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Lecture

Na transport & carb digestion

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Department
Physiology
Course
Physiology 3120
Professor
Tom Stavraky
Semester
Winter

Description
Human Physiology Wednesday, April 7, 2010 “Gastro VIII” Sodium transport (cont’d) • Primarily in the lower gut. Typified by secondary active transport using a Na/Cl symporter (1:1 ratio); the transporter is activated by a Na concentration gradient across the apical/luminal membrane. Binding of the Na (already has high affinity) increases the affinity for the Cl site for its substrate (i.e. chloride); when both ions bind, the protein undergoes some conformational change occurs to move the ions to the cytosolic side. On basolateral membrane, have a Na ATPase: functions to pump Na into blood, as well as maintain Na concentration across apical membrane (maintains high affinity for Na binding site); also have chloride channels here, so chloride drifts into EC compartment • Pathological situation where the above process is eliminated or overcome; associated with watery diarrhoea and cholera. Increase in content of prostaglandin E 2ssociated with cholera toxin. Cholera toxin does 2 things: (1) inhibits apical Na/Cl symporter, so can’t absorb NaCl, and (2) punches holes in apical membrane, causing Cl to leak out into the intestinal lumen (and water to follow). PGE 2s specific to the Na/Cl symporter, so giving electrolyte-rich juice (Ginger-Ale) can help overcome the net efflux of water.  Solvent drag: solvent moves and drags all other substances dissolved in it along for the ride Carbohydrate digestion • First digested by amylase in the mouth; followed by pancreatic enz
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