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Hypertriglyceridaemia delays pancreatic regeneration after acute pancreatitis in mice and patients
  1. Na Yang1,
  2. Baiqiang Li1,
  3. Yiyuan Pan1,2,
  4. Jianfeng Tu1,
  5. George Liu3,
  6. Guotao Lu1,4,
  7. Weiqin Li1
  1. 1 Surgical Intensive Care Unit (SICU), Department of General Surgery, Jinling Hospital, Medical School of Nanjing University, Nanjing, China
  2. 2 Intensive Care Unit (ICU), Suzhou Municipal Hospital (East Campus), Nanjing Medical University Affiliated Suzhou Hospital, Suzhou, China
  3. 3 Key Laboratory of Molecular Cardiovascular Science Ministry of Education, Institute of Cardiovascular Science, Peking University, Beijing, China
  4. 4 Department of Gastroenterology, Affiliated Hospital of Yangzhou University, Yangzhou University, Yangzhou, China
  1. Correspondence to Dr. Guotao Lu, Surgical Intensive Care Unit (SICU), Department of General Surgery Jinling Hospital, Medical School of Nanjing University Nanjing China; pkulgt{at}163.com and Pro. Weiqin Li, Surgical Intensive Care Unit (SICU), Department of General Surgery, Jinling Hospital, Medical School of Nanjing University, Nanjing 210029, China; njzy_pancrea{at}163.com

https://doi.org/10.1136/gutjnl-2017-315560

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    We read with great interest the recent publication by Barlass et al in which morphine was demonstrated to aggravate the severity of acute pancreatitis (AP) and delay pancreatic regeneration. These results indicated the risk of morphine use in AP-associated pain treatment.1 Similar to their observation, we found another interesting phenomenon that hypertriglyceridaemia (HTG), a prevalent metabolic disorder, delayed pancreatic regeneration after AP in mice and patients. Moreover, the delayed regeneration process could be ameliorated by lipid-lowering therapy.

    Two models of HTG (drug induced: poloxamer 407 (P407) and gene modified: glycosylphosphatidylinositol-anchored high-density lipoprotein-binding protein 1 (GPIHBP1) deficiency) were employed to explore the effect of HTG on AP repair. AP induced by caerulein infusion in both normal triglyceride (NTG) mice and HTG mice caused pancreatic acinar cell necrosis. The injured pancreas was reconstructed in 3 days and recovered its normal architecture in 7 days in the NTG mice (figure 1A–C). However, we observed reduced morphological recovery in the HTG mice, especially in the severe HTG mice that presented with prolonged necrosis until 7 days (figure 1A–C, online supplementary figures 1–3). Furthermore, the key cellular responses involved in AP repair, including the fibroinflammatory response and acinar cell proliferation,2 were significantly delayed in the HTG mice (online supplementary figures 4–6). The above results suggested the possibility that …

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