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Advanced: Fat Transportation
Terms in this set (28)
What are the three different types of fats?
*Triglycerides (TG) aka triacylglycerols (TAG)
*Sterols (cholesterol or cholesteryl ester)
Can we make cholesterol? Can we break it down?
Every cell in the body can make cholesterol, but only the liver can break it down.
What are plant sterols, what do they do, how well are they absorbed, and what are some examples?
*Examples: β-sitosterol, campesterol, stigmasterol.
*Approx 1-10% absorption.
*Phytosterols are known to displace cholesterol from micelles, which interferes with cholesterol absorption.
*Results in a ~10% reduction in plasma LDL cholesterol in most people.
What are fatty acids (FA), what are the different classifications, and how are they absorbed?
*Have a hydrocarbon chain and a carboxylic acid group.
*Very long chain FA = ≥20 carbons
*Long chain FA = 14-18 carbons
*Medium chain FA = 8-12 carbons
*Short chain FA = <8 carbons long
*FA 12 carbons or longer are absorbed in the lymphatic system. FA 10 carbons or less are absorbed directly into the portal circulation.
What is the composition of coconut oil (a fatty acid) and why is this a problem?
*Mostly saturated fatty acids.
*Mostly medium chain TG (MTC).
*Most of the MCT are Lauric acid, a saturated fat with 12 carbons.
*Althoug 95% of medium chain TG are absorbed through the portal vein, only 25-39% of lauric acid is absorbed through the portal vein.
What is the structure of lipoprotein particles?
*Composed primarily of nonpolar components:
*TAG aka TG
*Fat soluble vitamins
*Composed primarily of polar components:
What are some classifications of lipoproteins?
*VLDL (very low density lipoproteins)
*IDL (intermediate density lipoproteins)
*LDL (low density lipoproteins)
*HDL (high density lipoproteins
What is lipoprotein lipase (LPL)? How are fatty acids in lipoproteins absorbed into the cell?
*For fatty acids to enter the cell, circulating lipoproteins must be hydrolyzed.
*Extracellular enzymes called lipases bind to lipoproteins and release their contents.
*FFA are then taken up by cells, where they can directly enter metabolic pathways or be stored for later use.
The triglyceride lipase gene family includes:
*Hepatic triglyceride lipase
What is the function of chylomicrons?
The main function is to deliver fat soluble material, TAG, and cholesterol to the other parts of the body.
What are chylomicrons? What protein is found on its surface?
*Chylomicrons (CM) are the largest size of all the lipoproteins.
*The main protein added to the particle surface is called apolipoprotein B-48 (apoB-48). It helps stabilize the CM in the blood stream.
What are intestinal derived lipoproteins?
*Formed and secreted after the ingestion of fat.
*CM formation occurs in direct response to eating a fat-containing meal.
*The proportions of the various lipids in CM reflect that of the diet.
*Most of the at we consume are TAGs.
Where do CM go after they have taken up the fatty acids from the intestine? What happens to the fats? What role does insluin play?
*Adipocytes are the major storage site for TAG and the most likely target of CM following a fat-containing meal.
*Usually the amount of fat consumed by an individual in a single meal exceeds the immediate energy demands of tissues.
*Therefore, most dietary TAG must be stored, at least temporarily, until needed when energy demand exceeds energy intake.
*Insulin increases the uptake of free fatty acids and monoacylglycerols in adipocytes by stimulatin LPL (lipoprotein lipase).
*Insulin accelerates the entry of glucose into adipocytes and its conversion to fatty acids.
What happens to the CM after they are depleted of TAG?
*CM depleted by TAG are taken up by the liver.
*The components of the CM are incorporated into new lipoproteins.
*Chylomicron remnants can be a negative thing if they remain in circulation or if you have too many.
What is associated with a rapid rise in serum TAG levels after a high-fat meal?
*Clinical studies have found that rapid rise in serum TAG levels after a high-fat meal was significantly related to endothelial dysfunction.
*Both fasting and postprandial hypertriglyceridemia is positively associated with the morbidity of coronary heart disease. This is related to the increase in CM remnant lipoproteins produced from the intestine.
What are the effects of excess CM remnants on disease?
Related to many metabolic disorders:
*Chronic kidney disease
*Postprandial hypertriglyceridemia (Genetics and diet. If genetics, medication can help.)
What are some dietary interventions for postprandial hypertriglyceridemia?
*If getting excess fats, decrease fat intake
*Fiber (all types)
*Omega-3 and omega-6
*Increased intake of MCT (medium chain triglycerides) - Don't require CM transportation, but may cause GI distress
What is the typical western diet?
*High in processed meat (high in saturated fat, cholesterol)
*High in high-fat dairy
*High in Na
*Low in K and Ca
*High in refined sugar and grains
*High in sugary drinks
*Low in fruits, vegetables, whole grains, fiber
*Low in fish/seafood (low in omega-3)
What are the effects of remnant lipoproteins in the bloodstream?
