What is POMC and where is it produced?
Proopiomelanocortin is a product of a common gene. Chemically, it is a polypeptide chain comprising 265 amino acid residues.
Site of synthesis: POMC is produced in the anterior and intermediate lobes of the pituitary gland, as well as in the intestine and placenta.
Which hormones are derived from POMC?
As a result of processing, several biologically active substances are formed from the POMC molecule:
- Adrenocorticotropic hormone (ACTH).
- Melanocyte-stimulating hormone (MSH).
- $\beta$-endorphin and other peptides.
How is synthesis regulated?
The key regulator of POMC production is corticotropin-releasing hormone (CRH), a regulator of the hypothalamic-pituitary-adrenal axis.
Neurosecretory cells of the hypothalamus are activated under the influence of CNS structures, primarily the limbic system. CRH stimulates proopiomelanocortin-producing cells of the adenohypophysis.
Physiological effects of POMC derivatives
The cleavage products of POMC exhibit the following effects:
- Thermoregulation: ACTH, $\alpha$- and $\gamma$-MSH act as endogenous antipyretics. They modulate the activity of neurons in the septal area and other brain regions that transmit signals to the thermoregulatory center. This prevents an excessive rise in body temperature above 41–42 °C and prevents organism death.
- Energy metabolism: POMC derivatives are part of the leptin-melanocortin pathway, which regulates feeding behavior and energy metabolism.
- Role in the central nervous system: POMC derivatives include ACTH, $\alpha$- and $\gamma$-melanocyte-stimulating hormones.
Clinical significance
Addison's disease (primary adrenal insufficiency) In tuberculous or autoimmune damage to the adrenal cortex cells, corticosteroid synthesis decreases. This leads to a loss of negative feedback and increased ACTH secretion. Since ACTH and MSH are formed from a common precursor—POMC—an excess of ACTH and accompanying peptides stimulates melanocytes. A characteristic symptom develops: hyperpigmentation of the skin and mucous membranes ("bronze disease"). Associated symptoms include hypotension, muscle weakness, hyponatremia, hypoglycemia, and stress intolerance.
Monogenic obesity Mutations in the proopiomelanocortin, melanocortin receptor, or leptin genes disrupt the appetite regulation cascade. This leads to the development of a very rare form of genetically determined obesity. The disease manifests in the first months of life and is characterized by hyperphagia, rapidly progressive morbid obesity by preschool age, and secondary hypogonadism.
Class and exam questions
Why does the skin darken in Addison's disease?
In cortisol deficiency, negative feedback is lost, disinhibiting pituitary ACTH secretion. Since ACTH and melanocyte-stimulating hormone are formed from a common precursor—POMC—an excess of ACTH and accompanying peptides stimulates melanocytes, causing hyperpigmentation ("bronze disease").
What role do POMC derivatives play in thermoregulation?
POMC derivatives (ACTH, $\alpha$- and $\gamma$-MSH) act as endogenous antipyretics. They affect brain neurons that transmit signals to the thermoregulatory center, preventing an excessive rise in body temperature above 41–42 °C.
What does a POMC gene mutation lead to in children?
A mutation in the POMC gene disrupts the leptin-melanocortin pathway of appetite regulation. This leads to the development of early-onset monogenic obesity with hyperphagia and secondary hypogonadism.
What else to study on this topic
- Corticotropin-releasing hormone (CRH)
- Adrenocorticotropic hormone (ACTH)
- Leptin-melanocortin pathway
- Endogenous antipyretics
- Hypothalamic-pituitary-adrenal axis
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