Published online Sep 14, 2016. doi: 10.3748/wjg.v22.i34.7660
Peer-review started: June 4, 2016
First decision: July 12, 2016
Revised: July 25, 2016
Accepted: August 10, 2016
Article in press: August 10, 2016
Published online: September 14, 2016
Processing time: 96 Days and 6 Hours
After the first description of fatty pancreas in 1933, the effects of pancreatic steatosis have been poorly investigated, compared with that of the liver. However, the interest of research is increasing. Fat accumulation, associated with obesity and the metabolic syndrome (MetS), has been defined as “fatty infiltration” or “nonalcoholic fatty pancreas disease” (NAFPD). The term “fatty replacement” describes a distinct phenomenon characterized by death of acinar cells and replacement by adipose tissue. Risk factors for developing NAFPD include obesity, increasing age, male sex, hypertension, dyslipidemia, alcohol and hyperferritinemia. Increasing evidence support the role of pancreatic fat in the development of type 2 diabetes mellitus, MetS, atherosclerosis, severe acute pancreatitis and even pancreatic cancer. Evidence exists that fatty pancreas could be used as the initial indicator of “ectopic fat deposition”, which is a key element of nonalcoholic fatty liver disease and/or MetS. Moreover, in patients with fatty pancreas, pancreaticoduodenectomy is associated with an increased risk of intraoperative blood loss and post-operative pancreatic fistula.
Core tip: Nonalcoholic fatty pancreas disease is a very common yet neglected pathological condition. It can be considered an early marker of the metabolic syndrome and, as so, its clinical significance spaces between internal and surgical diseases, such as type 2 diabetes mellitus, atherosclerosis, acute pancreatitis and even pancreatic cancer. This review collects current knowledge of worldwide opinion leaders and researchers of this matter.