In human
malabsorption syndromes,
lipofuscin accumulation has been reported to occur exclusively within the muscle layers of the intestine. It has been widely speculated that this
lipofuscin deposition is related to
vitamin E deficiency. To determine whether
vitamin E deficiency leads to the same pattern of intestinal
lipofuscin accumulation as that seen in many human
malabsorption syndromes, the duodenums of rats that had been fed a
vitamin E-deficient diet for 17 or 34 wk were examined for the presence of
lipofuscin.
Lipofuscin did not appear in the muscle layers of the duodenum until 34 wk, at which time occasional fibers containing large amounts of
lipofuscin were present. An earlier and more pronounced deposition of
lipofuscin occurred within connective tissue cells of the intestinal villi. After 17 wk, many fibroblastlike cells in the lamina propria of the villi contained large amounts of
lipofuscin. By 34 wk, the numbers of these
lipofuscin-containing cells in the lamina propria had increased substantially, and scattered cells containing
lipofuscin were also seen in the submucosa. The difference in intestinal
lipofuscin distribution between
vitamin E-deficient rats and humans with
malabsorption syndromes suggests that other factors, in addition to
vitamin E, probably play important roles in regulating
lipofuscin accumulation in the intestine.