Cholestasis is associated with systemic accumulation of bile salts and by deficiency of bile in the intestinal lumen. During the past years bile salts have been identified as signaling molecules that regulate lipid, glucose and energy metabolism. Bile salts have also been shown to activate signaling routes leading to proliferation, apoptosis or differentiation. It is unclear, however, whether cholestasis affects the constitution and absorptive capacity of the intestinal epithelium in vivo. We studied small intestinal morphology, proliferation, apoptosis, expression of intestine-specific genes and carbohydrate absorption in cholestatic (1 wk bile duct ligation), bile-deficient (1 wk bile diversion) and control (sham) rats. Absorptive capacity was assessed by determination of plasma ²H- and ¹³C-glucose concentrations after intraduodenal administration of ²H-glucose and naturally-enriched ¹³C-sucrose, respectively. Small intestinal morphology, proliferation, apoptosis and gene expression of intestinal transcription factors (mRNA levels of Cdx-2, Gata-4 and Hnf-1, and Cdx-2 protein levels) were similar in cholestatic, bile-deficient and control rats. The (unlabeled) blood glucose response after intraduodenal administration was delayed in cholestatic animals, but the absorption over 180 minutes, was quantitatively similar between the groups. Plasma concentrations of ²H-glucose and ¹³C-glucose peaked to similar extents in all groups within 7.5 min and 30 min, respectively. Absorption of ²H-glucose and ¹³C-glucose in plasma was similar in all groups. The present data indicate that neither accumulation of bile salts in the body, nor their intestinal deficiency, two characteristic features of cholestasis, affect rat small intestinal proliferation, differentiation, apoptosis, or its capacity to digest and absorb carbohydrates.