Issues of Lipid Digestion - Essay Example

Lipids Lipid digestion is typically characterised by two challenges: lipids do not dissolve in water and fatty molecules are often too large to be absorbed into the body (Kamal, 2009). As a result, fat molecules clump together to form droplets that move into the small intestine. From the time of ingestion to the time the fat reaches the small intestine, it has usually undergone no digestion. Dietary fat thus reaches the small intestine as a large fat glob. Digestion starts in the small intestine (ileum) when bile from the gall bladder, coming via the bile duct, mixes with the fat droplets in the ileum. Bile is a solution that is composed of cholesterol, lecithin, bilirubin, and bile salts. Bile is normally produced in the liver and moved to the gallbladder for storage. The bile emulsifies the fat droplets, meaning it breaks them down into smaller droplets (Fahy et al., 2009). Please see Figure 1. Figure 1: Breakdown of a fat droplet in the small intestine (Kamal, 2009, p.3). The bile salt that is contained in the bile is responsible for breaking fats into finer particles with a larger surface area. The larger surface area aids in digestion, as the enzymes then act on them. The large surface area increases the contact with enzymes fat particles and hence faster digestion. The main enzyme in this process is called pancreatic lipase, and it acts on triglycerides (Fahy et al., 2009). Pancreatic lipase is produced by the pancreas and is released into the ileum to break down fats. Triglycerides2-monoglycerides + 2-free fatty acids In the above process, the pancreas also secretes a pancreatic collipase enzyme. This enzyme is activated by trypsin and interacts with triglycerides and the pancreatic lipase enzyme. In the lipid digestion process, its main function is to displace bile to allow it to be recycled. It also works to improve the action of pancreatic lipase by anchoring pancreatic lipase to the micelle, which is a complex lipid material that can be dissolved in water (Coleman & Lee, 2004). Please see Figure 2. Figure 2: Micelle that is formed by bile salts, triacylglycerols, and pancreatic lipase (Coleman & Less, 2004 p.13). The enzyme breaks the lipid into free fatty acids and 2-monoglycerides. The free fatty acids are further hydrolysed by the phospholipase, which are from phospholipids. Another enzyme called cholesterol esterase hydrolyses the fatty acids that are from the cholesterol esters. The micelle combines with 2-monoglycerides, free fatty acids, and vitamins that are fat soluble (i.e. Vitamin A, D, E, and K). The micelles that are mixed up then move to the mucosal cells of the intestine and release their content into the cells where they are then absorbed. The bile salts that were produced for digestion are also re-absorbed down into the gastro-intestinal tract and transported back to liver where recycling takes place before being released for another digestion process. The fatty acids, the 2-monoglycerides, cholesterol, and the esters from the cholesterol are absorbed by moving along the concentration gradient, where passive diffusion takes place. The passive diffusion involves the movement of the substances across the cell membranes without the use of the cell’s ATP energy. They are then re-packaged for transportation to the liver; this repackaging takes place in intestinal cells. Some of them go through a reformation and are turned into triglycerides that are coated with protein to form chylomicrons. The chylomicrons have soluble coats and hence can easily move outside the epithelial cell to get into lymphatic capillaries called the lacteals (Chirala & Wakil, 2004). Please see Figure 3. Lipid absorption Figure 3: Lipid absorption (Hajri & Abumrad, 2002, p. 391). Transport of lipids in the human body The means through which fat is transported through the human body is essential for one’s health and wellbeing. As stated by Hajri and Abumrad (2002), lipids are composed of phospholipids, sterols, and cholesterols. Cholesterol and triglycerides are hydrophobic molecules and thus cannot be transported in an aqueous environment like blood without being first incorporated in macromolecule complexes called lipoproteins. Thus, lipids require a specialized means of transport through the body and bloodstream: typically through lipoproteins. The composition of lipoproteins differs and their classification is normally based on their composition. They include the chylomicrons, low-density lipoproteins (LDL), very low-density lipoproteins (VLDL), and high-density lipoproteins (HDL) (Vance & Vance, 2002). Chylomicrons Chylomicrons are the largest lipoproteins and have the lowest density of all the lipoproteins. They normally transport triglycerides from the small intestine to lymph, blood and the rest of the blood cells. Chylomicrons pass through the blood stream and, through passive diffusion, lipids are removed from them. After all the lipids are removed from the chylomicrons, the remains (chylomicrons) are removed from the blood by liver cells and reassembled into newly synthesized triglycerides (Coleman & Lee, 2004). The liver is the most active site for the synthesis of lipids; it is where fatty acids are broken down to other forms of fatty acids and triglycerides. Very Low-Density Lipoproteins The very low-density lipoproteins are usually endogenously made in the liver, but a very small fraction is obtained from the diet. The very low-density lipoproteins transport triglycerides, which are about 50% lower in concentration than those transported in the chylomicrons. They also transport cholesterol and phospholipids. These types of very low-density lipoproteins travel in the body, and the triglycerides that they are carrying are removed from them by body cells. As the triglycerides are being removed, the cholesterol proportion in them increases, which