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The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.

Angptl4 Upregulates Cholesterol Synthesis in Liver via Inhibition of LPL- and HL-Dependent Hepatic Cholesterol Uptake

Lichtenstein, Laeticia, Berbée, Jimmy F.P., van Dijk, Susan J., van Dijk, Ko Willems, Bensadoun, André, Kema, Ido P., Voshol, Peter J., Müller, Michael, Rensen, Patrick C.N., Kersten, Sander·2007·Arteriosclerosis, Thrombosis, and Vascular Biology
DOI 10.1161/atvbaha.107.151894
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Abstract

Background— Dysregulation of plasma lipoprotein levels may increase the risk for atherosclerosis. Recently, angiopoietin-like protein 4, also known as fasting-induced adipose factor Fiaf, was uncovered as a novel modulator of plasma lipoprotein metabolism. Here we take advantage of the fasting-dependent phenotype of Angptl4-transgenic (Angptl4-Tg) mice to better characterize the metabolic function of Angptl4. Methods and Results— In 24-hour fasted mice, Angptl4 overexpression increased plasma triglycerides (TG) by 24-fold, which was attributable to elevated VLDL-, IDL/LDL- and HDL-TG content. Angptl4 overexpression decreased post-heparin LPL activity by stimulating conversion of endothelial-bound LPL dimers to circulating LPL monomers. In fasted but not fed state, Angptl4 overexpression severely impaired LPL-dependent plasma TG and cholesteryl ester clearance and subsequent uptake of fatty acids and cholesterol into tissues. Consequently, hepatic cholesterol content was significantly decreased, leading to universal upregulation of cholesterol and fatty acid synthesis pathways and increased rate of cholesterol synthesis. Conclusions— The hypertriglyceridemic effect of Angptl4 is attributable to inhibition of LPL-dependent VLDL lipolysis by converting LPL dimers to monomers, and Angptl4 upregulates cholesterol synthesis in liver secondary to inhibition of LPL- and HL-dependent hepatic cholesterol uptake.

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  • Multiple laboratories have confirmed the ability of ANGPTL4 to inhibit LPL.

    “In the years since, multiple laboratories have confirmed the ability of ANGPTL4 to inhibit LPL (49–55).”

    From Regulation of lipoprotein metabolism by ANGPTL3, ANGPTL4, and ANGPTL8 (2021) · cites this paper as [50]

    The indexed copy returns bibliographic material, including a title about inhibition of LPL- and HL-dependent hepatic cholesterol uptake, but no passage stating that ANGPTL4 inhibits LPL itself. Searches for ANGPTL4 inhibiting LPL and for lipoprotein lipase did not retrieve a decisive passage from the paper's body. (LLM, conf=0.70)

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  • There are conflicting reports of ANGPTL4's ability to inhibit hepatic lipase.

    “there are conflicting reports of its ability to inhibit hepatic lipase (16, 50)”

    From Regulation of lipoprotein metabolism by ANGPTL3, ANGPTL4, and ANGPTL8 (2021) · cites this paper as [50]

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Research works printed but not linked: 35

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Metadata

Authors
Lichtenstein, L., Berbée, J. F. P., van Dijk, S. J., van Dijk, K. W., Bensadoun, A., Kema, I. P., Voshol, P. J., Müller, M., Rensen, P. C. N., & Kersten, S.
Affiliations
From the Nutrigenomics Consortium (L.L., K.W.v.D., M.M., S.K.), TI Food and Nutrition, Wageningen, the Netherlands; Nutrition, Metabolism, and Genomics group (L.L., S.J.v.D., M.M., S.K.), Wageningen University, Wageningen, the Netherlands; the Departments of General Internal Medicine (J.F.P.B., K.W.v.D., P.C.N.R.), Endocrinology and Metabolic Diseases (J.F.P.B., P.J.V., P.C.N.R.), and Human Genetics (K.W.v.D.), Leiden University Medical Center, Leiden, the Netherlands; the Division of Nutritional...
Venue
Arteriosclerosis, Thrombosis, and Vascular Biology
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
2007-11
Volume
27
Issue
11
Pages
2420-2427
ISSN
  • 1079-5642
  • 1524-4636
DOI
10.1161/atvbaha.107.151894
Cited by
163
References
1
Language
en

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