How the Human Body Obtains Cholesterol

How the Human Body Obtains Cholesterol

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According to the scientific report from Gunness and Gidley (2010), the human body obtains cholesterol from two sources. The major source is liver. Liver synthesizes about 700-900 mg cholesterol per day. Another source is diet, which account for up to 300-500 mg/d.
The major route cholesterol eliminates from human body is to convert to bile salts (BS) and excrete from the gastrointestinal tract (Gunness & Gidley, 2010). Bile salts (BS) are synthesized from cholesterol in the liver. Hydroxyl (OH) groups are inserted at several points of cholesterol, and then the second ring of cholesterol loses its double-bond. Finally, the hydrocarbon tail is shortened by three carbons, and a carboxyl group is added to the end ( Masterjohn, September 2, 2005). BS functions as solution of fat soluble components such as cholesterol, fat soluble vitamins and other lipids. BS micelles deliver those solubilized components into the enterocytes and help them digested in small intestine (Gunness & Gidley, 2010). Once the role of BS is done, it is reabsorbed into the enterohepatic circulation by hepatic portal vein. The enterohepatic circulation is very efficient at reabsorbing and recycling of the BS, only approximately 5% of BS is excreted by fecal excretion (Gunness & Gidley, 2010). The vivo studies have shown that ingestion of SDF results in a 35% to 65% increase excretion of BS in feces, thus decrease the BS re-absorption into the enterohepatic circulation. The decrease of re-absorption causes a depletion of BS in liver, so cholesterol has to be quickly catabolized to replenish BS (Gunness & Gidley, 2010). Further, cholesterol esters are also metabolized. The production of LDL-C surface membrane receptors is increased to enhance the uptake of LDL-C from the blood stream. Thus, Excess excretion of BS leads to reduction of total plasma cholesterol and low density lipoprotein cholesterol (Gunness & Gidley, 2010).
Cholesterol level in human body is also regulated by modulation of 3-hydroxy 3-mathyglutaryl co-enzyme A reductase (HMG-Co AR), an enzyme which promotes hepatic cholesterol synthesis (Gunness & Gidley, 2010). Insulin is known as an activator of HMG-Co AR. Decreasing of insulin level will reduce HMG-Co AR activity, thus leads to reduction of cholesterol synthesis (Gunness & Gidley, 2010). Viscous SDF slow down the digestion and absorption of macronutrients by delaying digestive enzyme transport and gastric emptying. Glucose is a macronutrient, SDF slow down postprandial glucose absorption. Decline of postprandial glucose level in blood resulting in a decline of insulin level, potentially reduces the activity of HMG-Co AR.

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Consequently, hepatic cholesterol synthesis is reduced. However, the insulin activity on cholesterol synthesis is complex (Gunness & Gidley, 2010). Lundin, Zhang, Lairon, Tidehag, Aman, Adlercreutz and Hallmans (2004) argueed that low insulin level indeed leads to a reduction of cholesterol level, but this consequence is happened with the combination of enhanced BS excretion. As insulin affects so many dietary responses, it is hard to determine its exact role in cholesterol controlling reactions.
Cholesterol level is also regulated by SDF fermentation products (Gunness & Gidley, 2010). SDF neither digested or absorbed by small intestine, it undergoes fermentation by anaerobic reaction in the caecum and colon. The products of fermentation are short chain fatty acids such as acetate, propionate, and butyrate. Butyrate is used by the epithelial call of colon as their primary energy source, whereas acetate and propionate are partially absorbed into the hepatic portal vein. Propionate is known to be able to inhibit hepatic cholesterol metabolism thus decrease cholesterol level (Gunness & Gidley, 2010). More than one mechanism is involved in the reaction. They include the reduction of HMG-Co AR activity and the inhibition of acetyl-Co A reductase which catalyses the synthesis of acetyl-Co A from acetate. No matter these mechanisms work alone or work together, they make propionate intervenes in glycolysis, gluconeogenosis and ketogenosis activities in the liver (Gunness & Gidley, 2010). The role of propionate in blood cholesterol reduction has been tested in vitro and in vivo. In in vitro study, propionate is injected in isolated rat liver cell at different concentrations. In the study, cholesterol biosynthesis in rat liver cell is decreased with increase of propionate concentration. However, the in vivo test does not show specific relation between propionate intake and cholesterol reduction. In the in study, rats were fed propionates having no change in hepatic cholesterol synthesis. Moreover, there is no plenty evidences show the effect of short chain fatty acids on hepatic cholesterol metabolism in human body. Results from existing studies are inconsistent, further human study are needed to understand the role of short chain fatty acids in human cholesterol metabolism (Gunness & Gidley, 2010).
Even if there is enough evidence show soluble dietary fibre fermentation products reduce hepatic cholesterol synthesis, it is not likely to be the major mechanism. This is because SDF fermentation occurs irrespective of molecular size of polysaccharides, whereas cholesterol-lowering effects are associated with molecular size (Gunness & Gidley, 2010).
In summary, there are three potential mechanisms of SDF are involved in cholesterol metabolism. First, SDF is able to decrease the re-absorption of bile salt. Bile salts depletion in liver cause cholesterol quickly catabolized to replenish bile salts, thus cholesterol level in body is decreased. Second, SDF slow down glucose absorption and result in decline of insulin level, potentially reduces the activity of HMG-Co AR. Third, SDF fermentation product propionate reduces hepatic cholesterol synthesis. In conclusion, consume soluble dietary fibre potentially reduce blood cholesterol level. High blood cholesterol is a main cause of cardiovascular disease, so fibre has benefits to reduce the risk of having cardiovascular disease.

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