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) [1–8]. 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 [12–14]. With the role of unsaturated fatty acids (UFA) as propagators in SAP having recently come to light [15] 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.

Body mass index and the risk of acute pancreatitis by etiology: A prospective analysis of Korean National Screening Cohort

“…Adiposity itself increases triglyceride and local and systemic inflammation, which is involved in the development of AP. Complex factors, such as higher secretion of inflammatory mediators, lipotoxicity and necrosis of peripancreatic fat, diabetes/insulin resistance, elevated systemic inflammatory response, and low levels of anti‐inflammatory cytokines, have been implicated as pathogenic mechanisms associated with obesity in AP development . Further, elevated BMI increased the risk of symptomatic cholelithiasis, thereby increasing the risk of gallstone‐related AP.…”

Non-alcoholic fatty pancreas disease

“…Acute pancreatitis is often characterised by elevated serum amylase and lipase levels; however, according to Sepe et al ,18 there was no association between fatty pancreas and serum amylase and lipase concentrations. Recent studies identified obesity as a risk factor for severe acute pancreatitis associated with multisystem organ failure with a mortality rate of up to 30% 31. The implications of pancreatic fat with reference to its proximity to pancreatic acinar cells and the toxic effect on islets have been described 31.…”

“…Recent studies identified obesity as a risk factor for severe acute pancreatitis associated with multisystem organ failure with a mortality rate of up to 30% 31. The implications of pancreatic fat with reference to its proximity to pancreatic acinar cells and the toxic effect on islets have been described 31. Pancreatic steatosis with superimposed acute pancreatitis has been proven to intensify the inflammation, thereby having a direct toxic effect on pancreas parenchyma; in fact, fat infiltrates adjacent to acinar cells have been associated with more severe parenchymal damage in acute pancreatitis 34 35.…”

Elevated Omentin Serum Levels Predict Long-Term Survival in Critically Ill Patients

“…The visceral adipose tissue (VAT) was identified as critical source of bioactive proteins—so-called adipokines—during inflammatory diseases [1, 2]. By directly regulating hyperglycemia, glucose intolerance, and insulin resistance, adipokines function as prognostic indicators in several diseases [3, 4].…”