Digestion includes mechanical, chemical and absorptive events. Throughout its length the digestive tract is internally lined by a mucus-protected epithelium. Such mucus acts as a lubricant, thereby facilitating food movement and protecting the epithelium from mechanical abrasion. Mechanical events in digestion start with chewing, and continue along the digestive tract through diverse peristaltic movements.
Starch hydrolysis begins in the mouth, through the action of sallivary amylase. This enzyme cleaves starch into maltose, but its action is very short-lived since the enzyme is inactivated as soon as it reaches the low-pH environment of the stomach.
The stomach secretes hydrochloric acid and pepsinogen (an inactive protease). HCl affords some pretection against bacterial collonization, and converts pepsinogen into its active form, pepsin. The stomach itself is protected from HCl and pepsin due to the presence of a thick, alkaline, mucus that neutralizes the acid before it reaches the gastric epithelium.
At the parietal cells lining the stomach, carbonic anhydrase catalyses the reaction:
H2CO3 is a moderate acid, and decomposes into H+ and HCO3-. As H+ is secreted into the stomach through active transport (mediated by H+/ K+ ATPases), HCO3- is exported to the bloodstream, leading to an increase in blood pH. Pancreas uses the same reaction in order to produce HCO3-, which is secreted into the duodenum with a concomitant release of H+ towards the bloodstream (which re-establishes normal blood pH).
During a meal, secretion of gastric juices (containing HCl and pepsinogen) increases from a few mL / hour (the usual values between meals) to almost 1.5 L.
HCl and pepsinogen secretion occurs on three phases:
Cephalic phase (yields about 1/5 of total secretion)
- Psychologic stimuli (such as anticipating a meal, its smell, sight and texture) start gastric secretion even before food reaches the stomach.
Gastric phase.
- The presence of partially-digested food (especially peptides and aminoacids) in the stomach promotes the secretion of the hormone gastrin. This peptide hormome acts on the stomech, thereby stimulating secretion. Histamine and acetylcholine also stimulate secretion, and all three factors act synergistically, so that their total potentiating effect is markedly higher than the sum of their individual contribuions. Therefore, blocking only one of this factors is enough to ellicit a substantial decrease of total secretion.
Gastrin also increases gastric motility, leading to movement of the stomach contents (chyme) from the stomach and into the duodenum.
Enteric phase (yiels about 1/10 of total secretion):
- Duodenum pH is lowered by the arrival of (acidic) chyme. This increase in acidity stimulates the secretion of another hormone, secretin, which diminishes gastrointestinal motility and stops the transfer of chyme into the duodenum. Secretin acts on the stomach glands and inhibits HCl secretion. However, duodenum also secretes some gastrin, which counteracts this effect by stimulating HCl and pepsinogen secretion.
Secretin stimulates pancreas into secreting bicarbonate (HCO3-) into the duodenum. This anion neutralizes the hydrochloric acid just coming from the stomach, allowing duodenum pH to rise to the optimum values for the pancreatic enzymes (proteases, lipases, pancreatic amylase). These enzymes are secreted by the pancreas in response to cholecystokinin (CCK), a peptide hormone secreted by the duodenum when fatty acids are present in the chyme.
Cholecystokinin prompts the gallbladder to release bile into the duodenum. Bile contains bilirrubin, cholesterol and bile salts (cholesterol-derived amphipatic molecules, i.e., containing both hydrophilic and hydrophobic moieties, which allow the diet lipids to disperse in an aqueous medium, thereby forming an emulsion). The total amount ob bile salts released by the gallbladder during the digestion of a meal is far higher than the amount of bile salts present in the organism, because they are efficiently absorbed by the intestine and quickly shuttled back to the liver and gallbladder as the digestion progresses. This "recycling" of bile salts is dubbed "entero-hepatic circulation of bile salts".
In the absence of bile salts, diet lipids cannot be digested efficiently since the contact area between non-emulsified lipids and the aqueous solution where pancreatic enzymes lie is very small. This can happen e.g. when a gallstone (formed due to precipitation of excess cholesterol in the bile) blocks the bile duct. In more extre cases, gallstones may also block pancreatic secretions, since the pancreatic duct joins the bile duct before reaching the duodenum.
Intestine secretes a wide variety of digestive enzymes (maltase,lactase, saccharase, proteases, lipases, etc.) , and aborbs water, electrolytes and nutrients. Proteins are absorbed as small peptides and free aminoacids. On the other hand, carbohydrates may only be absorbed as monossacharides: the absence of maltase, sucrase or lactase (which hydrolyze the dissacharides maltose, sucrose and lactose, respectively) prevents the utilization of dissacharides. Unused dissacharides may be degraded by intestinal bacteria, leading to sudden increases of bacterial fermentation rates, and causing, nausea, vomiting, flatulence, and diarrhea. Lactose intolerance due to absence of lactase is the most common of these disorders.
Free fatty acids and monoglycerides are absorbed separately and packaged into triglycerides in the intestinal epithelial cells. They are then secreted into the lymph in chylomicrons (lipoproteins with a very high lipid content), which deliver said lipids to the cells upon entering the bloodstream. Chylomicrons depleted of most lipids (known as chylomicron remnants) are absorbed by the liver. Cholesterol and triglycerides produced endogenously are transported in Very Low Density Lipoproteins (VLDL). Upon delivering their triglycerides to cells, they become Intermediate Density Lipoproteins (IDL), enriched in cholesterol esters. Some of these IDl get taken up by the liver, and the remaining become Low Density Lipoproteins (LDL), which deliver cholesterol to cells. If the cells are unable to efficiently absorb LDL, they accumulate in the bloodstream and eventually precipitate cholesterol esters on the blood vessel walls (atherosclerose) (see this article for a review)
. Excess cholesterol from the cell membranes is taken up by High Density Lipoproteins (HDL), and then transferred to LDL or VLDL.
