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Peripancreatic fat necrosis worsens acute pancreatitis independent of pancreatic necrosis via unsaturated fatty acids increased in human pancreatic necrosis collections.
Gut. 2016 Jan; 65(1):100-11.Gut

Abstract

BACKGROUND AND AIMS

Peripancreatic fat necrosis occurs frequently in necrotising pancreatitis. Distinguishing markers from mediators of severe acute pancreatitis (SAP) is important since targeting mediators may improve outcomes. We evaluated potential agents in human pancreatic necrotic collections (NCs), pseudocysts (PCs) and pancreatic cystic neoplasms and used pancreatic acini, peripheral blood mononuclear cells (PBMC) and an acute pancreatitis (AP) model to determine SAP mediators.

METHODS

We measured acinar and PBMC injury induced by agents increased in NCs and PCs. Outcomes of caerulein pancreatitis were studied in lean rats coadministered interleukin (IL)-1β and keratinocyte chemoattractant/growth-regulated oncogene, triolein alone or with the lipase inhibitor orlistat.

RESULTS

NCs had higher fatty acids, IL-8 and IL-1β versus other fluids. Lipolysis of unsaturated triglyceride and resulting unsaturated fatty acids (UFA) oleic and linoleic acids induced necro-apoptosis at less than half the concentration in NCs but other agents did not do so at more than two times these concentrations. Cytokine coadministration resulted in higher pancreatic and lung inflammation than caerulein alone, but only triolein coadministration caused peripancreatic fat stranding, higher cytokines, UFAs, multisystem organ failure (MSOF) and mortality in 97% animals, which were prevented by orlistat.

CONCLUSIONS

UFAs, IL-1β and IL-8 are elevated in NCs. However, UFAs generated via peripancreatic fat lipolysis causes worse inflammation and MSOF, converting mild AP to SAP.

Authors+Show Affiliations

Departments of Medicine, Mayo Clinic, Scottsdale, Arizona, USA.Departments of Medicine, Mayo Clinic, Scottsdale, Arizona, USA.Departments of Medicine, University of Pittsburgh Medical Center, Pasavant, Pennsylvania, USA.Departments of Medicine, Mayo Clinic, Scottsdale, Arizona, USA.Departments of Medicine, Mayo Clinic, Scottsdale, Arizona, USA.Departments of Medicine, Mayo Clinic, Scottsdale, Arizona, USA.Departments of Medicine, Mayo Clinic, Scottsdale, Arizona, USA.Departments of Surgery, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania, USA.Departments of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.Departments of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.Departments of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.Departments of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.Departments of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.Departments of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.Departments of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.Departments of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.Departments of Medicine, University of Pittsburgh Medical Center, Pasavant, Pennsylvania, USA.Departments of Medicine, University of Pittsburgh Medical Center, Pasavant, Pennsylvania, USA.Departments of Medicine, Washington University, Saint Louis, Missouri, USA.Departments of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.Departments of Pathology, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.Departments of Medicine, Mayo Clinic, Scottsdale, Arizona, USA.

