GLOSSARY

Gluconeogenic Precursor include lactate, glycerol and certain amino acids.

Gluconeogenesis makes glucose from lactate, glycerol and some amino acids, with major hepatic and context-dependent renal contributions. It costs energy and is not a simple reversal of all glycolysis. Even-chain fatty-acid acetyl units do not normally provide direct net human glucose; glycerol and other routes require separate treatment. Endogenous production does not automatically eliminate exercise fueling needs, particularly at high demand, and precursor availability is only one part of pathway regulation.

Endogenous glucose production includes glycogen breakdown and new synthesis rather than gluconeogenesis alone. Cellular production and release into blood differ because local use occurs. Contributions change with fasting and activity. Tracers and pool definitions matter; a stable blood glucose can coexist with high turnover. It does not mean fuel is unnecessary or glucose use has stopped, nor does one circulating concentration isolate hepatic versus renal contributions to supply.

Alanine can move carbon and nitrogen between muscle and liver; hepatic carbon supports glucose pathways while nitrogen enters disposal handling. The alanine cycle differs from the lactate cycle despite interorgan links. Recycling does not replace adequate energy and protein. Increasing one amino acid does not guarantee useful activation or prevent muscle loss under every condition. Carbon routing, nitrogen transfer and net tissue balance are connected but require separate interpretation rather than one supplement inference.