Published online Jun 14, 2025. doi: 10.3748/wjg.v31.i22.106575
Revised: April 9, 2025
Accepted: May 26, 2025
Published online: June 14, 2025
Processing time: 103 Days and 6.2 Hours
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.