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

25500204

Citation

Noel, Pawan, et al. "Peripancreatic Fat Necrosis Worsens Acute Pancreatitis Independent of Pancreatic Necrosis Via Unsaturated Fatty Acids Increased in Human Pancreatic Necrosis Collections." Gut, vol. 65, no. 1, 2016, pp. 100-11.
Noel P, Patel K, Durgampudi C, et al. Peripancreatic fat necrosis worsens acute pancreatitis independent of pancreatic necrosis via unsaturated fatty acids increased in human pancreatic necrosis collections. Gut. 2016;65(1):100-11.
Noel, P., Patel, K., Durgampudi, C., Trivedi, R. N., de Oliveira, C., Crowell, M. D., Pannala, R., Lee, K., Brand, R., Chennat, J., Slivka, A., Papachristou, G. I., Khalid, A., Whitcomb, D. C., DeLany, J. P., Cline, R. A., Acharya, C., Jaligama, D., Murad, F. M., ... Singh, V. P. (2016). Peripancreatic fat necrosis worsens acute pancreatitis independent of pancreatic necrosis via unsaturated fatty acids increased in human pancreatic necrosis collections. Gut, 65(1), 100-11. https://doi.org/10.1136/gutjnl-2014-308043
Noel P, et al. Peripancreatic Fat Necrosis Worsens Acute Pancreatitis Independent of Pancreatic Necrosis Via Unsaturated Fatty Acids Increased in Human Pancreatic Necrosis Collections. Gut. 2016;65(1):100-11. PubMed PMID: 25500204.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Peripancreatic fat necrosis worsens acute pancreatitis independent of pancreatic necrosis via unsaturated fatty acids increased in human pancreatic necrosis collections. AU - Noel,Pawan, AU - Patel,Krutika, AU - Durgampudi,Chandra, AU - Trivedi,Ram N, AU - de Oliveira,Cristiane, AU - Crowell,Michael D, AU - Pannala,Rahul, AU - Lee,Kenneth, AU - Brand,Randall, AU - Chennat,Jennifer, AU - Slivka,Adam, AU - Papachristou,Georgios I, AU - Khalid,Asif, AU - Whitcomb,David C, AU - DeLany,James P, AU - Cline,Rachel A, AU - Acharya,Chathur, AU - Jaligama,Deepthi, AU - Murad,Faris M, AU - Yadav,Dhiraj, AU - Navina,Sarah, AU - Singh,Vijay P, Y1 - 2014/12/10/ PY - 2014/07/15/received PY - 2014/11/17/accepted PY - 2014/12/16/entrez PY - 2014/12/17/pubmed PY - 2016/4/5/medline KW - OBESITY KW - PANCREATITIS SP - 100 EP - 11 JF - Gut JO - Gut VL - 65 IS - 1 N2 - BACKGROUND AND AIMS: Peripancreatic fat necrosis occurs frequently in necrotising pancreatitis. Distinguishing markers from mediators of severe acute pancreatitis (SAP) is important since targeting mediators may improve outcomes. We evaluated potential agents in human pancreatic necrotic collections (NCs), pseudocysts (PCs) and pancreatic cystic neoplasms and used pancreatic acini, peripheral blood mononuclear cells (PBMC) and an acute pancreatitis (AP) model to determine SAP mediators. METHODS: We measured acinar and PBMC injury induced by agents increased in NCs and PCs. Outcomes of caerulein pancreatitis were studied in lean rats coadministered interleukin (IL)-1β and keratinocyte chemoattractant/growth-regulated oncogene, triolein alone or with the lipase inhibitor orlistat. RESULTS: NCs had higher fatty acids, IL-8 and IL-1β versus other fluids. Lipolysis of unsaturated triglyceride and resulting unsaturated fatty acids (UFA) oleic and linoleic acids induced necro-apoptosis at less than half the concentration in NCs but other agents did not do so at more than two times these concentrations. Cytokine coadministration resulted in higher pancreatic and lung inflammation than caerulein alone, but only triolein coadministration caused peripancreatic fat stranding, higher cytokines, UFAs, multisystem organ failure (MSOF) and mortality in 97% animals, which were prevented by orlistat. CONCLUSIONS: UFAs, IL-1β and IL-8 are elevated in NCs. However, UFAs generated via peripancreatic fat lipolysis causes worse inflammation and MSOF, converting mild AP to SAP. SN - 1468-3288 UR - https://www.unboundmedicine.com/medline/citation/25500204/Peripancreatic_fat_necrosis_worsens_acute_pancreatitis_independent_of_pancreatic_necrosis_via_unsaturated_fatty_acids_increased_in_human_pancreatic_necrosis_collections_ L2 - https://gut.bmj.com/lookup/pmidlookup?view=long&pmid=25500204 DB - PRIME DP - Unbound Medicine ER -