first-line treatment in an UNCONSCIOUS patient who cannot receive oral glucose and may not have IV access. GLUCAGON mechanism: (1) Activates GLYCOGEN PHOSPHORYLASE in LIVER → glycogenolysis → glucose-1-P → glucose-6-P → (G6Pase) → FREE GLUCOSE released into blood. (2) Activates GLUCONEOGENESIS via cAMP/PKA pathway. Result: RAPID BLOOD GLUCOSE ELEVATION within 10-15 minutes. Glucagon kits available for home use. Also: IV DEXTROSE (D50W) if IV access available. CAUTION: glucagon is ineffective if GLYCOGEN STORES ARE DEPLETED (prolonged fasting, chronic alcoholism, starvation) → IV dextrose essential in those cases.\ \ 📹 [VIDEO LINK]