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New drug targets that prevent fat absorption primarily act by inhibiting lipases in the stomach and small intestine which break down fat into single monoglyceride units which can subsequently be absorbed into the intestinal cells and then be transported to other parts of the body for storage. Its implications in the treatment of obesity have shown that it can function to induce weight loss in individuals in combination with other diet and lifestyle interventions, as well as improvements in other health parameters of the obese state.

Dietary fat is ingested in the form of triglycerides, which are three fatty acid molecules that are attached to a glycerol carbohydrate backbone. Upon ingestion, these triglycerides are normally broken down by lipases, or enzymes, which break the triglyceride into two fatty acid chains and the glycerol backbone still attached to one fatty acid chain in the upper portion of the small intestine (duodenum) as well as in the stomach itself. The signal that fat is in the gastrointestinal tract also causes the enzyme cholecycstokynin to excrete bile acid from the gall bladder. The broken-down fat emulsifies with the bile acid, thereby protecting the polar nature of the fatty acid chains from coming in contact with the aqueous water environment of the digestive tract.

Bile acids and free fatty acids combine to form the circular molecular known as the micelle, where the polar ends face inward and the nonpolar end of the fatty acid faces the aqueous water environment of the digestive tract. Consequently, they travel to the edge of the intestinal tract where finger-like intestinal villi cells where the micelle breaks down the free fatty acids are actively absorbed into the intestinal villi cells. Here, they are transported through the lymph fluid to the liver. In the liver, the fatty acid chains may be repackaged with the glycerol backbone and subsequently sent to other tissues in the body such as the fat storage tissue adipose, or they may be directly used for energy as their breakdown generates the energy molecule adenosine triphosphate (ATP). ATP subsequently is broken down to release energy that the body uses to function.

The primary drug that has been synthesized to work by inhibiting fat absorption is Orlistat. Other polymers that inhibit fat absorption by inhibiting lipases are still in development and have not been developed into actual pharmaceutical therapies. Orlistat exerts its influence by selectively inhibiting the gastric lipase and lipase from the pancreas. It does so by binding to the active site of lipase enzymes, thus preventing their action in breaking down triglycerides into the fatty acids chains that can be absorbed into the intestinal villi cells. Consequently, the undigested triglycerides are excreted in the feces and are not actively absorbed by the body where they can be stored as fat. Alli is a form of Oristat that is available without a prescription. Alli causes similar side effects as Orlistat (anal leakage, gas, loose stools), but is half the dose. Long-term studies are not yet available on the effectiveness of Alli.

In clinical trials, orlistat-treated patients had significantly higher weight loss at one year and subsequently maintained that weight loss at two years with continuation of the drug. Studies have shown that approximately 30 percent of the ingested fat is lost in the feces by the action of orlistat. The drug as well has been shown to exert itself in a dose-dependent manner, meaning the higher the dose, the greater the fat malabsorption. The U.S. Food and Drug Administration (FDA) approved a prescription version of the drug marketed as Xenical. Its usage has been recommended as three 120 milligram tablets to be taken along with meals. The highest recommended dosage of orlistat is 400 milligrams daily.

Orlistat also had a beneficial effect on a number of other unhealthy parameters of the obese state. The total serum cholesterol of patients taking orlistat was significantly lower than patients taking a control drug. Furthermore, a significant reduction was found in low-density lipoprotein cholesterol (LDL-C). LDL-C has been implicated as the leading cause of cardio disease, and the subsequent lowering by orlistat might signal its use not only to reduce fat absorption but also in the treatment of high cholesterol levels. Orlistat has also been implicated as an effective lowering agent of blood pressure. Additionally, orlistat studies in diabetic patients have shown improved control of their postmeal glycemic response, characterized as a much higher spike in diabetic patients in blood glucose upon ingestion of food.

Side effects of orlistat include abdominal pain, oily stool, increased defecation, and fecal incontinence as well as flatulence. In addition, it has been suggested that absorption of fat-soluble vitamins such as vitamins A, D, E, and K might be significantly inhibited because they require fat to be actively absorbed into the body. Consequently, decreases in blood coagulation associated with decreased vitamin K absorption have been suggested as possible with orlistat usage.

Alternatively, another approach to reduce absorption of ingested fat has been the development of a synthetic fat to be incorporated into food products. This synthetic fat subsequently cannot be readily broken down by gastric lipases and will simply be excreted intact. Olestra, a sucrose carbohydrate conjugated with six to eight fatty acid chains has the physical properties of fat but subsequently cannot be broken down in the intestine. Adding olestra to a reduced-energy diet has resulted in improved weight loss.

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