Background and objective: Fat accumulation in the pancreas has remained a relatively unknown disease since it was initially described in 1926. However, it has gained increasing attention in the past two decades with the emergence of the obesity epidemic. Pancreatic steatosis is a general term used for fat accumulation in the pancreas. It is further classified into fatty replacement, fatty infiltration, lipomatous pseudo-hypertrophy, non-alcoholic fatty pancreas disease (NAFPD) and non-alcoholic fatty steatopancreatitis (NASP). NAFPD is defined as obesity-associated accumulation of fat in the pancreas without significant alcohol consumption. Data on the prevalence of NAFPD are limited due to a lack of standardized screening tests.

Methods: MEDLINE/PubMed was searched to find relevant studies and abstracts on pancreatic steatosis.

Results: Pancreatic fat can be quantified by various imaging techniques including ultrasonography, computed tomography, magnetic resonance imaging and magnetic resonance spectroscopy. The pathophysiology of NAFPD has not been completely understood. Chronic exposure of β-cells to hyperglycemia and higher levels of free fatty acids results in increased intracellular triglyceride accumulation, which ultimately causes reduced insulin secretion, insulin resistance, cell apoptosis and subsequent fatty replacement. This vicious cycle likely is a determining factor in the development of diabetes mellitus and metabolic syndrome. There is no approved pharmacologic therapy for NAFPD. Caloric restriction might have a role in normalization of β-cell function by reducing pancreatic fat content. Troglitazone (blend of telmisartan and sitagliptin) has demonstrated effectiveness in animal models but is still in experimental stages.

Conclusion: The cause and effect relationship between the metabolic syndrome and NAFPD has not yet been established. Further studies are required to study the effect of NAFPD on glucose hemostasis.