The Digestion, Transport, and Storage of Lipids in the Human Body - Essay Example

Name Date Affiliation The digestion of lipids Introduction Lipids are considerably large molecules that are insoluble in water. Lipids are consumed as fats that are generated from plants and animals, and they are in the form of triacylglycerols (TAG) that normally consists of three fatty acids that are mainly linked to the glycerol group (Bauer, Jakob & Mosenthin, 2005, p.290). Many enzymes in the human body are water-soluble and, therefore, the enzyme responsible for breaking down lipids has an extra work to perform in order to make the lipids readily available for the body (Denning & Beckstein, 2013). The first step of digestion of lipids starts in the mouth as triacylglycerols and phospholipids encounter the saliva. The saliva helps in masticating the food (lipids) which makes it for the chewing purpose. The chewing and emulsification makes it possible for the digestive enzymes to start doing their tasks. The enzyme lipase coupled with the lingual lipase with other small amounts of the phospholipids, which acts as an emulsifier, makes the process of digestion practical and possible (Kong & Singh 2010). Emulsification and chewing increase the surface area of the lipids since they are broken down into tiny fragments that are easily accessed by the enzymes. Consequently, the fats become tiny droplets that are separable from the water components. When the lipids reach the stomach, the gastric lipase goes ahead and breaks the already broken Triacylglycerols into diglycerides and some fatty acids (Heyningen, 2009). It is estimated that exactly two hours after taking a fatty meal, at least 30%of the triacylglycerols are normally converted into the diglycerides and some fatty acids(Lattge, 2012p.14). The churning that takes place in the stomach helps in dispersing the fat molecules while the diglycerides that are derived of the process normally act as the emulsifiers. However, it is worth noting that minimal digestion of lipids takes place in the stomach. As posited above, the enzyme lipase is soluble in water, and it only works on the surfaces of fat globules where it breaks them into much smaller and finer emulsion droplets. The bile salts, amphiatic and the phospholipids molecules are normally present in the bile (Laforet & Vianey-Saban, 2010). The motility of that exists in the small intestines helps in breaking the fat globules into small droplets that are coated with some bile salts and the phospholipids in an attempt to deter the emulsion droplets from recombining. The emulsion droplets are the point where the digestion occurs since emulsification normally increases the surface area where the water-soluble lipase can act on the TAG (triacylglycerols). Moreover, colipase, which is an amphiatic protein normally, binds and anchors the surfaces of the emulsion droplets (Li, 2011). After digestion, the monoglycerides and the fatty acids associate with the bile salts and some phospholipids to form the micelles. The micelles are approximately 200 times smaller than the emulsion droplets (4-7 nm versus 1um for the droplets of the emulsion (Martin & Parton,2005). They are necessary since they can transport the monoglycerides and fatty acids that are poorly soluble into the enterocyte where they are easily absorbed. Moreover, the micelles contain some fat-soluble vitamins and cholesterol, and that explains its significance in the digestion process (Schmitz & Grandl, 2009). Micelles are known to constantly breakdown and reforming hence feeding a small amount of the fatty acids and the monoglycerides that are inform of the solution. The monoglycerides are normally non-polar and, therefore, they can easily diffuse across the enterocyte and the plasma membrane (Meams, 2013). Once the monoglycerides are in the enterocyte, the fatty acids and the monoglycerides are synthesized to form TAG that is packaged along with cholesterol of some fat-soluble vitamins. The Chylomicrons are form of lipoproteins and special particles that are normally designed for transporting the lipids in the entire circulation (Schmitz & Grandl,2009). The chylomicrons are later released through exocytosis into the basal, lateral surface of the enterocytes. The particles are normally too large to enter the typical capillaries. Instead, they normally enter the lacteals and lymphatic capillaries that normally poke up to the center of the villus. The chylomicrons normally deliver the absorbed TAG into the cell of the body (Heyningen, 2009). The TAG and the lipoproteins are normally hydrolyzed by the lipoprotein lipase that is an enzyme that is found in the capillaries of the endothelial cells. The monoglycerides and fatty acids that are released from the digestion later diffuse into the cells. Transportation of lipids After the lipids have been effectively digested, they are transported into the cells through the blood. However, the transportation of lipids is quite complicated since a series of chemical reactions that results to the formation of chemical compounds that are