American Journal of Clinical Nutrition, Vol 21, 495-501, Copyright © 1968 by The American Society for Clinical Nutrition, Inc.

Intestinal Transport, Coenzyme A, and Colitis in Pantothenic Acid Deficiency

¹ From the George H. Scott Research Laboratory and Department of Physiology, Western Reserve University Medical School, Cleveland, Ohio

Studlies of the effect of pantothenic acid deficiency on intestinal transport of water, sodium, potassium, and glucose were carried out in acute and chronic experiments in jejunal and colonic segments of 22 pigs. Assays of coenzyme A activity of cells of the colonic mucosa were performed in 16 animals.

1) In the jejunum, pantothenic acid deficiency produced an equal reduction in the bidirectional flux rates of sodium and mild reductions in net potassium and glucose transport. Net water and sodium movements were unaffected.

2) In the cecum, acute studies revealed that loss of body water and sodium into the gut lumen was produced or accentuated in pantothenic acid-deficient pigs or in pigs weaned from gifts fed a diet low in this vitamin. Chronic studies in two pigs, however, did not support these findings from 16 animals. In chronic studies, exsorption of sodium declined as well as net water, sodium, and potassium transport.

3) Early in the development of deficiency, large quantities of water, sodium, and potassium were lost into the gut lumen of two of four pigs with jejunal segments. The early period of deficiency also affected cecal transport in which large quantities of potassium were lost into the gut lumen. This change was accompanied by an increase in sodium absorption. Both of these effects disappeared as the deficiency state progressed.

4) Coenzyme A activity of cells from the colonic mucosa was reduced by more than 75% in pantothenic acid-dieficient pigs with bloody diarrhea and ulcerative mucosal lesions.