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The absorption of the fat begins in the intestine with the help of several enzymes which is closely regulated by local hormones.
More than 90% of dietary fat is in the form of triacylglycerol (TAG). The remainder of the fat is in the form of cholesterol, cholesteryl esters, phospholipids, and free fatty acids, which are unesterified. The mechanism of fat absorption includes degradation by the local enzymes, mediated by the hormones in the gastrointestinal system.
The digestion of the lipids begins in the stomach, when the food content is mixed with salivary lipase produced in the mouth. The gastric lipase is produced by the stomach and salivary lipase, which are resistant to gastric acidity, helps the breakdown of short- and medium-chain TAG molecules. Once the lipid-rich food reaches the duodenum, which is the first part of small intestine, the process of emulsification begins with the addition of bile salts and mechanical peristalsis. With the emulsification, the surface area of the lipid molecules is increased and also prevents their coalescing with other lipid molecules. Eventually, pancreatic enzymes play a major role in the absorption of dietary lipids. TAG is initially a larger molecule when it enters the intestine, and the pancreatic lipase removes the fatty acids from TAG to make it a smaller molecule, which is then taken up by intestinal villi.
Dietary cholesteryl esters in the form of cholesterol are in the nonesterified (free) form. Cholesterol esterase, a pancreatic enzyme, degrades cholesteryl esters into free fatty acids and cholesterol. Phospholipids in the food are degraded by the phospholipase, another pancreatic enzyme.
The lipid digestion is controlled by two important hormones in the intestine. Cholecystokinin (CCK) is a local hormone produced by jejunum and duodenum after the partially digested fat-rich food. CCK contracts the gall bladder to release bile and also act on the cells of pancreas to produce the pancreatic digestive enzymes. Bile fluid is produced from the liver and stored in the gall bladder, and it is rich in bile salts, phospholipids, and free cholesterol. Bile salts help in the emulsification process as mentioned before. Secretin, another small peptide hormone produced by the intestinal cells, act on the liver and pancreas to produce the watery solution rich in bicarbonates and this helps to alkalinize the gastric acidity when the food enters the duodenum. This helps to maintain the optimum pH for the action of all the above-described enzymes.
Free fatty acids, free cholesterol, and 2-monoacylglycerol are the final products of lipid digestion in the intestine. These end products along with bile salts and fat-soluble vitamins form mixed micelles. The micelles are disk-shaped clusters with water-soluble components located outside and water insoluble components located inside their surface. These mixed micelles are absorbed from the brush border of intestinal mucosal cells. Short- and medium-chain length fatty acids are directly absorbed without the assistance of micelles.
After the absorption of these lipids in the intestinal cells, the longer-chain fatty acids are further taken up by the endoplasmic reticulum of intestinal cells where the synthesis of complex lipids takes place. The longer fatty acids are activated by the enzyme, fatty acyl Co A synthetase, and are transformed into TAG with the help of TAG synthase. The small and medium-chain fatty acids are directly released into the portal circulation to the liver after binding to albumin.
Absorbed lipid components either go to liver through the portal vein or directly into systemic circulation to the rest of the body through the lymphatic system.
References and Further Reading
- Harvey, R. A., & Ferrier, D. R. (2008). Cholesterol and steroid metabolism. In R. A. Harvey (Ed.), Lippincott’s illustrated reviews biochemistry (pp. 173–180). Philadelphia: Wolters Kluwer/Lippincott Williams and Wilkins.Google Scholar