easily transported through the blood (Erdman, Macdonald & Zeisel, 2012). The mono and the diacylglycerols are converted into the triglycerides and packed into the lipoproteins that is found in the blood stream and are known as the chylomicrons. They normally travel in the blood stream through the lymph systems. The triacylglycerols are also known to be synthesized in the liver where they are normally packed as the low-density lipoproteins (VLDLs) and are later released into the blood stream. Once it arrives in the adipose tissue and the muscle cells, the lipoprotein lipase normally cleaves at the free fatty acids and the glycerol. The tissues normally take up the fatty acids, and the glycerol is later transported to the kidney where it is immediately converted to form dihydroxyacetone phosphate (intermediate glycolysis) by the glycerol kinase (Pol et al., 2005). Through adding a phosphate group, it is oxidized to form glycerol-3 phosphate dehydrose (DHAP).In the adipose tissues, the hydrolysis of fats to form fatty acids and glycerol is accomplished through hormone sensitive triacylglycerols lipase. The free fatty acids are later released into the blood stream where they bind with the albumin (Nelson et al,200). The complexes of the lipoproteins normally the lipids in the blood stream and this make it possible for very little cases of the lipid detection in the blood stream. The components of protein and the lipoproteins are normally synthesized in the intestinal mucosa cells and the liver. The classes of proteins and their properties make it possible for lipids to be efficiently transported in the blood (Meams, 2013). The lipoproteins are known to form micelles from lipid that is a mechanism of transporting them in the aqueous environment of the blood. There are five categories of lipoproteins that transport lipids that are found in the blood system to ensure effectiveness and efficiency in the end (Torres, et al, 2006). The chylomicrons normally transport the dietary fats and cholesterol from the intestines and the tissues. The VLDL is a second lipoprotein that transports the endogenous fats and the cholesterol from the liver to the tissues. Third, is the IDL that normally transports the endogenous lipids and cholesterol from the entire liver to the other tissues. The last lipoprotein involves, the HDL that transports the endogenous cholesterol from the immediate tissues to the liver (Van Meer, et al, 2006). The chylomicrons normally assemble the intestinal mucosa that carries the exogenous fats and the cholesterol through the lymphatic system to the large veins that are found in the body. The chylomicrons normally adhere to the inner surfaces of the capillaries of the skeletal muscles and the tissues of the adipose (Xu, et al, 2005). The fats are contained in them are later hydrolyzed the lipoprotein lipase hence freeing the fatty acids and the monoacylglycerol. The remaining shrunken portion of the chylomicrons structure is commonly known as chylomicrons remnant, and it contains the cholesterol that has dissociated from the capillary endothelium’s and later reenters the circulation where is delivered to the liver. Therefore, it is worth noting that the chylomicrons normally deliver the dietary fats to the adipose tissues and the muscles. Moreover, they carry the dietary cholesterol back to the liver (Meams, 2013). The liver synthesizes the VDLs and like the Chylomicrons; they are normally degraded by the lipoprotein lipase. The VLDL, LDL and the IDL are normally related, and the LDL appears in the circulation as the remnants of the VLDL. The VLDL is normally converted to LDL through removing all the proteins except the B-100 and esterification of most of the cholesterol (D’Avila et al, 2006, p.3087). The etherification normally occurs through transfer of the fatty acids from the lecithin to cholesterol, therefore, forming lysolecithin. The components of protein in the lipoproteins are known as apolipoproteins or the apoproteins. These proteins in as much as they are water-soluble, they have hydrophobic and hydrophilic character that is eminent in the alpha helices. The alpha helical regions are normally stabilized after the incorporation of the lipoproteins. HDL normally removes cholesterol from the tissues and finally deposits it in the liver (Ingraham 2011). It is created from the components and other degraded components of the lipoproteins. Normally, it converts cholesterol into the cholesterol ester through the LCAT enzyme that is activated by the Apo A-I in the HDL. It appears to get cholesterol to the liver through transferring the cholesterol ester to the VDL and after degradation from IDL to LDL is later taken from the liver through direct interactions between the HDL and the liver through specific receptors. Storage of fats in the human body Some lipids such as cholesterol, cholesteryl esters and the triglycerides are normally stored in the body inform of specialized cells by the name adipocytes. These specialized cells have some specialized fatty tissues that are known as the adipose tissues. The adipose