Lippincott's Biochemistry Chapter 18 - Cholesterol, Lipoprotein, and Steroid Metabolism

VLDL receptors are recycled, lipoprotein remnants are transferred to lysosomes for degradation, releasing reusable cholesterol, amino acids, fatty acids, and phospholipids.

Lipoprotein remnants are broken down in lysosomes by enzymes, releasing usable materials.

Cholesterol levels in cells are regulated by several mechanisms, including inhibiting cholesterol synthesis, and reducing LDL receptor production.

Enzyme crucial for cholesterol synthesis. Its expression is inhibited by high cholesterol.

Gene controlling LDL receptor protein production. Its expression reduces when cholesterol levels are high.

Fragments of chylomicrons left over after fat delivery in the bloodstream. They contribute to cellular cholesterol.

Intermediate-density lipoprotein; a cholesterol-carrying particle, a precursor of LDL.

Low-density lipoprotein; a major cholesterol-carrying particle in the blood.

Chylomicrons transport dietary triglycerides (TAG) to tissues. LPL breaks down TAGs, apo C-II is returned to HDL, and remnants carry cholesterol to the liver for uptake.

A genetic disorder characterized by a deficiency of lipoprotein lipase (LPL) or apo C-II, leading to high chylomicron levels in the blood.

After chylomicron TAGs are removed, remnants rich in cholesterol bind to liver receptors recognizing apo E for uptake and degradation.

A genetic disorder causing defective uptake of chylomicron remnants and IDL, resulting in elevated levels of these particles in the blood.

Liver-produced lipoprotein carrying triglycerides from the liver to peripheral tissues for energy.

Enzyme that breaks down triglycerides in lipoproteins (e.g., chylomicrons, VLDL) enabling their uptake by tissues.

A lipoprotein intermediate in the conversion of VLDL to LDL, containing a mix of lipids and apolipoproteins.

A lipoprotein that transports cholesterol from the liver to peripheral tissues, considered a "bad" cholesterol.

Receptor on cells that binds LDL, enabling its uptake and cholesterol delivery to cells.

A genetic disorder with defective LDL receptors, leading to high LDL cholesterol levels.

Enzyme responsible for cholesterol synthesis.

A lipoprotein involved in reversing cholesterol transport, considered a "good" cholesterol.

Protein components of lipoproteins that enable their transport and regulate lipid processing.

A genetic disorder resulting in defects in specific ABC proteins, impacting cholesterol and lipid transport.

A lipoprotein similar to LDL but with an additional apolipoprotein (apo(a)).

Apolipoprotein molecule linked to apo B-100 in Lp(a), similar to plasminogen.

High levels of Lp(a) are associated with increased risk of coronary heart disease, possibly by slowing blood clot breakdown.

A blood protein that breaks down blood clots (fibrin).

Proteins involved in lipid transport and have defects in diseases, including Tangier disease.

Dietary fats that increase levels of Lp(a).

A treatment that reduces Lp(a), LDL-C, and TAG, while increasing HDL-C.

Low-density lipoprotein, a type of cholesterol transport protein.

High-density lipoprotein, a type of cholesterol transport protein.

Negatively charged glycoproteins clustered in pits on the cell membrane, crucial for LDL uptake.

Issues with LDL receptor synthesis, causing high LDL-C in blood and increased risk of early atherosclerosis.

A genetic condition resulting from flawed LDL receptor synthesis, causing extremely high LDL cholesterol levels.

A cell's method of engulfing substances by trapping them within vesicles.

A protein that coats cell membrane pits aiding in receptor-mediated endocytosis.

Leftover particles from the absorption of dietary fat, taken up by the liver.

Larger vesicles formed after LDL complexes are internalized.

A protease that impacts LDL receptor's internalization and breakdown.

A genetic condition causing elevated blood cholesterol levels, often due to LDL receptor dysfunction.

Cholesterol is a vital component of cell membranes, and a precursor for bile acids, steroid hormones, and vitamin D.

Cholesterol comes from the diet, is synthesized by extrahepatic tissues, and by the liver itself.

The liver regulates cholesterol balance in the body. It takes in cholesterol, processes it, and releases it in various forms.

Cholesterol is eliminated from the liver as unmodified cholesterol in bile or converted into bile salts and secreted into the intestine.

Cholesterol can be part of lipoproteins that carry lipids to other tissues.

Imbalance between cholesterol intake and removal can cause its gradual buildup in tissues, especially blood vessel linings.

