BI3.1-6 | Chemistry and Metabolism of Carbohydrates — Summary & Reflection

REFLECT

Now that you've covered all of carbohydrate metabolism, test your understanding with these clinical reasoning exercises:

1. Trace the glucose molecule: You eat a roti. Trace the journey of one glucose molecule from your mouth to an ATP molecule in your quadriceps muscle. Name every enzyme at the key checkpoints (digestion, absorption, glycolysis, pyruvate dehydrogenase, TCA, ETC).

1. The 24-hour fast: A medical student skips dinner and breakfast (18-hour fast). Draw a timeline showing: (a) when liver glycogenolysis kicks in, (b) when gluconeogenesis becomes the primary source, (c) which hormones are driving each phase, (d) which precursors are being used for gluconeogenesis.

1. DKA vs HHS: A Type 1 diabetic (22 years old) and a Type 2 diabetic (65 years old) both present with blood glucose > 500 mg/dL. Explain why the Type 1 patient develops ketoacidosis but the Type 2 patient doesn't. Which emergency is more lethal, and why?

1. The lab puzzle: A neonate has a positive Benedict's test (reducing sugar in urine) but NEGATIVE glucose oxidase test. What is the most likely reducing sugar present, and what diagnosis should you suspect?

1. Cross-subject connection: Red blood cells have no mitochondria. Explain why they depend entirely on glycolysis, why they produce lactate instead of CO₂ + H₂O, and where the lactate goes (name the cycle).

KEY TAKEAWAYS

Key takeaways — your study checklist:

1. Classification (BI3.1): Monosaccharides (glucose, fructose, galactose), disaccharides (sucrose, lactose, maltose), polysaccharides (starch, glycogen, cellulose, GAGs). Three roles: energy, storage, structural.
2. Digestion & absorption (BI3.2): Salivary amylase → pancreatic amylase → brush border enzymes (maltase, sucrase, lactase). Absorption: SGLT-1 (glucose/galactose, active), GLUT-5 (fructose, passive). GLUT-4 is insulin-dependent (muscle/fat). ORS exploits SGLT-1.
3. Glycolysis (BI3.3): 10 steps, 2 phases. Net: 2 ATP + 2 NADH + 2 pyruvate. Rate-limiting: PFK-1 (regulated by ATP, AMP, F-2,6-BP). Occurs in cytoplasm. Only ATP source for RBCs.
4. TCA cycle (BI3.3): Mitochondrial matrix. Acetyl-CoA → 2 CO₂ + 3 NADH + 1 FADH₂ + 1 GTP per turn. Total per glucose: ~30-32 ATP. Rate-limiting: isocitrate dehydrogenase.
5. Gluconeogenesis (BI3.3): Liver/kidney. Precursors: lactate (Cori cycle), alanine (glucose-alanine cycle), glycerol. NOT from fatty acids. Three bypass enzymes. Reciprocally regulated with glycolysis.
6. Glycogen metabolism (BI3.3): Synthesis (glycogen synthase), breakdown (glycogen phosphorylase). Insulin = synthesis, glucagon/epinephrine = breakdown. GSDs: Von Gierke (G6Pase), McArdle (muscle phosphorylase), Pompe (lysosomal).
7. HMP shunt (BI3.3): Produces NADPH + ribose-5-phosphate. G6PD deficiency → haemolytic anaemia (oxidative stress triggers).
8. Minor pathways (BI3.4): Fructose metabolism (aldolase B deficiency → HFI), galactose metabolism (transferase deficiency → galactosaemia), polyol pathway (diabetic complications — cataracts, neuropathy).
9. Glucose homeostasis (BI3.5): Insulin (lowers) vs glucagon (raises). Type 1 DM (autoimmune, DKA), Type 2 DM (insulin resistance, HHS). Chronic damage: glycation/AGEs, polyol, PKC, oxidative stress.
10. Lab investigations (BI3.6): FPG (≥126 = DM), OGTT (≥200 at 2h), HbA1c (≥6.5%), lactate (anaerobic glycolysis marker), Benedict's vs glucose oxidase (non-glucose reducing sugars → galactosaemia).