Fructose is a ketohexose (6-carbon ketone sugar), while glucose, galactose are aldohexoses, and ribose is a pentose.

The Warburg effect describes the metabolic shift in cancer cells toward anaerobic glycolysis, producing lactate even in the presence of oxygen, resulting in high glucose consumption.

BCAA metabolism produces acetyl-CoA and increases the acetyl-CoA/CoA ratio, which inhibits pyruvate dehydrogenase, reducing glucose oxidation and affecting carbohydrate metabolism.

In muscle, phosphorylase a (phosphorylated form) is active. It is further activated by AMP, which signals energy depletion during exercise.

G6PD deficiency reduces NADPH production, decreasing reduced glutathione (GSH) levels. GSH protects RBC membranes from oxidative damage, so its depletion leads to hemolysis.

After 24-48 hours of fasting, muscle glycogen is depleted. Muscle shifts to oxidizing amino acids (from proteolysis) and utilizing ketone bodies produced by the liver.

Glucose-6-phosphatase catalyzes the dephosphorylation of glucose-6-phosphate to free glucose, which is the final and rate-limiting step of hepatic gluconeogenesis.

Von Gierke disease causes hepatomegaly, lactic acidosis, and hyperuricemia due to glucose-6-phosphatase deficiency, leading to increased glycolysis and purine metabolism.

Glucose-1-phosphate is converted to UDP-glucose by UDP-glucose pyrophosphorylase, which is the activated form used by glycogen synthase for glycogen synthesis.

Von Gierke disease (GSD Type I) involves glucose-6-phosphatase deficiency, leading to impaired glucose release. However, alternative glucose production through gluconeogenesis and pentose phosphate pathway increases.