Lipid Digestion Process

Study Notes

Begins in the stomach with lingual lipase and gastric lipase
- Both enzymes are acid stable.
- Lingual lipase primarily targets short and medium chain fatty acids (milk fat).
- Gastric lipase primarily targets long chain fatty acids.
- Lingual lipase also breaks down cholesterol esters.
Emulsification occurs in the small intestine (duodenum) with the help of peristalsis and bile salts.
- Bile salts have detergent properties, increasing the surface area of hydrophobic fat droplets for enzyme access.
Pancreatic enzymes in the small intestine degrade triglycerides, cholesterol esters, and phospholipids:
- Pancreatic lipase breaks down triglycerides into 2-monoacylglycerol and free fatty acids.
- Cholesterol esterase breaks down cholesterol esters into cholesterol and fatty acids.
- Phospholipase A2 (activated by trypsin) removes one fatty acid from carbon 2 of a phospholipid.
- Lysophospholipase removes the fatty acid at carbon 1 of a phospholipid to form glycerolphosphorylbase.

Cholecystokinin (CCK) is released from jejunum and lower duodenum in response to lipids and partially digested proteins.
- CCK stimulates gallbladder contraction and release of bile, and pancreatic exocrine cell release of digestive enzymes.
- It also decreases gastric motility.
Secretin is released from other intestinal cells in response to low pH (chyme).
- Secretin promotes release of a watery solution by pancreas and liver, high in carbonate, to create an optimal pH for pancreatic enzymes.

Absorbed in the mucosal cells of the small intestine (jejunum).
Jejunum absorbs:
- Free fatty acids
- Free cholesterol
- 2-monoacylglycerol
These are combined with bile and fat-soluble vitamins to form micelles.
Micelles are soluble in the aqueous intestinal environment and absorbed at the brush border of enterocytes.
Triglycerides and cholesterol esters are resynthesized in the endoplasmic reticulum.
- Long chain fatty acids are converted to fatty acyl CoA by fatty acyl CoA synthase.
- 2-monoacylglycerol uses fatty acyl CoA to revert into TAG through the action of triglyceride synthase (acyltransferase).

Leads to steatorrhea, increased lipid and fat-soluble vitamin excretion in feces.
Caused by defects in:
- Lipid digestion
- Lipid absorption
The presence of fat droplets in stool is a characteristic of steatorrhea.
- Stool may be bulky and difficult to flush.