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8 Cards in this Set
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chylomicron
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lowest density, mostly triglycerides; formed post-prandially from dietary fat; formed with cholesterol esters and ApoB48 in intestines, goes through lymph to veins to target tissues.
Target tissues: adipose when hi insulin (storage) or muscle when staved or exercise. Target uses lipoprotein lipase, regulated by ApoC-II (activates) and C-III (inhibits). Remnants are cholesterol esters, which go to liver for chol metab regulation. |
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VLDL
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contains full length ApoB100, ApoC-II and C-III, produced by liver. ApoB packages triglycerides into VLDL in the liver, driven by plasma free fatty acids, chylomicron remnants, and VLDL remnants
remnants of VLDL returning to the liver are IDL. which is recycled. Some forms LDL by degradation by hepatic triglyceride lipase → leading to loss of fatty acids, ApoC and ApoE proteins. more VLDL directly means more LDL by this process. with hypertriglyceridemia, VLDL enters the artery wall: macrophages have lipoprotein lipase, so the triglycerides in VLDL are broken down and the atherosclerotic lesions contain only cholesterol |
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LDL
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LDL-R recognition sites are found on ApoE and ApoB100, but not ApoB48, so LDL-R will bind chylomicron remnants and VLDL remnants as well as LDL
saturated fats and cholesterol intake downregulate LDL-R, leading to higher plasma levels of LDL of all the lipoproteins, LDL accumulates to the highest steady-state levels in plasma because of its slow turnover and long half-life LDL is highly pro-atherogenic, mostly due to ApoB100 high levels of LDL drive cholesterol transfer from HDL to VLDL by CETP, leading to more LDL and deposition in arterial walls over time |
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HDL
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HDL decreases the risk of atherosclerosis, is an antioxidant, inhibits endothelial adhesion molecules and monocyte migration, stabilizes prostacyclins, and promotes nitric oxide production
contains ApoA-I and ApoA-II → this nascent HDL then picks up cholesterol from macrophages in atherosclerotic lesions and transports it back to the liver most comes from the liver, with some also produced in the intestine the ABC A1 cholesterol transporter allows HDL to pick up cholesterol from macrophages, and cholesterol is then esterified by LCAT enzyme to form mature HDL, larger and with higher cholesterol content SR-B1 on the liver picks up the esterified cholesterol from the HDL, returning it to a nascent HDL low HDL levels are seen with hypertriglyceridemia, obesity, insulin resistance, and anabolic steroid use |
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Type 1 Hyperlipoproteinemia
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an accumulation of chylomicrons.
patients tend to present as infants with ab pain from acute pancreatitis resulting from severe hypertriglyceridemia → looks like appendicitis, but plasma is milky (full of triglycerides) severe hypertriglyceridemia results in eruptive, acneiform xanthomas that wax and wane with plasma triglyceride levels, and capillaries are infiltrated by fused, enlarged masses of chylomicrons triglycerides in retinal vessels produce a “cream of tomato soup” colored fundus called lipemia retinalis |
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Type 3 Hyperlipoproteinemia
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is due to a homozygous mutation for ApoE2, which is a low function mutant compared to the regular ApoE3 or ApoE4 proteins.
accumulate chylomicron remnants, leading to large accumulations over tendons called tuberous xanthomas an yellow streaks on the palms of the hands triglyceride uptake and accumulation in arteries, due to pro-atherosclerotic chylomicron remnants |
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familial hypercholesterolemia
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mutations in LDL-R, found with a heterozygote frequency of 1/300-1/450
HOMOZYGOUS: LDL plasma levels of 700-800 (normal is < 100), nl triglyceride levels, tuberous xanthomas over many joints and xanthelasmas over their eyelids; joints have constant low-grade chronic inflammation, so macrophages within the joint pick up LDL and extravascular atherosclerotic lesions tend to form over the joints heart attack before the age of 10 |
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hyerptriglyceridemia
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results from many conditions, including caloric excess, high dietary simple carbohydrates, obesity, insulin resistance, diabetes mellitus, ethanol (produces a body-wide reduced state), and hormone therapy (estrogen)
patients with genetic defects in the lipoprotein system, with 50-70% normal protein activity, can have hypertriglyceridemia exacerbated by environmental and lifestyle risk factors in an obese person, as adipose content increases and becomes saturated with triglycerides, the liver cannot keep up with triglyceride transport and becomes fatty and filled with VLDL with caloric excess (from any source), lipogenesis occurs in the liver, increasing the risk of fatty liver disease. insulin resistance → non-responsive adipose tissue continues to release free fatty acids into the blood even in the presence of hyperinsulinemia. in type I DM, triglyceride breakdown leads to ketone body synthesis combined hyperlipidemia assoc w/ low HDL, variable LDL, high triglycerides, insulin resistance, metabolic syndrome, and early cardiovascular disease. |