EP366: LDL is a Remnant or a Waste Product of Lipid Metabolism

[@faylouise8169]

points of clarity, not included: substrate molecules from ingestion if you want to compare dietary fats vs liver-made fats. Chylomicrons carry all the lipid molecules, and they are varied, fats(triglycerides and free fatty acids) from diet are different than triglycerides made from liver conversion of sugars. Chylomicrons are taken up in the liver, the repackaging of those to be further decreased as VLDL that are recycling intestinal fats (then into IDL, LDL) are carrying and made for different substrates transport than carbohydrate synthesized fats into VLDL, IDL, LDL) Different functional profiles of creation, both with the intent of delivery to tissues of triglycerides, you can affirmatively say that elevated triglycerides are a traffic congestion of denovou synthesis of glucose into fats, whereas the profile of low triglycerides and "normal" to elevated LDL from fatty acids of ingestion are pointedly carry and affect a whole host of signaling and inflammatory profiles, this being a low inflammatory profile vs the high trigs and resultant dyslipidemia of high carb generated fats, which is a state of heightened inflammation. To note that very few cells of the body rely on circulating cholesterol. again different system. systemic liver synthesized cholesterol is but a product synthesized for the molecule formation of carrying (on loads and offloads, exchanges) from dietary molecules. All cells that have the enzymes for the mevalonate pathway will make the needed cellular components on that pathway, crucial and essential, cholesterol is but one. Well known is the reduction of cholesterol will upregulate receptor uptake, that is how statins work, (not the decrease of cholesterol itself but a down regulation of that pathway, cholesterol is one of the products. HDL and LDL apoproteins are both made in the liver, HDL is also made in the intestines, both are highly active in receptor communication for immune functions. If you take the focus away from cholesterol and look at the functions and pathway synthesis actions, you will have a better metabolic understanding, and it may very well change how you approach doctoring.

[@jarichards99utube]

😊👍 -70SomethingGuy

[@ariskoktsidis4442]

So does eating too much* dietary fat for too long* damage how well each cell is able to uptake LDL for use? When does the turnover become negative? And is every person different? Aren’t there multiple factors if dietary cholesterol gets utilized or not ?