Fed, fasting and starvation states !

The body switches fuel with the time since the last meal: it stores in the fed state and draws on reserves while fasting.

Updated 2026-11-01

Key facts

The insulin/glucagon ratio rules: high after a meal (store), low in fasting (mobilise).
Liver glycogen keeps blood glucose up for the first hours and runs out around 24 hours of fasting; after that glucose comes from gluconeogenesis.
In prolonged starvation the brain draws much of its energy from ketone bodies, which lowers the glucose need and spares muscle protein.
The red cell (no mitochondria) always depends on glucose; muscle and heart prefer fatty acids in fasting.
The switches work at three levels: allosteric (seconds), enzyme phosphorylation (minutes) and gene expression (hours to days).

Fed state (0–4 h): insulin rises. The liver takes up glucose through GLUT2 and glucokinase, fills glycogen and turns the surplus into fatty acids exported in VLDL; muscle and fat take up glucose through GLUT4, and adipose lipoprotein lipase stores the triglycerides.
Post-absorptive (4–24 h): insulin falls and glucagon rises. The liver breaks down glycogen (glycogen phosphorylase) and starts gluconeogenesis; adipose tissue releases fatty acids through hormone-sensitive lipase.
Early fasting (1–3 days): with no liver glycogen, glucose comes from lactate (Cori cycle), glycerol and muscle alanine (glucose–alanine cycle); the liver oxidises fatty acids and makes ketone bodies.
Starvation (over 3 days): ketones rise sharply and the brain uses them; muscle proteolysis slows and the kidney adds glucose made from glutamine. T3 and leptin fall and energy expenditure drops.
Key fasting switches: PKA phosphorylates and inactivates glycogen synthase, liver pyruvate kinase and acetyl-CoA carboxylase, and fructose 2,6-bisphosphate falls; cortisol and glucagon induce PEPCK and glucose 6-phosphatase.
Survival in starvation depends mostly on the fat reserve; death comes when protein loss hits the breathing muscles, heart and immunity.

Defects of gluconeogenesis, glycogen or beta-oxidation show up as fasting hypoglycaemia (von Gierke disease, MCAD deficiency).
Refeeding a malnourished patient with a lot of carbohydrate triggers insulin and drives phosphate, potassium and magnesium into cells: refeeding syndrome.
Kwashiorkor and marasmus are the severe forms of childhood malnutrition; diabetic ketoacidosis is a metabolic fast with high glucose because insulin is missing.

Think of the answer, then tap the question to see it.

What keeps blood glucose up during the first hours of fasting?

Liver glycogen, which runs out around 24 hours; after that glucose comes from gluconeogenesis.

Why does prolonged starvation use less muscle protein than a 2-day fast?

Because the brain switches to ketone bodies and needs less glucose, so less gluconeogenesis from amino acids is required.

Which cell always depends on glucose, even in starvation?

The red blood cell, because it has no mitochondria and makes ATP only by glycolysis.

Which hormone dominates the fed state, and what does it do to adipose lipoprotein lipase?

Insulin; it raises adipose lipoprotein lipase so the triglycerides of chylomicrons and VLDL are stored.

Educational information, not medical advice. For any symptom, see a health professional.

Sources: Hypoglycemia: MedlinePlus (MedlinePlus, US National Library of Medicine, 2026); Malnutrition: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2026); INS: Insulin (human) (UniProt, 2026); GCG: Pro-glucagon (human) (UniProt, 2026); Textbook of Biochemistry for Medical Students, 6th ed. (Jaypee Brothers Medical Publishers (Vasudevan DM, Sreekumari S, Vaidyanathan K), 2011).

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Representative model, for educational purposes only.