Body protein pools, turnover and their hormonal control
- Regulation
- For completeness
Body protein is built and broken down all day; insulin, GH and testosterone tip the balance to building, cortisol to breaking down.
Also called: Amino acid pool, Anabolic and catabolic hormones, Plasma proteins
See it in 3D: Liver
What it is
Amino acids circulate at low concentration and are pumped into cells by active carriers. Cells build and break down protein continuously, and the liver makes the plasma proteins, which exchange with tissue protein. The body cannot store extra protein: once cells are full, surplus amino acids are burned or turned into glucose and fat. Hormones decide whether the net flow is toward muscle or away from it.
Key facts
- Plasma amino acid concentration is low and tightly held; after a protein meal it rises only modestly because cells, especially liver, take amino acids up quickly.
- Uptake into cells is active (many are Na⁺-coupled carriers), so cell amino acid concentrations exceed plasma.
- The kidney reabsorbs almost all filtered amino acids in the proximal tubule.
- About half of body protein is in skeletal muscle; even in rest, a few hundred grams of protein are made and broken down daily.
- The liver makes albumin, most globulins (other than immunoglobulins) and fibrinogen; tissue macrophages can take up plasma proteins and release their amino acids.
- Some nitrogen is lost every day even on a protein-free diet (obligatory loss), so a minimum intake is always needed.
How it works, step by step
- Digested protein enters portal blood as amino acids and small peptides; the liver takes up a large share.
- Insulin and amino acids (leucine) activate mTOR and raise muscle uptake and synthesis; insulin also suppresses proteolysis.
- GH stimulates amino acid transport and synthesis, largely through IGF-1, and spares protein by shifting fuel use to fat.
- Testosterone increases muscle protein mass; this is why males usually have more muscle after puberty.
- Cortisol activates muscle proteolysis and releases amino acids (alanine, glutamine) that the liver turns into glucose.
- When intake exceeds what cells can hold, surplus amino acids are deaminated in the liver and the nitrogen is excreted as urea.
Approximate values (70 kg adult)
| Parameter | Value | Note |
|---|---|---|
| Total body protein | ≈ 10–12 kg | about half in muscle |
| Daily protein turnover | ≈ 250–300 g/day | |
| Plasma total protein | 6–8 g/dL | |
| Plasma albumin | 3.5–5 g/dL | half-life ≈ 3 weeks |
| Obligatory nitrogen loss | ≈ 20–30 g protein/day | on a protein-free diet |
Approximate values for a healthy adult at rest; each laboratory sets its own ranges.
Regulation
- +Insulin: More amino acid uptake and synthesis in muscle; less proteolysis.
- +Growth hormone / IGF-1: More amino acid transport and synthesis; growth of muscle and organs.
- +Testosterone: More muscle protein; positive nitrogen balance.
- −Cortisol: Breaks down muscle protein; amino acids go to the liver for gluconeogenesis.
- −Thyroid hormone (excess or low calories): Speeds turnover so breakdown outpaces synthesis; muscle wasting in hyperthyroidism.
- −Glucagon and catecholamines: Increase liver amino acid uptake for gluconeogenesis; favour net loss in fasting and stress.
Clinical notes
- Long-term glucocorticoid use or Cushing syndrome causes proximal muscle wasting, thin skin and easy bruising from protein breakdown.
- Kwashiorkor: inadequate protein with relatively preserved calories; low albumin lowers oncotic pressure, causing edema and a fatty liver.
- Serum albumin falls in acute illness even when intake is fine, so it is a marker of inflammation and prognosis more than of recent nutrition.
- Untreated type 1 diabetes causes muscle wasting because insulin's anabolic and anti-proteolytic effects are lost.
Test yourself
Think of the answer, then tap the question to see it.
What happens to amino acids eaten in excess of what the cells can use?
They are deaminated, mostly in the liver; the nitrogen becomes urea and the carbon skeletons are used for energy or stored as glycogen or fat. There is no protein store.
How can cortisol be catabolic in muscle yet raise protein synthesis in the liver?
It breaks down muscle protein and sends amino acids to the liver, where it increases uptake, gluconeogenic enzymes and synthesis of some liver and plasma proteins.
Why does serum albumin fall within days in sepsis?
Cytokines (IL-6) shift liver synthesis toward acute-phase proteins, and capillary leak moves albumin out of the plasma; intake is not the main cause.
Which hormones have a net anabolic effect on skeletal muscle protein?
Insulin, growth hormone acting through IGF-1, and testosterone.
Connections
See it in 3D1
The structures of Durgical's 3D anatomy where it happens.
In Biochemistry3
In Pharmacology1
Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.
Sources: Hypercortisolism (Cushing Syndrome) (StatPearls (NCBI Bookshelf), 2025); Kwashiorkor: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2025); Amino acid transport across the plasma membrane (Reactome, 2025).
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Representative model, for educational purposes only.