Hexose absorption from jejunal loops in situ in zinc-deficient and Zn-supplemented rats.

1. Immature, male Wistar rats were given a low-zinc semi-synthetic diet (2 mg Zn/kg) for 22-28 d. Control groups received a similar diet supplemented with 58 mg Zn/kg either ad lib., or in amounts matched to the consumption of the Zn-deficient group. There was a rapid onset of reduced food consumption and growth retardation in the Zn-depleted animals. 2. Serosal surface area of small intestines taken from Zn-deficient rats was significantly reduced compared with that of control animals. Villi, dissected from samples of proximal jejunum, were markedly smaller than those of control rats and were present in greater numbers per unit area of serosa. 3. Luminal loss of galactose from jejunal loops in situ was significantly greater in the Zn-deficient rats compared with controls when expressed in terms of unit dry weight of intestine and serosal or villous surface area. Since only a small proportion of the total galactose remained in the mucosal tissue and associated extracellular space, this loss could only be accounted for by an increased efficiency of net trans-epithelial transport. Differences in total galactose absorption per unit length of jejunum were not so marked. 4. This intestinal adaptation to Zn-deficiency allows the maintenance of normal, and possibly increased, rates of hexose transfer into the body of animals exhibiting severe growth retardation, reduced food utilization and abnormal glucose metabolism.