Biochemistry Study Guide 2026

When acetyl-CoA from fatty acid oxidation exceeds the capacity of the TCA cycle (e.g., during fasting), the liver converts excess acetyl-CoA into ketone bodies (acetoacetate, β-hydroxybutyrate, acetone).

Humans lack uricase and therefore cannot convert uric acid to allantoin as most other mammals do; uric acid is thus the terminal product of purine breakdown, and its accumulation causes gout.

During fasting, when the body's glycogen stores are depleted, gluconeogenesis becomes the primary process to synthesize new glucose. This pathway, mainly in the liver, produces glucose from non-carbohydrate precursors like amino acids, lactate, and glycerol. Gluconeogenesis is vital for maintaining blood glucose levels to supply energy to glucose-dependent tissues, such as the brain.

Methotrexate competitively inhibits DHFR, preventing reduction of dihydrofolate to tetrahydrofolate; without THF cofactors, one-carbon transfer reactions required for both purine ring synthesis and dTMP formation are blocked.

The primary function of the phospholipid bilayer in the cell membrane is to form a selective barrier that controls the movement of molecules into and out of the cell. Its hydrophobic interior prevents the free passage of most polar molecules, while its overall structure maintains cellular integrity and homeostasis. This selectivity is vital for cell function.

Passive transport describes the movement of substances across a cell membrane down their concentration gradient, meaning from an area of higher concentration to an area of lower concentration. This process does not require the cell to expend metabolic energy (ATP) because it is driven by the natural tendency of molecules to spread out. Examples include simple diffusion and facilitated diffusion.