Why does the effect of the cholera toxin on the epithelial sodium transport protein contribute to both the diarrhea and metabolic acidosis?

The cholera toxin binds to GM1 ganglioside receptors on the enterocytes (epithelial cells of intestines). This results in the uptake of the toxin by endocytosis. Once inside the cells, the toxin undergoes a biological pathway that causes an increase in the production of cyclic-AMP. This activates the cystic fibrosis transmembrane conductance regulator (CFTR) thereby resulting in an efflux of ions (mostly sodium) from the cells. Water efflux follows due to a change in osmotic pressure thereby causing watery diarrhea.

The cholera toxin in the sodium epithelial transport protein promotes the release of cyclic adenosine monophosphate in the cells of the intestinal mucosa, promoting diarrhea and metabolic acidosis.

Explanation:

Cholera toxin has the ability to bind sodium transport protein. as a result, the protein will bind to the intestinal mucosa and promote the exaggerated release of cyclic adenosine monophosphate into the cells of the intestinal mucosa. This molecule stimulates the release of water and salt, which will promote diarrhea and metabolic acidosis.

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