makes them become denser and hence become low-density lipoproteins (Vance & Vance, 2002). Low-density lipoproteins Low-density lipoproteins are composed mainly of cholesterol, which forms approximately 50% of the low-density lipoprotein. The low-density lipoprotein normally circulates to different body parts. The triglycerides that they are carrying are released into the body’s cells. In the process, cholesterol and phospholipids are also released. The lipids that are collected by the body cells are stored for later use, and the low-density lipoproteins are removed from circulation by the liver (Hajri & Abumrad, 2002). High-density lipoproteins: High-density lipoproteins transport cholesterol from the cells to the liver where it is then disposed of. This is normally called good cholesterol, because it carries a low risk of causing heart disease (Hajri & Abumrad, 2002). Storage of lipids in the body The human body derives energy from the oxidation of carbohydrates and lipids. Fats normally act as an energy reserve in the human body. Lipids yield 9 kcal of energy per gram; conversely, carbohydrates and proteins yield 4 kcal per gram. Lipids are normally stored in all the body’s connective tissues, forming the adipose tissues (Kamal, 2009). These stored fats have various functions: providing cushion for the body’s vital organs (i.e. liver, kidney, and heart); giving structural support to the organs; and insulating the body from high and low temperatures. Lipids that are stored in the body include cholesterol, triglycerides, and cholesterol esters. These types of lipids are stored in specialized cells of the body called the adipocytes. The adipocytes make up a specialized tissue for the storage of fats called adipose tissues. Adipocytes store lipids in cell organelles called lipid droplets. The adipocytes have a role as the fuel tank for triglyceride storage. Additionally, adipose tissue consists of white and brown varieties (Kamal, 2009). Please see Figure 4. Figure 4: Overview of lipid digestion, absorption, storage, and use in the body (Kamal 2009, p.12). Disorders of lipid metabolism Hypobetalipoproteinemia This is an autosomal recessive disorder associated with lipid metabolism. The disorder normally arises if levels of the low-density lipoprotein and apolipoprotein B are low. The disorder occurs when the liver is unable to synthesize VLDL (Brun et al., 2009). The anomaly in the synthesis of VLDL and its subsequent transportation causes triglycerides to accumulate in the liver. This leads to a condition called macrovesicular steatosis. Patients with this disorder are characterised by steatorrhea, failure to thrive, neurologic impairment, and degenerative ataxia. The management and treatment of the disorder involves having a fat restricted diet. In addition, consuming supplements of fat soluble vitamins have been found to help in managing the disorder. Combined hyperlipidemia Combined hyperlipidemia is a lipid metabolism disorder that results from an overproduction of apoB-100. The overproduction leads the liver to produce excessive VLDL, and peripheral and hepatic lipid levels are subsequently increased (Brun et al., 2009). The characteristic emergence of hyperlipidemia can be reduced through lifestyle changes, such as having fat restricted diet, increasing one’s physical exercise, and avoiding smoking (Mozaffarian & Willet, 2007). Weber Christian disease This is a disorder associated with the abnormal metabolism of fat. Symptoms include a fever, skin lesions, and painful subcutaneous nodules on the extremities. The disease is also associated with a fatty infiltration of the liver caused by macrovesicular steatosis. The etiology of the disease is still unclear. Immunosuppressive regimes have been developed but have achieved limited success (Miles et al., 2009). Lipodystrophy This disorder occurs when adipose tissue is not evenly distributed in the body. The disorder is characterized by severe fat loss, an avid appetite, and accelerated linear growth, especially in children. Complications from the disorder relate to diabetes mellitus, in which insulin resistance occurs (Brun et al., 2009). Treatments include taking medications for hypoglycaemia and insulin. If diet restrictions fail to control the serum lipid, medications are used to treat the metabolic aberrations. References Brun, L. D, Gagne, C., Julien, P., Tremblay, A., Moorjani, S., Bouchard, C., and Lupien, P. J. (2009). Familial lipoprotein lipase activity deficiency: Study of total body fatness and subcutaneous fat tissue distribution. Metabolism, 38(1), 1005–1009. Chirala, S., and Wakil, S. (2004). Structure and function of animal fatty acid synthase. Lipids, 39(11), 1045–53. Coleman, R. A., and Lee. D. P. (2004). Enzymes of triglyceride synthesis and their regulation. Progress in Lipid Research, 43(2), 134–176. Fahy, E., Subramaniam, S., Murphy, R., Nishijima, M., Raetz, C., Shimizu, T., Spener, F., Van Meer, G., Wakelam, M., and Dennis E. A. (2009). Update of the lipid metabolism: Comprehensive classification system for lipids. Journal of Lipid Research, 50(1) pp.9-14. Hajri, T., and Abumrad, N. A. (2002). Fatty acid transport across membranes: Relevance to nutrition and metabolic pathology. Annual Review Nutrition Journal, 22(1), 383–415. Kamal H. (2009). Lipid metabolism, digestion, absorption, and transport. Amsterdam: Elsevier. Miles, J. M., Park, Y. S., Walewicz, D., Russell-Lopez C., Windsor, S., and Isley, W. (2005). Systemic and forearm triglyceride metabolism: Fate of lipoprotein lipase-generated glycerol and free fatty acids. Diabetes, 53 (1), 521–527. Mozaffarian, D., and Willett, W. C. (2007). Trans fatty acids and cardiovascular risk: A unique cardio metabolic imprint. Current Atherosclerosis Reports, 9(6), 486–493. Vance, J. E., and Vance D. E. (2002). Lipids and lipoproteins. Amsterdam: Elsevier. Read More