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Select item 34012941.

Endotext [Internet].

Feingold KR, Adler RA, Ahmed SF, et al., editors.

South Dartmouth (MA): MDText.com, Inc.; 2000-.

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Select item 44036682.

StatPearls [Internet].

Treasure Island (FL): StatPearls Publishing; 2026 Jan-.

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Select item 14589843.

GeneReviews® [Internet].

Adam MP, Bick S, Mirzaa GM, et al., editors.

Seattle (WA): University of Washington, Seattle; 1993-2026.

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Select item 26591824.

Database of Abstracts of Reviews of Effects (DARE): Quality-assessed Reviews [Internet].

York (UK): Centre for Reviews and Dissemination (UK); 1995-.

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Select item 41868385.

Optimal strategies for monitoring lipid levels in patients at risk or with cardiovascular disease: a systematic review with statistical and cost-effectiveness modelling.

Perera R, McFadden E, McLellan J, et al.

Southampton (UK): NIHR Journals Library; 2015 Dec. (Health Technology Assessment, No. 19.100.)

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Select item 14152806.

Madame Curie Bioscience Database [Internet].

Austin (TX): Landes Bioscience; 2000-2013.

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Select item 53679107.

Prevention and Treatment of Atherosclerosis: Improving State-of-the-Art Management and Search for Novel Targets [Internet].

von Eckardstein A, Binder CJ, editors.

Cham (CH): Springer; 2022.

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Select item 48841288.

Familial hypercholesterolaemia: identification and management: Evidence reviews for case-finding, diagnosis and statin monotherapy.

London: National Institute for Health and Care Excellence (NICE); 2017 Nov. (NICE Guideline, No. 71.)

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Select item 31723569.

Diet and Health: Implications for Reducing Chronic Disease Risk.

National Research Council (US) Committee on Diet and Health.

Washington (DC): National Academies Press (US); 1989.

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Select item 243457210.

Fat Detection: Taste, Texture, and Post Ingestive Effects.

Montmayeur JP, le Coutre J, editors.

Boca Raton (FL): CRC Press/Taylor & Francis; 2010.

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Select item 221488611.

Screening for Intermediate Risk Factors for Coronary Heart Disease [Internet].

Helfand M, Buckley D, Fleming C, et al.

Rockville (MD): Agency for Healthcare Research and Quality (US); 2009 Oct. (Evidence Syntheses, No. 73.)

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Select item 555402812.

Inclisiran (Leqvio): CADTH Reimbursement Review: Therapeutic area: Primary hypercholesterolemia [Internet].

Ottawa (ON): Canadian Agency for Drugs and Technologies in Health; 2022 Apr.

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Select item 573513813.

Food Sources of Saturated Fat and Risk of Cardiovascular Disease: A Systematic Review [Internet].

Gardner C, Hoelscher DM, Tobias D, et al.

Alexandria (VA): USDA Nutrition Evidence Systematic Review; 2024 Nov.

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Select item 261902614.

Biosocial Surveys.

National Research Council (US) Committee on Advances in Collecting and Utilizing Biological Indicators and Genetic Information in Social Science Surveys; Weinstein M, Vaupel JW, Wachter KW, editors.

Washington (DC): National Academies Press (US); 2008.

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Select item 430903415.

Lipid Screening in Childhood and Adolescence for Detection of Familial Hypercholesterolemia: A Systematic Evidence Review for the U.S. Preventive Services Task Force [Internet].

Lozano P, Henrikson NB, Dunn J, et al.

Rockville (MD): Agency for Healthcare Research and Quality (US); 2016 Aug. (Evidence Syntheses, No. 141.)

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Select item 466662216.

Mechanisms of Vascular Disease: A Reference Book for Vascular Specialists [Internet].

Fitridge R, Thompson M, editors.

Adelaide (AU): University of Adelaide Press; 2011.

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Select item 457697817.

Dementia: Assessment, management and support for people living with dementia and their carers.

London: National Institute for Health and Care Excellence (NICE); 2018 Jun. (NICE Guideline, No. 97.)

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Select item 576984418.

Review of Evidence on Alcohol and Health.

National Academies of Sciences, Engineering, and Medicine; Health and Medicine Division; Food and Nutrition Board; Committee on Review of Evidence on Alcohol and Health; Stone KB, Calonge BN, editors.

Washington (DC): National Academies Press (US); 2025 Apr 23.

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Select item 547968819.

Screening for Lipid Disorders in Children and Adolescents: An Evidence Update for the U.S. Preventive Services Task Force [Internet].

Guirguis-Blake JM, Evans CV, Coppola EL, et al.

Rockville (MD): Agency for Healthcare Research and Quality (US); 2023 Jul. (Evidence Synthesis, No. 229.)

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Select item 485381620.

LiverTox: Clinical and Research Information on Drug-Induced Liver Injury [Internet].

Bethesda (MD): National Institute of Diabetes and Digestive and Kidney Diseases; 2012-.

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Figure 2.

Routes of exit of cholesterol from trophoblasts and fetal endothelial cells. Cholesterol exits these cells by being effluxed out of cells to acceptors in the plasma or by being secreted. There are several routes for efflux to occur, and all proteins involved have been found in the cell types listed; aqueous diffusion to acceptors (with lipid-poor acceptors being most efficient), SR-BI mediated, ABCG1-mediated, and ABCA1-mediated. In trophoblasts, studies have shown that cells can secrete lipoproteins and apolipoproteins which will carry sterols to the circulation as they exit the cell. Finally, exosomes carry cholesterol as they exit cells.

