Induction of hyperlipidemic pancreatitis by different fatty acids: A narrative review

Abstract

Epidemiological evidence suggests that there is a direct relationship between the degree of obesity and acute pancreatitis severity. Intake of different fatty acids leads to different types of hyperlipidemias. Adipose degradation by pancreatic lipase generates different free fatty acids, which can exacerbate pancreatitis. Saturated fatty acids (SFAs) play an inflammatory role in human metabolic syndrome and obesity, whereas unsaturated fatty acids (UFAs) are “good fats” that are thought to enhance overall health status. However, it appears that serum UFAs correlate with severe acute pancreatitis. Additionally, the “obesity paradox” suggests that UFAs potentially minimize direct harm to the organ. This review provides an in-depth overview of the role of SFAs and UFAs in acute pancreatitis of hyperlipidemia and discusses potential prevention targets for severe acute pancreatitis.

Keywords: Severe acute pancreatitis; Hypertriglyceridemia; Saturated fatty acid; Unsaturated fatty acid; M1 macrophage polarization

Core Tip: This review explores the potential causes of hyperlipidemic pancreatitis. The increased intake of saturated fatty acids (SFAs) initially elevates pancreatic lipase activity, accelerating lipolysis and fat necrosis, which in turn increases free fatty acids levels and creates a permissive inflammatory environment in severe acute pancreatitis. This process accelerates immune response of M1 macrophage polarization and subsequent acinar damage. Over time, unsaturated fatty acids (UFAs) exacerbate acinar cell damage and impair β-cell function in the pancreas, leading to diabetes. This cumulative effect is a consistent and damaging process. Therefore, the ratio of UFAs to SFAs is crucial in the pathogenesis of severe acute pancreatitis, and the progression is complex. It is essential to clearly define the primary roles of SFAs and UFAs in the development of severe acute pancreatitis.