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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