Figure 3.

The exocrine pancreas is a rich source of pancreatic lipases that result in the hydrolysis of TG, resulting in the liberation of a large amount of free fatty acids that, once exceeding the binding capacity of albumin, leads to mitochondrial toxicity, oxidative stress, and creates proinflammatory milieu and acinar cell damage, culminating in pancreatic acinar necrosis. In addition, chylomicronaemia and free fatty acids via micelle formation increase the viscosity of blood and, thereby, impede the blood flow to the pancreas, leading to ischemia and worsening acidosis, which potentiates FFA-mediated acinar cell damage. A certain amount of pancreatic lipase, rather than entering the lumen of the gut, finds its way into the capillary circulation of the pancreas. Normally, this does not matter. However, when the pancreatic microcirculation is sluggish in chylomicronaemia, there is time for it to release fatty acids and lysolipids, which are cytotoxic [22,58,59]. ER: endoplasmic reticulum; NO: nitric oxide; PGI2: prostacyclin I2; ROS: reactive oxygen species; TXA2: thromboxane A2.