tissue has the capacity of storing the fats in the cell organelles in form of the lipid droplets that grow very large in terms of size (Lattge 2012). The liver is also adopted to synthesize the fatty acids, triglycerides and the cholesterol from proteins and the carbohydrates from the diet. The excess dietary protein is not stored in the body since its toxic to the functioning of the body; instead, it is later broken down into amino acids that are later broken down through a pathway of carbon units and incorporated with the lipids (Pol, etal, 2005). Similarly, the glucose that is derived from the diet is broken down through a process known as glycolysis, and it later incorporated with the lipids (Li, 2011). The lipids that are synthesized in the internal sections of the liver are normally utilized and stored in the lipid droplets or shipped to other tissues as components of the lipoproteins. Source: Mescar and Koshland. A new model for protein stereospecificity (other than 3 point binding). Nature. 403, pg 614 (2000) Source: Mescar and Koshland. A new model for protein stereospecificity (other than 3 point binding). Nature. 403, pg 614 (2000) Disorders of lipid metabolism As posited earlier, lipids are an integral source of energy in the body. The storage of fats in the body is constantly broken down and reassembled into the body energy needs and the food that is generally available. Groups of specific enzymes normally help the body to break down and process the fats. Some abnormalities in the enzymes can lead to building up of the fatty content that would have been broken down. Piling of these fats leads to the development of some complications some of which are fatal (Laforet & Vianey-Saban 2010). First, is the abetalipoproteinemia that is an autosomal recessive disorder that is mainly caused by mutation of the gene encoding through the microsomal triglyceride transfer (MTTP) protein. MTTP is normally an endoplasmic reticulum protein that transfers the triglycerides to the apolipoproteins B-100 in the renowned hepatocyte and the apolipoproteins B-48 in the enterocyte. A mutation that occurs in the MTTP normally prevents the apoB 100 and the apo -B48 from combining with the triglycerides hence forming low-density lipoproteins (VLDL) and the chylomicrons (Vergas, 2009, p.357). The malfunctioning of the chylomicrons normally inhibits the effectiveness of lipid absorption in the intestines hence leading to hypolipidemia that is fat mal absorption coupled with some neurologic disorders. The absence of the VDL leads to accumulation of the triglycerides in the hepatocyte hence leading to steatosis. The symptoms are normally reduced through low-fat diet, supplementation with the fat-soluble vitamins and total parental nutrition (TPN) (Lattge 2012). The second complication related to the lipids is the hypobetalipoproteinemia commonly known as the (FHBL) which means Familial hypobetalipoproteinemia and it is an autosomal recessive disorder related to lipid metabolism. The complication is attributed to lowered level of the low-density lipoprotein (LDL) and the apolipoproteins B. Missence mutation in the apo B100 genes normally results in the disability of the liver to synthesize the VLDL. The synthesis that is impaired and the exportation of the VLDL normally causes the triglycerides to continue accumulating in the liver hence resulting in macro vesicular steatosis (Ingraham 2011). The clinical characteristics of FHBL are similar to those of the ABL where patients present failure to thrive the steatorrhea and the neurologic impairment especially the spinocerebellar degenerative ataxia. The best treatment for the complication involves fat restricted diets and supplementation of the fat-soluble vitamins (Adibhatla, 2008). Familial combined hyperlipidemia (FCHL) is normally an autosomal dominant lipid disorder that is caused by excessive production of the apoB-100. The overproduction normally leads to escalated VLDL production in the liver and the significant increase in hepatic and the peripheral levels of the lipid. Changes in lifestyle especially reducing the amount of fats taken, increasing the exercise, smoking cessation and reductase inhibitors in an attempt to reduce the characteristic of hyperlipidemia (Vergas, 2009). A glycogen storage disease is a disorder that is caused by inefficient metabolism of lipids. The disease results from abnormal storage of glycogen. Twelve forms of GSD have been described which are 0,I,iii,iv,vi and the phosphorylase kinase deficiencies are the most commonly associated with the liver disease (Torres et al, 2006). Glycogen is normally in the liver and later released while fasting to the immediate tissues that are unable to synthesize glucose. Hypoglycemia and hepatomegaly normally result from altered metabolism of glycogen in the liver. Patients with the disorder exhibit early growth retardation, lactic acidosis and delay of development. The adults who have the GSD are normally at risk of progression of the liver disease to cause liver cirrhosis and the development of the hepatic adenoma (Torres et al, 2006). The treatment should involve avoiding fasting, ingestion cornstarch that is slowly absorbed in the form of glucose. In some cases, liver transplantation is the only form of treatment. Weber-Christian disease is a disorder highly linked with complications in lipid metabolism. Usually a nodular and non-supportive form of pannicults is associated with abnormal metabolism of the fats. Patients normally exhibit fever, myalgias, skin lesions, arthragias and some painful nodules in the subcutaneous layer of the skin. Lipodystrophy is characterized by the abnormal redistribution of the adipose tissues in the entire body. Congenital Lipodystrophy is characterized by autosomal recessive disorder and has a frequency of 1person in 10 million people (Laforet & Vianey-Saban, 2010). . It is characterized by severe loss of fats, voracious appetite and escalated levels of linear growth. Moreover, advanced, bone ages are characteristics of infants who have this disorder. The disease may start in early childhood or later in the adolescent in previously individuals who are healthy. Another possible cause of the acquired Lipodystrophy is the chronic use of the nucleoside analogs or the most active antiretroviral therapies (HAART) that is used for treating HIV. The complications of acquired Lipodystrophy are normally similar to the congenital lipodystrophy such as diabetes mellitus, hyperinsulinemia, and hypertriglyceridemia and the low-high density lipoprotein (HDL) levels. The hepatic involvement is normally severe in the congenital cases than in the acquired cases with the progression to cirrhosis in at least 20% of the patients’. The insulin, hypoglycemic medications, metformin are useful agents that are highly effective in the treatment (Laforet & Vianey-Saban, 2010). Bibliography Adibhatla, R. M. (2008). Altered lipid metabolism in the brain injury and the disorders. In springer Netherlands, Dordecht, pp. 241-268. Bauer, E., Jakob, S., & Mosenthin, R. (2005). Principles of physiology of lipid digestion. Asian- Australasian Journal of Animal Sciences, 18(2), 282-295. Denning, E. J., & Beckstein, O. (2013). Influence of lipids on protein-mediated transmembrane transport. Chemistry and Physics of Lipids, 169, 57-71. D’Avila, H., Melo, R. C., Parreira, G. G., Werneck-Barroso, E., Castro-Faria-Neto, H. C., & Bozza, P. T. (2006). “Mycobacterium bovis bacillus Calmette-Guerin induces TLR2- mediated formation of lipid bodies: intracellular domains for eicosanoid synthesis in vivo”. The Journal of Immunology, 176(5), 3087-3097. Erdman, J. W., Macdonald, I. A. & Zeisel, S. H. (2012). Lipids: Absorption and transport. Oxford, UK: Wiley-Blackwell. Heyningen. (2009). Lipid metabolism: reviews of the HDL and cholesterol effluxes, ethanol and the hepatic lipid metabolism and the lipid disorders during childhood. Current opinion in lipidology, 20(1), 77-78. Ingraham, H. A. (2011). Metabolism: A lipid for fat disorders. Nature, 474(7352), 455-456. Kong, F., & Singh, R. P. (2010). Human Gastric Simulator (HGS) To the Study Food of the Digestion In the Human Stomach. Journal of Food Science, 75(9), E627-E635. Lattge, U. (2012). A contest of the lipids: The oil-carbohydrate and protein complement of plant seed storage. European Journal of the Lipid Science and the Technology, 114(2), 101-102. Laforet, P., & Vianey-Saban, C. (2010). Disorders of the muscle lipid and the metabolism: Diagnostic and therapeutic challenges. Neuromuscular Disorders, 20(11), 693-700. Li, P. (2011). CIDE proteins and lipid storage and secretion. Chemistry and Physics of Lipids, 164, S15-S15. Martin, S., & Parton, R. G. (2005). Caveolin, cholesterol, and lipid bodies. In Seminars in cell & developmental biology (Vol. 16, No. 2, pp. 163-174). Academic Press. Meams, B. M. (2013). Liporprotein. Nature Reviews Cardiology. 10(4), 180 Nelson, D. L. Lehninger, A. L. & Cox, M. M. 2008, Lehninger principles of biochemistry. W. H. Freeman, New York. Schmitz, G., & Grandl, M. (2009). The Endolysosomal phospholipids, the cytosolic lipid droplets storage, and the release in macrophages. Biochimica and Biophysica Acta (BBA) Molecular and the Cell Biology of the Lipids, 1791(6), 524-539. Vergas, B. (2009). Lipid disorders in type 1 diabetes. Diabetes & Metabolism, 35(5), 353-360. Pol, A., Martin, S., Fernández, C., & Parton, R. G. (2005). Cholesterol and fatty acids regulate the dynamic of the caveolin trafficking through the Golgi complex and between the cell surface and lipid bodies. Molecular biology of the cell, 16(4), 2091-2105. Torres, N., Torre-Villalvazo, I., & Tovar, A. R. (2006). Regulation of the lipid metabolism by soy protein .The Journal of nutritional biochemistry, 17(6), 365-373. Van Meer, G., Halter, D., Sprong, H., Somerharju, P., & Egmond, M. R. (2006). ABC the lipid transporters: extruders, flippases, or flopless activators?. FEBS letters, 580(4), 1171- 1177. Xu, C., Li, C. Y. T., & Kong, A. N. T. (2005). Induction of phase I, II and III of the drug metabolism/transport by the xenobiotics. Archives of pharmacal research, 28(3), 249- 268. Read More