holera toxin, produced by Vibrio cholerae, a pathogenic intestinal bacterium, ca

Question

holera toxin, produced by Vibrio cholerae, a pathogenic intestinal bacterium, causes an indirect reduction in the activity of the Na+/K+ ATPase in intestinal epithelial cells. This results in reduced uptake of small sugars and amino acids from the intestine. How is this reduction in uptake coupled to impaired Na+/K+ ATPase function? (1 pt) How would you approach the anti-cholera drug development process? Hnt (you can use the provided mechanism) (2 pts) 2 Na /glucose symporter GLUT2 Glucose Glucose Glucose Na* 2 Na* 2 Na Na ATP Na /k ATPase ADP+P Apical membrane K* K* Basolateral membrane Tight junction Cytosol Low Na High K Intestinal lumen Dietary glucose Blood High Na" Low K High dietary Na C

Explanation / Answer

Glucose enters inside the cytosol from intestinal lumen by Na+ glucose symporter(Na+ enters via it's down to gradient concentration and glucose enters with Na+) for which Na+ concentration should be low inside the cytosol, otherwise Na+ could not enter. Na+ concentration is maintained by Na+/K+ ATPse pump present on the basolateral membrane which uses one ATP to drive one Na+ out and one K+ inside the cytosol. Thus always Na+ concentration is maintained at low inside cytosol and glucose enters via symport.

Anti-cholera drug should target the Na+/K+ ATPase pump and more precisely the beta subunit of this pump which is the regulatory subunit. Anti cholera drug may be developed such that it blocks the beta subunit so that cholera toxin can't bind over there.

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