Effect of diabetes and adrenocortical state on intestinal transport capacity and (Na+ + K+)-activated adenosine triphosphatase activity.
(Na+ + K+)-activated adenosine triphosphatase activity in the mucosal homogenate of rat small intestine estimated under conditions of experimental diabetes, application of corticosteroids, adrenalectomy or inhibition of adrenocortical function suggests a general parallelism between the capacity for monosaccharide absorption and enzyme activity. Studying the kinetic parameters it has been found that the maximal velocities of monosaccharide uptake as well as of (Na+ + K+)-activated adenosine triphosphatase reaction are significantly different, whereas sugar concentrations for halfmaximal transport velocities and enzyme-substrate affinity constants remain unaltered. From studies with purified brush borders and basolateral plasma membranes it has been shown that the activity changes were caused exclusively by that part of (Na+ + K+)-activated adenosine triphosphatase which is localized in the basolateral plasma membranes. The enzyme activity in the brush border region remains unchanged. These findings support a concept of intestinal transport mechanism which suggests that the basolateral part of (Na+ + K+)-activated adenosine triphosphatase is responsible for metabolic energy supply.
D000305:Adrenal Cortex Hormones / Q000502:physiology*; D000315:Adrenalectomy; D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000201:enzymology / Q000378:metabolism*; D005260:Female; D005947:Glucose / Q000378:metabolism*; D007408:Intestinal Absorption; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism*
D000305:Adrenal Cortex Hormones; D000254:Sodium-Potassium-Exchanging ATPase; D005947:Glucose