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Module 1 Lecture n5

Theme:

Common notions about qualitative nutrition diet. Carbohydrates, Lipids and Proteins digestion in the gastrointestinal tract. Absorption ways for products of digestion. Protein putrefaction in the large intestine. Nitrogen balance.

Carbohydrates Digestion in Gastrointestinal Tract

Food sources for carbohydrates:

Starch is represented in several food products, Glycogen is in the liver and muscles of animals. Lactose is in the milk, and sucrose is in sugar.

Digestion of starch and glycogen begins in the oral cavity. Salivary amylase is the main enzyme to destroy α–1,4-glycoside bonds in the structure of polysaccharides (pH opt =6-8):

( C6H10O5)n (C6H10O5)n-3 + C12H22O11 + C6H12O6

Starch Olygosaccharide Maltose Glucose

The second stage of digestion begins in the small intestine, only. That is because gastric juice has very low pH. The digestion of carbohydrates is stopped in the stomach.

Pancreatic amylase (pHopt =8-8,4) continues the digestion in the small intestine, cleaving the same type of bond (α –1,4- glycoside). But you know that there is another type of bond: α –1,6 glycoside in the structure of oligosaccharides. It is destroyed by oligo-1,6-glycosidase and amylo-1,6-glycosidase produced by mucosa cells.

Cellulose is composed of chains of β–D-glucose units joined by β–1,4 –glycoside bonds. There is no any enzyme in GIT to destroy cellulose. But it is very important in the food digestion for GIT because cellulose is used in the formation of chymus volume to promote normal smooth muscles contraction in GIT.

Maltose is destroyed due to maltase (products: 2 moles of glucose).

Sucrose is destroyed due to sucrase (products: 1 mole of glucose and 1 mole of fructose).

Lactose is destroyed due to lactase (products: 1 mole of glucose and 1 mole of galactose). All these enzymes are produced by mucosa cells of the small intestine.

The end-products of carbohydrates digestion in GIT are monosaccharides that are absorbed usually due to the active transport mechanism (Na+,K+-ATP pump). Glucose and galactose are absorbed faster then others. The time of the whole digestion of a portion of the food, containing carbohydrates, and their products absorption is about one hour. The essential hyperglycemia occurs after glucose absorption in the small intestine. Hyperglycemia: the concentration of glucose in the blood plasma is higher then 6, 11 mmol/lit (higher then 100mg%).

Then we have to consider some catabolic and anabolic pathways of glucose utilization in tissues controlled by hormone insulin.

Digestion of lipids

Triacylglycerols (TG) are the major dietary lipids of nutritional value , although many other lipid compounds are digested. Digestion of lipids in adults begins in duodenum, when the entrance of the acidic chyme from the stomach stimulates the secretion of enteric hormones by the duodenal mucosa. The bile salts and phosphatidyl choline (which is also from the bile) act as detergents in the duodenum due to their amphipathic structure; in this capacity they aid in the formation of mixed micelles. The micelles` associations of lipids are the substrates for hydrolyzing by enzymes.

There are three lipid-specific enzymes in the pancreatic juice:

1) Lipase, which cleaves TG to 2-monoacyl glycerol and two free high Fatty Acids (HFA); it is activated by bile salts;

2) Cholesterol esterase which cleaves cholesterol ester to free cholesterol and HFA;

3) Phospholipase A2 which hydrolyzes phospholipid to lysophospholipid and HFA.

But there are another Phospholipases (A1, C and D) that are produced by mucosa cells and give end-products: 2-monoacyl glycerol, HFA, glycerol, amino derivatives.

The gastric lipase action we have to consider during neonatal period, only, when pancreatic lipase may be low in activity and milk fats need to be digested. The pH optimum for this enzyme is broad, from approximately 3,0 to 6,0.

The main factor for all the products absorption in the small intestine is bile salts. Bile salts are used for micelles formation which help to absorb 2-monoacyl glycerol, HFAs and cholesterol by passive diffusion.

Then there is lipids resynthesis in the mucosa cells of the small intestine wall to form lipoproteins.

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