Fetal and Neonatal Sterol Metabolism.

Feingold KR, Ahmed SF, Anawalt B, et al., editors. Endotext [Internet]. South Dartmouth (MA): MDText.com, Inc.; 2000-.
Figure 3

AS lipid-binding domain modeled as an α11/3 helix. Repeats 1-4 and 5-7 are projected as a helix with 11 residues per 3 turns (or 3.67 residues per turn). In this configuration, residues at similar positions within the 11mer repeat align at the same position along the radius of the helix. Individual amino acid residues are indicated as basic (yellow), acidic (red), positively polar (green) and negatively polar (blue); uncolored residues are nonpolar. Superimposed on this structure are labels that classify residues as either lipid-exposed (Lp), solvent-exposed (Sv), or in an intermediate environment (˜), as determined by Jao et al.18 Unlabelled positions were not tested. The positions of the PD-association mutants A30P and E46K are indicated. According to this model, A30P falls within the lipid-exposed domain, while E46K is solvent-exposed. A53T falls within a 4 amino acid gap separating repeats 4 and 5. The concentration of basic residues at the polar/nonpolar interface is a conserved feature of the exchangeable apolipoproteins.10 Adapted from George et al. Neuron 1995; 15:361-372, Bussell and Eliezer, J Mol Biol 2003; 329(4):763-778, and Jao et al. Proc Natl Acad Sci USA 2004; 101(22):8331-8336.

α-Synuclein Physiology and Membrane Binding.

Madame Curie Bioscience Database [Internet]. Austin (TX): Landes Bioscience; 2000-2013.
Figure 2.

Lipoprotein Metabolism in Insulin Resistance. A combination of excess production and disposal processes results in secondary HTG and atherogenic dyslipidemia in the insulin resistant state. Chylomicrons and VLDL production originating from the intestine and liver are increased. Mobilization of free fatty acids (FFA) from fat cells by hormone sensitive and TG lipases (HSL/TGL) provides the liver with substrate for VLDL formation. Dietary intake of fat provides the intestine with TG for chylomicron formation, which is upregulated in insulin resistance. Hepatic VLDL containing excess Apo C-III relative to Apo E is increased; Apo C-III delays receptor-mediated hepatic uptake of VLDL and chylomicron remnants resulting in formation of intermediate density lipoproteins (IDL, not shown) and smaller and denser low-density lipoproteins (LDL). Lipoprotein lipase (LPL) is inhibited by Apo C-III and decreased by insulin resistance and/or deficiency. Cholesterol ester transfer protein (CETP) is upregulated resulting in exchange of TG and cholesterol ester (CE), leading to TG enrichment of LDL and HDL. Both become substrates for hepatic triglyceride lipase (HTGL), which is upregulated and acts on TG-enriched HDL and LDL to make them smaller, atherogenic and dysfunctional. Apolipoproteins A-I, B-48, B-100, C-I, C-II, C-III (C), and E are labelled and play important roles in lipoprotein metabolism.

Secondary Hypertriglyceridemia.

Feingold KR, Ahmed SF, Anawalt B, et al., editors. Endotext [Internet]. South Dartmouth (MA): MDText.com, Inc.; 2000-.
Figure 1

Transport-clearance hypothesis for Aα regulation in the brain (shown on next page). Transport-mediated clearance of Aα across the BBB. LRP1, a member of the LDL receptor family which is central to metabolism of cholesterol, mediates Aα transcytosis across the BBB, possibly metabolizing the peptide during transport out of the CNS.23 P-glycoprotein (P-gly), a member of the ABC superfamily of transporters may participate in removing the excess of Aα from brain endothelium across the luminal site of the BBB.47 ApoE and α₂-macroglobulin (α₂M), the LRP1 ligands and transport proteins for Aα in biological fluids, may influence transport-mediated clearance of Aα. Transport of plasma-deived Aα across the BBB. LRP2, a receptor for ApoJ at the luminal site of the BBB, transports ApoJ and ApoJAα complexes from circulation into the brain.34 Under physiological conditions, LRP2 is saturated by ApoJ which may preclude transport of Aα into the CNS. The role of other apolipoproteins (Apo) that bind Aα in plasma is not presently known. RAGE mediates relatively rapid influx of free, unbound Aα.43^,54 In AD, RAGE is upregulated in the vascular system and may act as a “pathogenic” receptor amplifying Aα accumulation. Aα sequestering agents. Soluble form of the RAGE receptor, sRAGE,56^,57 anti-Aα IgG46^,61 and/or serum amyloid P component (SAP)59 can all mop up the Aα in plasma reducing its influx across the BBB. Eliminating contributions of the circulating pool of Aα to its central pool could be important in sporadic AD in particular in the presence of defects of the efflux transport systems at the BBB, such as downregulated LRP1.23^,25

Transport-Clearance Hypothesis for Alzheimer's Disease and Potential Therapeutic Implications.

Madame Curie Bioscience Database [Internet]. Austin (TX): Landes Bioscience; 2000-2013.