The steroid hormones and bile acids are important to digestive tract structure and function. Glucocorticoids administered during pregnancy have been shown to induce cleft palate in the offspring in several species. Postnatally, a significant rise in corticosterone during week 3 in the rat coincides with profound morphological and biochemical changes in the small intestine toward the adult state. Exogenous glucocorticoids given suckling rats leads to precocious development of these changes. In the adult, glucocorticoids increase brush border enzyme levels, while adrenal insufficiency decreases mucosal weight, enzyme activity, and absorptive functions. Water and sodium absorption and potassium excretion are enhanced in both small and large intestine. The jejunum, through its sense of food, provides the entraining signal that governs corticosterone rhythm. In the stomach, high doses of glucocorticoids inhibit prostaglandin biosynthesis, thereby inhibiting the gastric alkaline response and producing severe gastric lesions. However, in man, peptic ulcer disease is not clearly associated with glucocorticoid therapy. Exacerbation of subclinical intestinal infections and perforative lesions have been observed in both animals and man given glucocorticoids. The female sex hormone estrogen, when given to rats, stimulates intestinal enzyme levels and facilitates absorption. Progesterone inhibits both circular and longitudinal smooth muscle contractile activity. Virtually the entire pool of bile acids is found in the enterohepatic circulation. The dihydroxy secondary bile acids, regardless of their conjugation states, are physiologically and morphologically more damaging to mucosal cell membranes than are the trihydroxy primary bile acids.