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Comment
. 2023 Jan;72(1):212-214.
doi: 10.1136/gutjnl-2022-326958. Epub 2022 Apr 22.

Alcohol predisposes obese mice to acute pancreatitis via adipose triglyceride lipase-dependent visceral adipocyte lipolysis

Xinmin Yang  1   2 , Linbo Yao  1   3 , Lei Dai  4 , Mei Yuan  1 , Wenhua He  5 , Tingting Liu  1 , Xianghui Fu  6 , Jing Xue  7 , Robert Sutton  8 , Qing Xia  9 , Wei Huang  9   2   3
Affiliations
Comment

Alcohol predisposes obese mice to acute pancreatitis via adipose triglyceride lipase-dependent visceral adipocyte lipolysis

Xinmin Yang et al. Gut. 2023 Jan.
No abstract available

Keywords: ACUTE PANCREATITIS; ALCOHOL; OBESITY.

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Conflict of interest statement

Competing interests: None declared.

Figures

Figure 1
Figure 1
Alcohol predisposes obese mice to AP with systemic organ injury. (A) Experimental protocol of establishing OA-AP. C57BL/6 J mice were fed a CD (lean) or HFD (obese) for 12 weeks, then were injected intraperitoneally with 2 g/kg EtOH two times at 1 hour apart: (B) Body weight. (C) Representative images of pancreatic histopathology and histopathological scores (oedema, inflammation and necrosis; magnification ×200), (D) Serum amylase and lipase and (E) pancreatic MPO, lung MPO, and serum IL-6 levels of the OA-AP mice. (F) Serum FFA levels and (G) FFA and glycerol release in collected adipose tissues. (H) Amylase and lipase levels in epididymal adipose tissue. (I) Immunoblot analysis of ATGL proteins in epididymal adipose tissue. In all experiments, mice were sacrificed at 12 hours after the first injection of EtOH and assessed for disease severity and/or lipolytic parameters. *P<0.05, **P<0.01, ***P<0.001. AP, acute pancreatitis; ATGL, adipose triglyceride lipase; CD, control diet; Ctrl, control; EtOH, ethanol; FFA, free fatty acid; HFD, high-fat diet; IL, interleukin; MPO, myeloperoxidase; ns, not significant; OA-AP, obese alcoholic acute pancreatitis.
Figure 2
Figure 2
Obesity and acute alcohol intake cause AP through visceral adipocyte lipolysis mediated by ATGL. Lean mice received intraperitoneal injection adipocytes 1 hour prior to two injection of 2 g/kg EtOH at a 1-hour interval: (A) Representative images of pancreatic histopathology (magnification ×200) and histopathological scores. (B) Serum amylase and lipase, and (C) pancreatic MPO, lung MPO and serum IL-6 levels. (D) Serum ALT and AST levels, (E) serum urea and creatinine and urea levels, and (F) serum FFA levels. In another experiment, the effect of an ATGL inhibitor, atglistatin, and a pancreatic lipase inhibitor, orlistat, in the OA-AP mice was tested. (G) Representative images of pancreatic histopathology (magnification ×200) and histopathological scores. (H) Serum amylase and lipase activity, (I) serum IL-6 levels, (J) serum ALT and AST levels, (K) serum urea and creatinine levels, and (L) serum FFA levels. In all experiments, mice were sacrificed at 12 hours after the first injection of EtOH and were assessed for disease severity and/or lipolytic parameters. *P<0.05, **P<0.01, ***P<0.001. ALT, alanine aminotransferase; AP, acute pancreatitis; AST; aspartate aminotransferase; ATGL, adipose triglyceride lipase; Ctrl, control; EtOH, ethanol; FFA, free fatty acid; HFD, high-fat diet; IL, interleukin; MPO, myeloperoxidase; ns, not significant; OA-AP, obese alcoholic acute pancreatitis.
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Comment on

References

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