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Digestion, Absorption and nutritional principles (Nutritional principles…
Digestion, Absorption and nutritional principles
Carbohydrates
Poly, di and monosaccharides
Starches (gulcose polymers) and derivatives are the only polysaccharides that are digested to any degree in the human GIT by human enzymes.
Amylopectin (75% of dietary starch) is a branched molecule, whereas amylose is a straight chain with only 1:4a linkages
Disaccharides
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Also ingested, along with mono-saccharides fructose and glucose
Mouth
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Remains partially active even once it moves to the stomach despite acidic gastric juice as active site is protected in presence of substrate to some degree.
Small intestine
Both salivary and pancreatic a-amylase act on ingested polysaccharides, both hydrolyze internal 1:4a linkages but spare 1:6a linkages
End producted of a-amylase digestion: oligosaccharides, disaccharide maltose, trisaccharide maltotriose and a-limit dextrins (polymers of glucose containing an average of about 8 glucose molecules with 1:6a linkages)
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Absorption
Hexoses rapidly absorbed across wall of small intestine, removed before the remains of the meal reach the terminal part of the ileum
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Transport of glucose and galcatose depends on Na+ in intestinal lumen
- High conc of Na+ on mucosal surface facilitates sugar influx into the epithelial cells while low concentration inhibits sugar influx
As these sugars share the same cotransporter (SGLT1)
- resemble GLUTs for facilitated diffusion in membrane crossing
intracellular Na+ is maintained low by transporting to the lateral intercellular spaces, while glucose is transported by GLUT2 into the interstitum and then into capillaries
Energy for glucose transport is indirectly by active transport of Na+ out of cell, maintain conc gradient across luminal border of cell
When SGLT is congenitally defective, resulting glucose/galactose malabsorption cause severe diarrhea that is often fatal if sugars not removed from diet
- Glucose and its polymers can also be used to retain Na+ in diarrheal disease
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Insulin has little effect on intestinal transport of sugars
- this processes will be normal in diabetes, but depressed by drugs (normal maxixmal rate of glucose absorption 120g/h)
Proteins
Digestion
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Small intestines
Polypeptides formed by digestion in the stomach are further digested by the powerful proteolytic enzymes of the pancreas and intestinal mucosa
Trypsin, chymotrypsins and elastase act at interior peptide bonds in the peptide molecules and are called ENDOPEPTIDASES
Formation of active endopeptidases from their inactive precursors occurs only when they have reached their site of action, secondary to the action of the brush border hydrolase, enterokinase
Trypsinogen converted to trypsin by enterokinase when pancreatic juice enters the duodenum, enterokinase contains 41% polysaccharides, and high polysaccharide content apparently prevents it from being digested before it exerts its effect
Trypsin converts chymotrypsinogens into chymotrypsins and other proenzymes into active enzymes, and can also further active more trypsinogen (auto-catalytic chain reaction)
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Carboxypetpidases of the pancreas are exopetidases that hydrolyze amino acids at the carboxyl ends of the polypeptides (A remove C-terminal with neutral AA, B remove C terminal with basic AA)
Some free A.A. are liberated in intestinal lumen, some at cell surface by aminopeptidases, carboxypeptidases, endopeptidases and dipeptidases in brush border of the mucosal cells
Some dipeptides and tripeptides are actively transported into intestinal cells and hydrolyzed by intracellular peptidases with the A.A. entering the bloodstream.
