Inflammation, autophagy, and obesity: common features in the pathogenesis of pancreatitis and pancreatic cancer

Gastroenterology. 2013 Jun;144(6):1199-209.e4. doi: 10.1053/j.gastro.2013.02.007.


Inflammation and autophagy are cellular defense mechanisms. When these processes are deregulated (deficient or overactivated) they produce pathologic effects, such as oxidative stress, metabolic impairments, and cell death. Unresolved inflammation and disrupted regulation of autophagy are common features of pancreatitis and pancreatic cancer. Furthermore, obesity, a risk factor for pancreatitis and pancreatic cancer, promotes inflammation and inhibits or deregulates autophagy, creating an environment that facilitates the induction and progression of pancreatic diseases. However, little is known about how inflammation, autophagy, and obesity interact to promote exocrine pancreatic disorders. We review the roles of inflammation and autophagy, and their deregulation by obesity, in pancreatic diseases. We discuss the connections among disordered pathways and important areas for future research.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Review

MeSH terms

  • Animals
  • Autophagy*
  • Humans
  • Inflammation / complications*
  • Inflammation / immunology
  • Inflammation / metabolism
  • Inflammation / pathology
  • Inflammation Mediators / metabolism
  • Obesity / complications*
  • Obesity / immunology
  • Obesity / metabolism
  • Obesity / pathology
  • Pancreas / immunology
  • Pancreas / metabolism
  • Pancreas / pathology*
  • Pancreatic Neoplasms / etiology*
  • Pancreatic Neoplasms / immunology
  • Pancreatic Neoplasms / metabolism
  • Pancreatic Neoplasms / pathology
  • Pancreatitis / etiology*
  • Pancreatitis / immunology
  • Pancreatitis / metabolism
  • Pancreatitis / pathology
  • Risk Factors
  • Signal Transduction


  • Inflammation Mediators