In regards to eating meat

[Tenet Nosce]

Here is an excerpt from one of the nutrition books I used in school. This is long. I am not posting this simply to be wry. I see that several people in various ways have expressed a keen interest in the topics of digestive enzymes, lipase, and fat metabolism.

Advanced Nutrition and Human Metabolism - 3rd ed

Chapter 6 - Lipids - Digestion

Because fats are hydrophobic, their digestion poses a special problem because their digestive enzymes, like all proteins, are hydrophobic, and normally function in an aqueous environment. However, the surface area of dietary lipid, targeted for digestion, is greatly enhanced by a very efficient emulsification process mediated mainly by the bile salts. Consequently, accessibility of the fat to digestive enzymes is greatly increased by bile salt action.

Triacylglycerols, phospholipids (Primarily phosphatidylcholine) and sterols (mainly cholesterol) provide the lipid component of the typical Western diet. Of these, triacylglycerols, customarily called fats, are by far the major contributor with a consumption rate of about 150 g daily on average. Digestive enzymes involved in the breakdown of dietary lipids in the gastrointestinal tranct are esterases that cleave the ester bonds within triacylglycerols (lipase), phospholipids (phosopholipases), and cholesterol esters (cholesterol esterase).

Most dietary triacylglycerol digestion is completed in the lumen of the small intestine, although the process actually begins in the stomach. Digestive activity at these two sites is attributed to the two different forms of lipases: (1) lingual lipase, secreted by the serous glands lying beneath the tongue, and (2) pancreatic lipase. Basal secretion of lingual lipase apparently occurs continuously but can be stimulated by neural (sympathetic agonists), dietary (high fat), and mechanical (sucking and swallowing) factors. Lingual lipase accounts for the limited digestion of fat in the stomach, made possible by the enzyme's particularly high stability at the low pH of the gastric juices. It can readily penetrate milk fat globules without substrate stabilization by bile salts, a feature that makes it particularly important for fat digestion in the suckling infant, whose pancreatic function may not be fully developed. Lingual lipases act preferentially on triacylglycerols containing medium- and short-chain length fatty acids. It preferentially hydrolyzes fatty acids at the sn-3 position. Short- and medium-length fatty acids are metabolizes more directly than long chain fatty acids.

For dietary fat in the stomach to be hydrolyzed by lingual lipase, some degree of emulsification must occur to expose sufficient surface area of the substrate. Muscle contractions of the stomach, and the squirting of the fat through a partially opened pyloric sphincter,m produce shear forces sufficient for emulsification. Also, potential emulsifiers in the acid milieu of the stomach include complex polysaccharides, phospholipids, and peptic digests of dietary proteins. However, quantitative hydrolysis and absorption, especially of the long-chain fatty acids, require less acidity, appropriate lipases, more effective emulsifying agents (bile salts), and specialized absorptive cells. These conditions are provided in the lumen of the upper small intestine. The presence of undigested lipid in the stomach delays the rate of emptying of the stomach contents, presumably by way of the hormone enterogastrone, which inhibits gastric motility. Fats therefore have a “high satiety value”.

The partially hydrolyzed lipid emulsion leaves the stomach and enters the duodenum as fine lipid droplets. Effective emulsification takes place because as mechanical shearing continues, it is complemented by bile that is released from the gallbladder as a result of stimulation by the hormone cholecystokinin (CCK). Bicarbonate is simultaneously released from the pancreas, elevating the pH to a level suitable for pancreatic lipase activity. In combination with triacylglycerol breakdown products, bile salts are excellent emulsifying agents. Their emulsifying effectiveness is due to their amphipathic properties- that is, their possessing both hydrophilic and hydrophobic “ends.” Such molecules tend to arrange themselves on the surface of small fat particles with their hydrophobic ends turned inward and hydrophilic regions outward toward the water phase. This chemical action, together with the help of peristaltic agitation, converts the fat into small droplets with a greatly increased surface area. These particles can then be readily acted on by pancreatic lipase.

Pancreatic lipase activation is complex, requiring the participation of the protein colipase, calcium ions, and bile salts. Colipase is formed by the hydrolytic activation by trypsin of procolipase, also of pancreatic origin. It contains approximately 100 amino acid residues and possesses distinctly hydrophobnic regions that are believed to act as lipid-biding sites. Colipase has been shown to associate strongly with pancreatic lipase and therefore may act as an anchor, or linking point, for attachment of the enzyme to the bile salt-stabilized micelles described later.

The action of pancreatic lipase on ingested triacylglycerols results in a complex mixture of diacyleglycerols, monoacylglycerols, and free fatty acids. Its specificity is primarily toward sn-1-linked fatty acids ans secondarily to sn-3 bonds. Therefore, the main path of this digestion progresses from triacylglycerols to 2,3-diacylglycerols to 2-monoacylglycerols. Only a small percentage of the triacylglycerols is hydrolyzed totally to free glycerol. That which does occur probably follows the isomerization of the 2-monoacylglycerol to the 1-monoacylglycerol, which is then hydrolyzed. Esterified cholesterol, meanwhile, undergoes hydrolysis to free cholesterol and a fatty acid, catalyzed by the enzyme cholesterol esterase. The C-2 fatty acid of lecithin is hydrolytically removed by a specific esterase called phospholkipase A2, producing lysolecithin and still another free fatty acid.

The products of the partial digestion of lipids, primarily 2-monoacylglycerols, lysolecithin, cholesterol, and fatty acids, combine with bile salts, forming negatively charged polymolectular aggregates called micelles. These have a much smaller diameter (~5 nm) than the unhydrolyzed precursor particles, allowing them access to the intramicrovillus spaces (50-100) nm of the intestinal membrane.