Role of pancreatic fat in the outcomes of pancreatitis

Abstract

The role of obesity in relation to various disease processes is being increasingly studied, with reports over the last several years increasingly mentioning its association with worse outcomes in acute disease. Obesity has also gained recognition as a risk factor for severe acute pancreatitis (SAP).The mortality in SAP may be as high as 30% and is usually attributable to multi system organ failure (MSOF) earlier in the disease, and complications of necrotizing pancreatitis later [9-11]. To date there is no specific treatment for acute pancreatitis (AP) and the management is largely expectant and supportive. Obesity in general has also been associated with poor outcomes in sepsis and other pathological states including trauma and burns. With the role of unsaturated fatty acids (UFA) as propagators in SAP having recently come to light and with the recognition of acute lipotoxicity, there is now an opportunity to explore different strategies to reduce the mortality and morbidity in SAP and potentially other disease states associated with such a pathophysiology. In this review we will discuss the role of fat and implications of the consequent acute lipotoxicity on the outcomes of acute pancreatitis in lean and obese states and during acute on chronic pancreatitis.

Keywords: Fibrosis; Lipotoxicity; Multi system organ failure; Obesity; Outcomes; Pancreatitis.

Figure 1. Schematics describe the influence of adipocyte mass and fibrosis on the progression of an acute pancreatitis attack

An attack induced by an insult in lean (A), obese (B) and chronic pancreatitis (CP, C) patients progresses differently. The lipases released by the insult increase UFA formation when the increased adipocyte mass, such as in obesity is adjacent to the acinar cells. This UFA formation is reduced by fibrosis walling-off the adipocytes in CP.