A potentially life-threatening condition where cholesterol buildup narrows blood vessels, increasing the risk of cardiovascular diseases.

A steroid alcohol found in animal tissues, crucial for cell membranes, bile acids, steroid hormones, and vitamin D.

A complex of lipids and proteins that transport lipids, like cholesterol, through the bloodstream.

Cholesterol comes from diet, is synthesized in the liver and other parts of the body (extrahepatic).

The liver plays a central role in regulating cholesterol levels by absorbing, processing, and releasing it.

Cholesterol is removed from the liver in bile as unmodified cholesterol or converted into bile salts, then released into the intestine.

Cholesterol can be transported in lipoproteins to different tissues.

Imbalance in cholesterol intake and removal leads to gradual buildup in tissues, mainly blood vessels.

A potentially harmful condition resulting from cholesterol buildup, narrowing blood vessels.

Cholesterol synthesis is controlled by factors such as sterol levels, insulin, and glucagon.

When cellular cholesterol levels are low, SREBP-2 is activated by proteases, upregulating HMG CoA reductase.

High sterol levels induce binding of HMG CoA reductase to INSIG proteins, leading to its degradation.

Insulin activates, while glucagon and epinephrine deactivate HMG CoA reductase.

SCAP protein's region that detects sterol levels in the ER membrane.

ER membrane proteins involved in regulating HMG CoA reductase activity, mainly by inhibiting its activity.

Steroid compounds synthesized in the liver, essential for fat digestion.

Cholic acid and chenodeoxycholic acid, main bile acid types.

Ionized forms of bile acids.

Multi-step process in the liver where hydroxyl groups are added, double bonds adjusted, and chains shortened.

Attachment of glycine or taurine to bile acids before release from the liver.

A bile acid conjugated with glycine.

A bile acid conjugated with taurine.

Enzyme in the liver crucial for bile acid synthesis; the rate-limiting step.

VLDL lipoproteins are created in the liver.

VLDL is primarily comprised of endogenous triglycerides.

VLDL transports triglycerides from the liver to peripheral tissues.

VLDL are secreted directly into the bloodstream by the liver, as nascent particles with apo B-100.

Nascent VLDL gains apo C-II and apo E from HDL in circulation.

The process where cholesterol absorbed by HDL is esterified by the enzyme lecithin:cholesterol acyltransferase (LCAT).

Plasma enzyme that esterifies cholesterol using phosphatidylcholine as a fatty acid source.

Nascent HDL, initially discoidal, transforms into spherical HDL3 and then cholesteryl ester-rich HDL2, carrying cholesteryl esters.

Cholesteryl esters are sequestered in the HDL core, maintaining a cholesterol concentration gradient, allowing continued cholesterol efflux.

Transfers cholesteryl esters from HDL to VLDL in exchange for triglycerides.

LCAT is activated by apo A-1 (a protein found on HDL).

Hepatic lipase is an enzyme involved in the conversion of HDL2 to HDL3 by degrading triglycerides and phospholipids.

A hydrophobic compound with four fused hydrocarbon rings (A-D) and an eight-carbon branched chain attached to ring D. Ring A has a hydroxyl group at carbon 3, and ring B has a double bond between carbons 5 and 6.

Cholesterol entering the liver comes from de novo synthesis and dietary intake.

Cholesterol leaves the liver via secretion in VLDL and HDL lipoproteins.

Intestinal uptake of cholesterol is mediated by the Niemann-Pick C1-like 1 protein.

Substances like sitosterol that are poorly absorbed by humans compared to cholesterol.

A rare condition caused by defects in the efflux transporter ABCG5/8.

Cholesterol combined with a fatty acid; a hydrophobic form of cholesterol not found in membranes.

Cholesterol absorbed by HDL is converted to a cholesteryl ester form by the enzyme LCAT.

The creation of cholesterol mainly done by the liver, intestine, adrenal cortex, and reproductive tissues (ovaries, testes, placenta).

Cholesterol and its esters are transported through lipoproteins and aided by phospholipids/bile salts

Plant compounds that decrease dietary cholesterol absorption by interfering with its uptake

Lipids carried in the blood stream, complex of lipids and proteins.

A type of lipid, that attaches to cholesterol at carbon 3 for cholesterol ester formation.

Sources of cholesterol include diet, liver and extrahepatic tissues.

Cholesterol is a steroid alcohol, vital for cell membranes, bile acids, hormones and vitamin D.