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Early in starvation, hepatic glycogen remains available but declines; glycogen breakdown supplies much of the blood glucose during the first hours. As stores approach depletion, gluconeogenesis increases, using lactate, glycerol, and alanine as substrates. Meanwhile, adipose tissue releases fatty acids and glycerol. Fatty-acid oxidation supplies energy and helps spare glucose, while hormonal and enzyme changes direct liver metabolism toward glucose production. The brain, red blood cells, and renal medulla continue to rely on glucose at this stage. Ketone production remains limited in short-term starvation, and muscle protein breakdown contributes amino acids for gluconeogenesis. Together, these adaptations support blood glucose as the body shifts from the fed state to early fasting.