Simultaneous manipulation of intestinal capacities and nutrient loads in mice

To study the relationship between capacity and load in the small intestine, we simultaneously varied dietary nutrient load and intestinal capacity in mice. Intestinal transection alone caused an increase in intestinal mass, because of increased serosal mass. Because virgin mouse intestine possesses 180% reserve uptake capacity before resection and the intestine regenerates after resection, resection of up to 50% had no effect on food intake, digestive efficiency, intestinal brush-border glucose uptake rate, or mass of all organs measured except the cecum. Regeneration of intestinal mass and glucose uptake capacity was quantitatively complete, because intestinal mass 10 wk after resection was similar to that in unresected mice. Resected intestinal mass in lactating mice was four times larger than that immediately after resection in virgin mice. Cecal mass increased in 50%-resected lactating mice with high food intakes, suggesting nutrient spillage into the distal gut as a signal for regeneration. Mice failed to survive 70% resection of the intestine, possibly because intestinal reserve uptake capacity was exhausted immediately after surgery, making regeneration impossible.

Humoral growth factor after small intestinal resection in the dog

The serum of dogs with a 50% proximal small bowel resection is capable of growth stimulation in small intestinal epithelioid cells in monolayer culture. This overstimulation by postresection serum is not seen when dogs undergo either a small intestinal transection or a simple laparotomy or with baby hamster kidney fibroblast cells in culture. The effect does not seem to be represented by a gastrinlike molecule. This study lends support to the hypothesis that a humoral factor is involved in small intestinal adaptation after partial resection.