I know that the saturated fats you ingest is broken down in the intestines by the bile acids from liver and then re synthesized as triglycerides after crossing the enterocytes. Then these triglycerides along with cholesterol (either from diet, or from the liver in form of Bile acid) is packaged into lipoprotein particles called chylomicrons..and they leave the intestines through the lymphathic Systems. These chylomicrons deliver triglycerides (converted to FFA) to adipose, muscular and other peripheral tissues.The remnants of the Chylomicrons are taken up back by the liver at a LRP receptor? Once these Chylomicrons remnants are taken up by the liver..it somehow triggers greater synthesis of ApoB particles and VLDL, as well as down regulation of LDL receptors on liver. Then the VLDL particles (loaded with Triglycerides and endogenous cholesterol?) leave the Liver and deliver FFA to peripheral tissues (similar to Chylomicrons)...and progressively lose their Triglyceride content and become IDL (reptaked by the liver). and finally LDL..since LDL receptors are also downregulated and their is presumably no other equally effective mechanism for LDL reuptake this leads to a net increase in LDL particles in Serum and measured Serum cholesterol. My question is How does Chylomicron remnants returning to the liver trigger the synthesis/Genesis of greater amount of ApoB and VLDL production? Do these remnants act as a signal to the liver to produce more VLDL/ApoB, or are Components from Chylomicrons used to produce the VLDL, and how about LDL reuptake downregulation. I am an engineer with no background in physiology/biochemistry. Could you please provide a relatively layman's explanation of the mechanism. Thank you.
Through what mechanism does ingesting Saturated Fat (but not Mono unsaturated Fat/PUFA) increase Serum Cholesterol.?
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