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[Biochemistry](https://durgical.com/en/biochemistry/) · Topic

# 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).

## In detail

- 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.

**Also called**
Metabolic integration, Fed–fast cycle

## Clinical notes

- 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.

## Pathways

- [Glycolysis](https://durgical.com/en/biochemistry/pathways/glycolysis/)
- [Gluconeogenesis](https://durgical.com/en/biochemistry/pathways/gluconeogenesis/)
- [Glycogen metabolism](https://durgical.com/en/biochemistry/pathways/glycogen-metabolism/)
- [Fatty acid synthesis (lipogenesis)](https://durgical.com/en/biochemistry/pathways/fatty-acid-synthesis/)
- [Fatty acid β-oxidation](https://durgical.com/en/biochemistry/pathways/fatty-acid-oxidation/)
- [Ketogenesis (ketone body synthesis)](https://durgical.com/en/biochemistry/pathways/ketogenesis/)

## Related conditions

- [Kwashiorkor](https://durgical.com/en/conditions/kwashiorkor/)
- [Marasmus](https://durgical.com/en/conditions/marasmus/)
- [Von Gierke disease (glycogen storage disease type I)](https://durgical.com/en/conditions/von-gierke-disease/)
- [Medium-chain acyl-CoA dehydrogenase (MCAD) deficiency](https://durgical.com/en/conditions/medium-chain-acyl-coa-dehydrogenase-deficiency/)
- [Diabetic ketoacidosis](https://durgical.com/en/conditions/diabetic-ketoacidosis/)

## Related

- [Insulin signalling](https://durgical.com/en/biochemistry/topics/insulin-signalling/)
- [Glucagon signalling](https://durgical.com/en/biochemistry/topics/glucagon-signalling/)
- [Cori cycle](https://durgical.com/en/biochemistry/topics/cori-cycle/)
- [Glucose–alanine cycle](https://durgical.com/en/biochemistry/topics/glucose-alanine-cycle/)
- [Hormone-sensitive lipase (HSL)](https://durgical.com/en/biochemistry/enzymes/hormone-sensitive-lipase/)
- [Lipoprotein lipase (LPL)](https://durgical.com/en/biochemistry/enzymes/lipoprotein-lipase/)
- [β-Hydroxybutyrate](https://durgical.com/en/biochemistry/molecules/hydroxybutyrate/)
- [Glycogen](https://durgical.com/en/biochemistry/molecules/glycogen/)
- [Glucose](https://durgical.com/en/biochemistry/molecules/glucose/)
- [Protein kinase A (PKA)](https://durgical.com/en/biochemistry/enzymes/protein-kinase-a/)
- [Exercise metabolism](https://durgical.com/en/biochemistry/topics/exercise-metabolism/)
- [Leptin, appetite and obesity](https://durgical.com/en/biochemistry/topics/leptin-appetite-and-obesity/)

## Test yourself

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.

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

Sources: [Hypoglycemia: MedlinePlus](https://medlineplus.gov/hypoglycemia.html) (MedlinePlus, US National Library of Medicine, 2026); [Malnutrition: MedlinePlus Medical Encyclopedia](https://medlineplus.gov/ency/article/000404.htm) (MedlinePlus, US National Library of Medicine, 2026); [INS: Insulin (human)](https://www.uniprot.org/uniprotkb/P01308/entry) (UniProt, 2026); [GCG: Pro-glucagon (human)](https://www.uniprot.org/uniprotkb/P01275/entry) (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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