Absence of luminal riboflavin disturbs early postnatal development of the gastrointestinal tract.

An increase in the size and cellularity of duodenal crypts and a decreased incidence of bifurcating crypts is observed in response to very short-term feeding of a riboflavin-deficient diet to weanling rats. A study was conducted to determine whether the absence of riboflavin in the lumen of the small intestine impairs gastrointestinal development. Forty-eight female weanling Wistar rats were allocated to one of two treatment regimens, to receive either a riboflavin-deficient diet and a daily intraperitoneal injection of flavin mononucleotide (luminally deficient group) or a complete diet and a daily intraperitoneal injection of saline (control group). Animals were killed at 93, 141, or 165 hr from feeding. The flavin injection regimen maintained normal systemic riboflavin status in the luminally deficient group. In this group, however, crypt hypertrophy and reduced crypt bifurcation were evident by 141 hr of luminal riboflavin deprivation. The absence of riboflavin in the duodenal lumen impairs normal development, suggesting that a crypt sensing mechanism may be involved in the response to riboflavin deficiency.