title: Endogenous hypertriglyceridemia intensifies the course of cerulein-induced pancreatitis in rat: relation with changes in the VLDL composition.
abstract: OBJECTIVE
  To study if the course of cerulein-induced pancreatitis in rats changes in a state of triglyceride-rich lipoprotein metabolism alteration.
  
  
  METHODS
  Two groups of rats received control diet during a 90-day period (A) and sucrose-rich diet to induce endogenous hypertriglyceridemia (B). Subgroups A2 and B2 received i.p. 45 microg cerulein/kg body weight (to induce acute pancreatitis). Histological examination of pancreas tissue, serum pancreatic lipase, lipoprotein profile and VLDL chemical composition were assessed. Then, pancreatic lipase hydrolytic activity on VLDL-triglycerides was evaluated in vitro.
  
  
  RESULTS
  Cellular vacuolization was observed in all of the cerulein-injected rats, but only in subgroup B2 fat necrosis was present. Serum triglycerides were higher in subgroup B1 than in subgroup A1 (mean +/- SEM, mg/dl 123,77 +/- 25.7 vs. 65.8 +/- 7, p < 0.01). Triglycerides from rats fed with sucrose-rich diet, decreased after cerulein-induced pancreatitis (80.38 +/- 11.3 vs. 123,77 +/- 25.7, p < 0.02). Moreover, the endogenous hypertriglyceridemic rats showed an increment of VLDL triglyceride content, which decreased when rats were injected with cerulein. A negative correlation was found between VLDL-triglyceride content and serum pancreatic lipase activity (r = 0.58, p < 0.02). The in vitro assay showed a decrease in VLDL-triglyceride content post incubation with pancreatic lipase enriched serum (mean +/- SD: 59.2 +/- 27.7%, p < 0.01).
  
  
  CONCLUSIONS
  The endogenous hypertriglyceridemia intensifies the course of cerulein-induced pancreatitis and it could be related to the decrease in VLDL-triglycerides as a consequence of pancreatic lipase hydrolytic activity.
authors.affiliation: Department of Physiology, School of Medicine, University of Buenos Aires, Buenos Aires, Argentina. oponzo@fmed.uba.ar
authors.forename: O
authors.initials: O
authors.lastname: Ponzo
authors.forename: L
authors.initials: L
authors.lastname: Schreier
authors.forename: R
authors.initials: R
authors.lastname: Resnik
authors.forename: G
authors.initials: G
authors.lastname: Negri
authors.forename: P
authors.initials: P
authors.lastname: Scacchi
authors.forename: M A
authors.initials: MA
authors.lastname: Cresta
authors.forename: R
authors.initials: R
authors.lastname: Wikinski
mesh_terms: D000208:Acute Disease; D000818:Animals; D002108:Ceruletide / Q000633:toxicity; D015243:Cholesterol, VLDL / Q000737:chemistry* / Q000378:metabolism; D015228:Hypertriglyceridemia / Q000378:metabolism*; D008049:Lipase / Q000097:blood / Q000378:metabolism*; D008079:Lipoproteins, VLDL / Q000097:blood / Q000378:metabolism*; D008297:Male; D010195:Pancreatitis / Q000139:chemically induced / Q000378:metabolism*; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D014280:Triglycerides / Q000097:blood / Q000378:metabolism*
chemical_list: D015243:Cholesterol, VLDL; D008079:Lipoproteins, VLDL; D014280:Triglycerides; C030106:very low density lipoprotein triglyceride; D002108:Ceruletide; D008049:Lipase