Gastric secretion lipids

Cholecystokinin Endocrine cells in mucosa of duodenum Breakdown products of lipid and, to a small extent, protein digestion in duodenum Inhibits gastric emptying and gastric secretion stimulates contraction of gallbladder stimulates secretion of digestive enzymes from pancreas... 

Dietary fat depresses gastric secretion, slows gastric emptying and stimulates biliary and pancreatic flow, thereby facilitating the digestive process. Often, the acceptance of food and its palatability depends upon flavor and aroma. Although TAG in the pure state are relatively tasteless, they absorb and retain flavor of food. Furthermore, in combination with other nutrients, lipids provide a texture that enhances palatability and contributes to a feeling of satiety. Finally, dietary lipids serve as carriers for fat-soluble vitamins A, D, E, and K, and as an aid to then-absorption in the intestine. 

Regarding phytochemicals, polyphenols and llavonoids in particular, their major route of entry is by oral ingestion, since they are consumed as part of a normal diet. Their bioavailability, similarly to what happens with other xenobiotics ingested orally, can be influenced by several factors. The physicochemical characteristics of the compound, such as the size of the molecule, its lipid/water solubility, or its pKa, can dictate its ability to cross a membrane by simple diffusion or not. For example, due to its size, larger molecules may imply other transport processes rather than diffusion. If the compound is hydrophiUc, it is unlikely to cross a membrane freely, but if it is too lipophilic, it may not be completely soluble in gastric secretions which can also make its absorption difficult. In addition, if the compound has ionic charge, it is not probable to cross biological membranes by diffusion and may involve other process to enter the cell. 

At neutral pH proton pump inhibitors are chemically stable, lipid-soluble, weak bases that have no inhibitory activity. In an acid environment they become protonated and a sulfenamide is formed. This sulfenamide binds covalently to the K+H+-ATPase proton pump in the gastric parietal cells, inhibiting this enzyme irreversibly and thus the entry of H+ ions into lumen. Omeprazole metabolizes at a pH of about 3.9. 1, whereas rabeprazole metabolizes at a pH of about 4.9. Secretion of acid only becomes possible again after new molecules of K+H+-ATPase are formed. 

The presence of lipids in the GI tract stimulates gall bladder contracts and biliary and pancreatic secretions, including bile salts, phospholipids, and cholesterol. These products, along with the gastric shear movement, form a crude emulsion, which promotes the solubilization of the coadministered lipophilic drug. Exogenous surface-active agents incorporated into the formulation may further stimulate the solubilization of the lipophilic compound. 

This Gram-negative, microaerophilic bacterium infects areas of the stomach and duodenum it can result in peptic ulcers, gastritis, duodenitis and cancers. H. pylori s hehcal shape and flagella favour its motility in the mucus layer. Adhesins are produced by the bacterium, which binds to membrane-associated lipids and carbohydrates to maintain its attachment to epithelial cells. Large amounts of the enzyme urease are produced, both inside and outside of the bacterium. Urease metabolises urea (which is normally secreted into the stomach) to carbon dioxide and ammonia (which neutralises gastric acid), and is instrumental in the survival of the bacterium in the acidic environment. 

It was soon recognized that gastric HVK -ATPase is the site of action for omeprazole [27,43] and that enzyme inhibition parallels inhibition of gastric acid secretion in laboratory animals [38]. Physico-chemically, omeprazole represents a lipid-permeable weak base with a pK of 4 [42]. At physiological pH, it is predominantly unionized and this neutral form passes freely across biological membranes. However, in an acidic environment with a pH below 4, it is predominantly protonated. This results in a limited permeability of the drug [28]. Due to the unique structure of the gastric... 

Yuk, H.G. and Marshall, D.L. 2005. Influence of acetic, citric and lactic acids on Escherichia coli 0157 H7 membrane lipid composition, verotoxin secretion, and acid resistance in simulated gastric fluid. Journal of Food Protection 68 673-679. 

Gastric inhibitory peptide (GIP) is found in the K cells of the duodenum and jejunum It consists of 43 amino acid residues and occurs in multiple molecular forms. Its secretion is stimulated by the presence of glucose and lipids in the duodenum. It has two main functions ... 

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