therefore, FINAL digestion in three locations: intestinal lumen, brush border and cytoplasm of mucosal cells
Absorption
At least 7 different transport systems that transport A.A. into enterocytes, 5 require Na+ and cotransports in a similar fashion as glucose, two of these 5 also require Cl-
- in 2 of the systems, transport is independent of Na+
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Transported from enterocytes to their basolateral borders by at least 5 transport systems, entering the hepatic portal blood from there
Absorption rapid in the duodenum and jejunum, little absorption in the ileum in health because majority of the free A.A. have already been assimilated at that point
About 50% of digested protein comes from ingested food, 25% in digestive juices, and 25% from desquamated mucosal cells (also where iron is excreted)
- only 2-5% of protein in the small intestine escapes digestion and absorption, some of which are eventually digested by bacterial action in the colon
almost all protein in stools is not of dietary origin but comes from bacteria and cellular debris (excreted epithelium)
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Congenital defect in mechanism that transports neutral A.A. in the intestine and renal tubules: hartnup disease
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However, most patients dont experience nutritional deficiencies because peptide transport compensates
In infants, moderate amts of undigested proteins are also absorbed
- e.g. IgAs, crossing through transcytosis and enter the circulation of the infant from the intestine
Absorbtion of intact proteins declines sharply after weaning, but adults still absorb small quantities
- e.g. allergic reactions, where some foods are considered more allergenic than others
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Nucleic acids
split to nucleotides in the small intestines by pancreatic nucleases, and then into nucleosides and phosphoric acid by enzymes that appear to be located on luminal surfaces of mucosal cells
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Bases absorbed by active transport, with smoe passsive and secondary acgive nucleoside transporters at the apical membrane of enterocytes
Lipids
Fat digestion
lingual lipase secreted by Ebner glandsd on the dorsal surface of tongue, stomach also secretes a lipase, but are of little quantitative significance for lipid digestion other than in the setting of pancreatic insufficiency, but may generate free fatty acids
Most fat digestion starts in duodenum, pancreatic lipase being one of the most important enzymes
Pancreatic lipase
hydrolyzes the 1- and 3- bonds of the triglycerides with relative ase, but acts on the 2-bonds at a very low rate
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Colipase
Protein also secreted in pancreatic juice, and when this molecule binds to the -COOH terminal domain of pancreatic lipase, opening of the lid is facilitated
Is secreted in inactive proform, activated in the intestinal lumen by trypsin
also critical for action of lipase because it allows lipase to remain associated with droplets of dietary lipid even in presence of bile acids
Cholesterol esterase
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Catalyzes hydrolysis of cholesterol esters, esters of fat-soluble vitamins and phospholipids as well as triglycerides (very similar enzyme found in human milk)
Fats relatively insoluble, limiting ability to cross the unstirred layer and reach surface of mucosal cells
They are finely emulsified in the small intestine by detergent action of bile acids, phosphatidycholine and monoglycerides
Lipids and bile acids interact spontaneously to form micelles, this cylindrical aggregates take up lipids, and although lipid concentration varies, they generally contain fatty acids, monoglycerides and cholesterol in the hydrophobic centers
Micelle formation further solubilizes lipids and provides a mechanism for their transport to the enterocytes, moving down their conc gradient through the unstirred layer to the brush border of the mucosal cells
Lipids then diffuse out of the micelles and a saturated aqueous solution of lipids is maintained in contact with the brush border of the mucosal cells
Steatorrhea
Fatty, bulky, clay-colored stools because of impaired digestion and absorption of fats (pancreatomized)
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Acid inhibits lipase, ,and lack of alkaline secretion from pancreas also contributes by lowering pH of intestine contents, and in some cases, hypersecretion of gastric acid can cause steatorrhea
Defective reabsorption of bile acids in distal ileum can cause this too, up to 50% of ingested fat appears in the feces, a severe malabsorption of fat soluble vitamin also results
- enterohepatic circulation is interrupted and liver cannot increase the rate of bile acid production
Fat absorption
used to think it enters through passive diffusion, but some evidence now suggest carriers are involved
Inside cells, lipids are rapidly esterified, maintaining a facorable concentration gradient from the lumen into the cells
There are also carriers that export certain lipids back into the lumen, limiting their oral availability
Size
<10-12 C: water soluble enough that they pass through the enterocyte unmodified and are actively transported into the portal blood
- circulate as free fatty acids (unesterified)
10-12 C: too insoluble, re-esterified to triglycerides in the enterocytes (SER)
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Triglycerides and cholestrol esters are then coated with a layer of protein, cholesterol and phospholipid to form chylomicrons, leave the cells and enter the lymphatics as too large to go into capillaries
in mucosal cells, most triglyceride is formed by acylattion of absorbed 2-monoglycerides, in SER
Some is formed from glycerophosphate, is also converted into glycerophopholipids that participates in chylomicron formatio
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Carbohydrate moieties are added to the proteins in the GA, finished chylomicrons extruded by exocytosis from basolateral aspect of the cell
Abosrption of long chain fatty acids greatest in upper parts of the small intestine, but appreciable amounts are also absorbed in the ileum
On moderate fat intake, 95% or more ingested fats are absorbed
- process involved in fat absorption are not fully mature at birth, and infants fail to absorb 10-15% of ingested fat, thus more susceptible to ill effects of disease processes that reduce fat absorption
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Control of food intake
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Higher function also modulate response to both central and peripheral cues that either trigger or inhibit food intake
Food preferences, emotions, environment, lifestyle and circadian rhythms may all have profound effects on whether food is sought and the type of food ingested.
Many hormones and other factors that are released coincident with a meal and may play other important roles in digestion and absorption are also involved in the regulation of feeding behavior
e.g., CCK produced by either I cells in intestine or released by nerve endings in the brain inhibits further food intake and is thus defined as a satiety factor or anorexin.
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Nutrition
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Mineral requirements
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iron (blood), cobalt(B12, megaloblastic anemia), iodine, zinc, copper, chromium, fluorine
can be toxic if present in large amounts, e,g, severe iron overload: hemochromatosis
Vitamins
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Fat soluble: A,D,E,K
-poorly absorbed in absence of bile/ pancreatic lipase
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