1、SummaryClinical LipidologyOctober 2013, Vol. 8, No. 5, Pages 587-594 , DOI 10.2217/clp.13.44(doi:10.2217/clp.13.44)ReviewHypertriglyceridemia-induced acute pancreatitisNils EwaldHypertriglyceridemia is a well established cause of acute pancreatitis and accounts for up to 10% of all acute pancreatiti
2、s cases and even up to 50% of all acute pancreatitis cases in pregnancy. Hydrolysis of triglycerides by pancreatic lipase and excessive formation of free fatty acids with inflammatory changes, capillary injury and hyperviscosity are postulated to account for the development of hypertriglyceridemia-i
3、nduced pancreatitis (HTGP). The clinical features of those patients are generally no different from patients with acute pancreatitis of other etiologies. HTGP, however, seems to be associated with a higher severity and complication rate. There is no clear evidence as to which hypertriglyceridemia pa
4、tients will develop acute pancreatitis and which will not. Insulin, heparin, plasmapheresis and different antihyperlipidemic agents, as well as dietary modifications, are key features in the management of HTGP.Annals of Surgery:May 2013 - Volume 257 - Issue 5 - p 943951doi: 10.1097/SLA.0b013e318269d
5、536Original ArticlesFat Necrosis Generates Proinflammatory Halogenated Lipids During Acute PancreatitisFranco-Pons, Neus PhD*; Casas, Josefina PhD; Fabris, Gemma PhD; Gea-Sorl, Sabrina PhD*; de-Madaria, Enrique MD, PhD; Gelp, Emilio PhD*,; Closa, Daniel PhD*AbstractObjective: To evaluate the generat
6、ion of halogenated fatty acids in the areas of fat necrosis during acute pancreatitis and to evaluate the effects of these molecules on the ensuing inflammatory process.Background: Lipid mediators derived from adipose tissue have been implicated in the progression of acute pancreatitis, although the
7、ir precise role remains unknown.Methods: Acute pancreatitis was induced in rats by intraductal infusion of 3.5% sodium taurocholate. Fatty acid chlorohydrins (FA-Cl) were measured in adipose tissue, ascitic fluid, and plasma by mass spectrometry. Chlorohydrins were also instilled in the rats periton
8、eal cavity, and their effects on peritoneal macrophages activation and in systemic inflammation were evaluated. Finally, they have also been measured in plasma from human patients with acute pancreatitis.Results: Induced acute pancreatitis results in a substantial release not only of free fatty acid
9、s but also of the chlorohydrins of both oleic and linoleic acids from adipose tissue. In plasma, only the chlorohydrin of oleic acid was detected. Administration of 250-M lipid chlorohydrins, which is the concentration found in ascitic fluid, induces the expression of TNF and interleukin-1 in perito
10、neal macrophages and increases the systemic inflammatory response in pancreatitis. Finally, increased concentrations of oleic acid chlorohydrin have been found in plasma of human patients with pancreatitis.Conclusions: During acute pancreatitis, adipose tissue release FA-Cl, which exacerbate the sys
11、temic inflammatory response.Generation of fatty acid chlorohydrins by adipose tissue in acute pancreatitisAutor : Franco-Pons, NeusCasas, JosefinaFabris, GemmaGea-Sorl, SabrinaGelp, EmiliClosa, DanielFecha de publicacin :jun-2011Citacin : 10th World Congress on Inflammation (2011)Resumen : Backgroun
12、d: Acute pancreatitis is an inflammatory process of the pancreatic gland that in the severe forms triggers the inflammation in remote organs. An additional characteristic of pancreatitis is the necrosis of peripancreatic adipose tissue due to the release of lipolytic enzymes. These areas of adipose
13、tissue release in turn inflammatory mediators. Here we have evaluated the generation of halogenated free fatty acids by necrotic adipose tissue in a model of acute pancreatitis. Methods: Pancreatitis was induced in male rats by intraductal administration of 3.5% sodium taurocholate. We obtained samp
14、les of adipose tissue and ascitic fluid 3, 6 and 18 h after induction, and the levels of free fatty acids as well as fatty acid chlorohydrins were evaluated by GCMS. In additional experiments we administered fatty acid chlorohydrins, generated by chlorination of adipose tissue lipid extracts, on the
15、 peritoneum of control animals. Three hours later we obtained peritoneal macrophages and the expression of TNFa on these cells was evaluated by RT-PCR. Results: During pancreatitis, necrotic areas of adipose tissue generate and release free fatty acids as well as its chlorohydrins. We identified ole
16、ic acid chlorohydrin and mono- and bis-chlorohydrin of linoleic acid in both adipose tissue and ascitic fluid. Administration of chlorinated lipids in the peritoneal cavity results in an increased expression of TNFa by peritoneal macrophages. Conclusion: We conclude that during severe acute pancreat
17、itis, the necrotic areas of the peripancreatic adipose tissue generate chlorinated fatty acids. These halogenated lipids could activate macrophages and plays a role in the progression of the systemic inflammation.Descripcin : Trabajo presentado al 10th World Congress on Inflammation celebrado en Paris del 25 al 29 de junio de 2011.