*Remnant lipoproteins exist in the systemic bloodstream continuously.
Many experiments have shown that remnant lipoproteins directly and indirectly correlate with the following:
*Platelet activation and coagulation
*The proliferation of smooth muscle cells
*The adhesion of monocyte cells to endothelial cells
*Remnant lipoproteins can directly penetrate the arterial wall, infiltrate the sub-endothelial space, and accelerate macrophage foam cell formation.
What are VLDLS? What do they do, and what happens once they do this? Where do the TAGs in VLDLs come from?
*A type of lipoproteins.
*The liver has limited capacity to store TAGs and must continually move them out for transport to peripheral tissues where they can be stored or used for energy.
*Made by the liver to deliver fat to the peripheral tissue.
*VLDLs eventually become depleted of TAG, and go from VLDL to IDL to LDL. This means they progressively contain less TAG and more cholesterol.
*VLDL remnants can be taken up directly by the liver or remain in circulation to continue to deliver fat.
The TAG that are contained in VLDLs are made from lipogenesis:
*Non-lipid precursors: glucose, fructose, and amino acids.
*Preformed lipids: delivered from chylomicrons, LDL, and HDL.
*Free FA bound to albumin.
What are LDLs? What do they do and what happens to them once they have done this? What factors influence the amount of LDL receptors?
*A type of lipoprotein.
*High amount of cholesterol and lower amount of TAG as compared to other lipoproteins.
*LDL receptors are found on many cell types: smooth muscle cells, liver cells, and epithelial cells of GI tract.
*LDL are taken up by the cell.
*LDL particles fuse with the lysosome and are degraded.
*LDL particles can also be taken up by macrophages.
*It is imperative that LDL, as the major carrier of cholesterol, is removed from the blood to prevent the accumulation of LDL cholesterol.
Factors influence the number of receptors on the cell surface which impact LDL-cholesterol concentration in the blood:
*Increased central adiposity reduces number of LDL receptors.
*High intakes of saturated and trans FA decrease LDL receptors.
*Soluble fiber and phytosterols increase LDL receptors.
What is HDL? Where are they made and what are their functions?
*Type of lipoprotein.
*Made in the liver and small intestines.
*Reverse cholesterol transport (picks up cholesterol from peripheral tissues, macrophages, and foam cells).
*Reduce blood clots.
*Healing the endothelium.
*Possess anti-inflammatory, antioxidant, and antithrombotic properties.
How can you increase HDLs? What is the lipoprotein(a)?
Food to increase HDL:
*Breaking fat up throughout the day.
*Moderate amounts of alcohol (AHA: "If you do not drink, do not start).
Lipoprotein(a) or Lp(a):
*Precise function and metabolism of Lp(a) is unclear.
*Lp(a) contributes to the process of atherogenesis.
What is the atherogenic lipid triad?
*High serum TG.
*Low serum HDL and/or small HDL.
*Small LDL particles and/or high serum LDL.
*This is a major CVD risk factor.
What does healthy functional adipose tissue do?
*Decrease VLDL₁ and VLDL₂
*Increase large LDL, decrease small LDL
*Increase large HDL₂ and decrease small HDL₃
What does dysfunctional adipose tissue do?
*Increase VLDL₁ and VLDL₂
*Decrease large LDL, increase small LDL
*Decrease large HDL₂ and increase small HDL₃
What happens to LDLs and HDLs when there are very large VLDLs due to excess TAG?
*Too many TAGs, the VLDLs become larger and there is more of them.
*When you have larger VLDLs with lots of TAGs, the enzyme CETP (cholesteryl ester transfer protein) is upregulated.
*CETP trades TAGs in the larger VLDLs for for cholesterol in LDLs or HDLs (LDLs have more cholesterol).
*Now the LDL or HDL has more TAGs than before, so they are good substrates for hepatic triglyceride lipase, which allows the liver to uptake the excess TAG.
*The LDL or HDL becomes smaller and denser because it lost some of its content, but remains in circulation.
*Smaller HDL has less cholesterol content and becomes more sensitive to degradation and increased clearance from the blood (overall lower HDLs). Smaller LDLs are highly atherogenic.
What is the problem with small, dense LDL?
*They are highly atherogenic.
*Small LDL particles bind less efficiently to LDL receptors, which are their normal route of clearance, which increases their time and number in the circulation.
*Insulin resistance worsens LDL clearance by reducing the ability of insulin to stimulate expression of the LDL receptors.
*Small LDL particles favor binding to the endothelial cells of the arterial wall.
*Small LDL particles are very sensitive to chemical modification (oxidation, etc) once inside the artery wall.
*Macrophages recognize the modified LDLs as foreign and engulf them.
What are foam cells?
*Foam cells are fat laden macrophages seen in atherosclerosis.
*They are an indication of plaque build-up, or atherosclerosis, which is commonly associated with increased risk of heart attack and stroke.
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