Dietary Lipid Digestion

Dietary lipid digestion begins in the stomach and continues in the small intestine (Fig. 1 ). Cholesteryl esters, phospholipids, and triacylglycerols (TAG) containing long-chain-length fatty acids (FA) are degraded in the small intestine by pancreatic enzymes. The most important of these enzymes are cholesterol esterase, phospholipase A2, and pancreatic lipase.
In cystic fibrosis, thickened mucus prevents these enzymes reaching the intestine. In contrast, TAG in milk fat contain short- to medium-chainlength FA and are degraded in the stomach by acid lipases (lingual lipase and gastric lipase). The hydrophobic nature of lipids requires that dietary lipids be emulsified for efficient degradation. Emulsification occurs in the small intestine using peristaltic action (mechanical mixing) and bile salts (detergents). The primary products of dietary lipid degradation are 2-monoacylglycerol, nonesterified (free) cholesterol, and free FA. These compounds, plus the fat-soluble vitamins, form mixed micelles that facilitate dietary lipid absorption by intestinal mucosal cells (enterocytes).
These cells use activated long-chain FA to regenerate TAG and cholesteryl esters and also synthesize protein (apolipoprotein [apo] B-48), all of which are then assembled with the fat-soluble vitamins into lipoprotein particles called chylomicrons. Short- and medium-chain FA enter blood directly.
Chylomicrons are first released into the lymph and then enter the blood, where their lipid core is degraded by lipoprotein lipase (with apo C-II as the coenzyme) in the capillaries of muscle and adipose tissues. Thus, dietary lipids are made available to the peripheral tissues. Fat maldigestion or malabsorption causes steatorrhea (lipid in the feces). A deficiency in the ability to degrade chylomicron components, or remove chylomicron remnants after TAG has been degraded, results in accumulation of these particles in blood.

Figure 1: Key concept map for metabolism of dietary lipids. TAG = triacylglycerols.