Juvenile pythons undergo large rapid upregulation of intestinal mass and in
testinal transporter activities upon feeding. Because it is also easy to do
surgery on pythons and to maintain them in the laboratory, we used a pytho
n model to examine signals and agents for intestinal adaptation. We surgica
lly isolated the middle third of the small intestine from enteric continuit
y, leaving its mesenteric nerve and vascular supply intact. Intestinal cont
inuity was restored by an end-to-end anastomosis between the proximal and d
istal thirds. Within 24 h of the snake's feeding, the reanastomosed proxima
l and distal segments (receiving luminal nutrients) had upregulated amino a
cid and glucose uptakes by up to 15-fold, had doubled intestinal mass, and
thereby soon achieved total nutrient uptake capacities equal to those of th
e normal fed full-length intestine. At this time, however, the isolated mid
dle segment, receiving no luminal nutrients, experienced no changes from th
e fasted state in either nutrient uptakes or in morphology. By 3 days postf
eeding, the isolated middle segment had upregulated nutrient uptakes to the
same levels as the reanastomosed proximal and distal segments, but it stil
l lacked any appreciable morphological response. These contrasting results
for the reanastomosed intestine and for the isolated middle segment suggest
that luminal nutrients and/or pancreatic biliary secretions are the agents
triggering rapid upregulation of transporters and of intestinal mass and t
hat systemic nerve or hormonal signals later trigger transporter regulation
but no trophic response.