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Lipases are a family of enzymes that break down triglycerides into free fatty acids and glycerol. There are expressed and active in multiple tissues; for example, hepatic lipases are in the liver, hormone-sensitive lipases are in adipocytes, lipoprotein lipase is in the vascular endothelial surface, and pancreatic lipase is in the small intestine. [1] Lipases in pancreatic secretions are responsible for digestion and hydrolysis of fat and absorption of fat-soluble vitamins. Understanding the lipase function is crucial for the pathophysiology of fat necrosis and acute and chronic pancreatitis. Also, lipases play an essential role in the mechanism of some cholesterol-lowering medications. This review will explore the lipase enzyme's function, pathophysiology, and clinical significance.[2]

Fat necrosis can generally result from non-enzymatic and enzymatic cellular processes. During traumatic events, such as physical injury in breast tissue, non-enzymatic fat necrosis takes place.[8] In acute pancreatitis, saponification of peripancreatic fat occurs. This is due to the damage to fat cells causing the release of lipase, triglyceride breakdown, and the release of fatty acids. These fatty acids are charged negatively, and once released in the bloodstream, they bind to positively charged calcium ions. This process of salt formation between negatively charged fatty acids and positively charged calcium ions is called saponification.[9] Histologically, saponified cells appear as dead fat cells outlining the tissue, which do not contain peripheral nuclei. The saponification of the fatty acid and calcium ion combined on hematoxylin and eosin staining appears dark blue.[10]