title: Does increased crypt cell proliferation impair cholesterol absorption after proximal gut resection?
abstract: BACKGROUND
  The effects of proximal small-bowel resection on absorption and synthesis of cholesterol are unclear.
  
  
  METHODS
  To study cholesterol absorption and synthesis after proximal gut resections of variable length, plasma plant sterols, cholestanol, and cholesterol precursors were measured 1 and 2 months after 50% and 75% proximal small-bowel resection or transection. To examine the effect of increased crypt cell proliferation and brush border development on cholesterol absorption, the results were related to the mucosal morphology, crypt cell proliferation, and disaccharidase activities of the remaining small bowel.
  
  
  RESULTS
  Campesterol levels in proportion to cholesterol decreased markedly more, and those of cholestanol markedly less, than would be expected simply due to the amount of proximal small intestine removed, whereas sitosterol proportions decreased in proportion to the length of gut resection. Campesterol proportions markedly (P = 0.06) increased between 1 and 2 months after 50% resection but remained unchanged after 75% resection. Crypt cell proliferation was only increased in the 75% resection group (P < 0.05). The longer the proximal gut resection, the lower was the mucosal enzyme activity. Both resection groups showed increased plasma cholesterol precursor proportions and crypt depth (P < 0.05), whereas villus height remained unchanged. After massive proximal resection campesterol and sitosterol proportions were inversely related to crypt cell proliferation (r = -0.86-0.83, P < 0.01).
  
  
  CONCLUSIONS
  Increased crypt cell proliferation activated by massive proximal gut resection may act as a previously unrecognized factor in aggravating cholesterol malabsorption and retarding its recovery during the early postoperative period. These findings warrant further investigation.
authors.affiliation: Dept. of Gastrointestinal Surgery, Helsinki University Central Hospital, University of Helsinki, Finland.
authors.forename: M P
authors.initials: MP
authors.lastname: Pakarinen
authors.forename: T A
authors.initials: TA
authors.lastname: Miettinen
authors.forename: J
authors.initials: J
authors.lastname: Lauronen
authors.forename: J
authors.initials: J
authors.lastname: Halttunen
mesh_terms: D000818:Animals; D002455:Cell Division; D002784:Cholesterol / Q000031:analogs & derivatives* / Q000378:metabolism*; D004186:Disaccharidases / Q000378:metabolism; D007408:Intestinal Absorption; D007413:Intestinal Mucosa / Q000166:cytology / Q000378:metabolism*; D007421:Intestine, Small / Q000601:surgery*; D010840:Phytosterols; D012855:Sitosterols / Q000378:metabolism; D013552:Swine
chemical_list: D010840:Phytosterols; D012855:Sitosterols; C021273:campesterol; C025473:gamma-sitosterol; D002784:Cholesterol; D004186:Disaccharidases