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Apolipoprotein A-V; a potent triglyceride reducer.

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Apolipoprotein A-V; a potent triglyceride reducer. / Nilsson, Stefan K; Heeren, Jörg; Olivecrona, Gunilla; Merkel, Martin.

In: ATHEROSCLEROSIS, Vol. 219, No. 1, 1, 2011, p. 15-21.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Nilsson, SK, Heeren, J, Olivecrona, G & Merkel, M 2011, 'Apolipoprotein A-V; a potent triglyceride reducer.', ATHEROSCLEROSIS, vol. 219, no. 1, 1, pp. 15-21. <http://www.ncbi.nlm.nih.gov/pubmed/21831376?dopt=Citation>

APA

Nilsson, S. K., Heeren, J., Olivecrona, G., & Merkel, M. (2011). Apolipoprotein A-V; a potent triglyceride reducer. ATHEROSCLEROSIS, 219(1), 15-21. [1]. http://www.ncbi.nlm.nih.gov/pubmed/21831376?dopt=Citation

Vancouver

Nilsson SK, Heeren J, Olivecrona G, Merkel M. Apolipoprotein A-V; a potent triglyceride reducer. ATHEROSCLEROSIS. 2011;219(1):15-21. 1.

Bibtex

@article{21354389599c4618a351d53d56df896c,
title = "Apolipoprotein A-V; a potent triglyceride reducer.",
abstract = "Since its discovery, apolipoprotein A-V has been considered to be a potent factor affecting plasma triglycerides (TG) in humans and mice. Several single nucleotide polymorphisms in the APOA5 gene are associated with increased TG levels in humans, and some nonsense mutations affecting protein structure predispose for familial hypertriglyceridemia and late onset chylomicronemia. It is not clear, how apoA-V decreases plasma TG. There are three major hypotheses: apolipoprotein A-V could work through (1) an intracellular mechanism affecting VLDL production in the liver, (2) stimulation of proteoglycan-bound lipoprotein lipase at the endothelium of capillaries in peripheral organs, or (3) enhancing the clearance of TG-rich lipoproteins via lipoprotein receptors in the liver. There is good evidence for a role of apoA-V in extracellular TG metabolism and increasing support for an additional function of ApoA-V as a receptor ligand. The intracellular role of apoA-V for lipoprotein assembly and secretion is still speculative. This review discusses these possible mechanisms.",
keywords = "Animals, Humans, Mice, Liver/metabolism, Apolipoproteins A/genetics/*physiology, Chylomicrons/blood, Hepatocytes/physiology, Hyperlipoproteinemia Type IV/*physiopathology, Lipoprotein Lipase/blood, Triglycerides/blood/*metabolism, Animals, Humans, Mice, Liver/metabolism, Apolipoproteins A/genetics/*physiology, Chylomicrons/blood, Hepatocytes/physiology, Hyperlipoproteinemia Type IV/*physiopathology, Lipoprotein Lipase/blood, Triglycerides/blood/*metabolism",
author = "Nilsson, {Stefan K} and J{\"o}rg Heeren and Gunilla Olivecrona and Martin Merkel",
year = "2011",
language = "English",
volume = "219",
pages = "15--21",
journal = "ATHEROSCLEROSIS",
issn = "0021-9150",
publisher = "Elsevier Ireland Ltd",
number = "1",

}

RIS

TY - JOUR

T1 - Apolipoprotein A-V; a potent triglyceride reducer.

AU - Nilsson, Stefan K

AU - Heeren, Jörg

AU - Olivecrona, Gunilla

AU - Merkel, Martin

PY - 2011

Y1 - 2011

N2 - Since its discovery, apolipoprotein A-V has been considered to be a potent factor affecting plasma triglycerides (TG) in humans and mice. Several single nucleotide polymorphisms in the APOA5 gene are associated with increased TG levels in humans, and some nonsense mutations affecting protein structure predispose for familial hypertriglyceridemia and late onset chylomicronemia. It is not clear, how apoA-V decreases plasma TG. There are three major hypotheses: apolipoprotein A-V could work through (1) an intracellular mechanism affecting VLDL production in the liver, (2) stimulation of proteoglycan-bound lipoprotein lipase at the endothelium of capillaries in peripheral organs, or (3) enhancing the clearance of TG-rich lipoproteins via lipoprotein receptors in the liver. There is good evidence for a role of apoA-V in extracellular TG metabolism and increasing support for an additional function of ApoA-V as a receptor ligand. The intracellular role of apoA-V for lipoprotein assembly and secretion is still speculative. This review discusses these possible mechanisms.

AB - Since its discovery, apolipoprotein A-V has been considered to be a potent factor affecting plasma triglycerides (TG) in humans and mice. Several single nucleotide polymorphisms in the APOA5 gene are associated with increased TG levels in humans, and some nonsense mutations affecting protein structure predispose for familial hypertriglyceridemia and late onset chylomicronemia. It is not clear, how apoA-V decreases plasma TG. There are three major hypotheses: apolipoprotein A-V could work through (1) an intracellular mechanism affecting VLDL production in the liver, (2) stimulation of proteoglycan-bound lipoprotein lipase at the endothelium of capillaries in peripheral organs, or (3) enhancing the clearance of TG-rich lipoproteins via lipoprotein receptors in the liver. There is good evidence for a role of apoA-V in extracellular TG metabolism and increasing support for an additional function of ApoA-V as a receptor ligand. The intracellular role of apoA-V for lipoprotein assembly and secretion is still speculative. This review discusses these possible mechanisms.

KW - Animals

KW - Humans

KW - Mice

KW - Liver/metabolism

KW - Apolipoproteins A/genetics/physiology

KW - Chylomicrons/blood

KW - Hepatocytes/physiology

KW - Hyperlipoproteinemia Type IV/physiopathology

KW - Lipoprotein Lipase/blood

KW - Triglycerides/blood/metabolism

KW - Animals

KW - Humans

KW - Mice

KW - Liver/metabolism

KW - Apolipoproteins A/genetics/physiology

KW - Chylomicrons/blood

KW - Hepatocytes/physiology

KW - Hyperlipoproteinemia Type IV/physiopathology

KW - Lipoprotein Lipase/blood

KW - Triglycerides/blood/metabolism

M3 - SCORING: Journal article

VL - 219

SP - 15

EP - 21

JO - ATHEROSCLEROSIS

JF - ATHEROSCLEROSIS

SN - 0021-9150

IS - 1

M1 - 1

ER -