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The DOI matches its Crossref record; 5 of the 5 references it cites were found in a registry or an index.

Hepatic ANGPTL3 regulates adipose tissue energy homeostasis

Wang, Yan, McNutt, Markey C., Banfi, Serena, Levin, Michael G., Holland, William L., Gusarova, Viktoria, Gromada, Jesper, Cohen, Jonathan C., Hobbs, Helen H.·2015·Proceedings of the National Academy of Sciences
DOI 10.1073/pnas.1515374112
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Abstract

Significance: Here we show that angiopoietin-like protein 3 (ANGPTL3) plays a major role in the trafficking of energy substrates to either storage or oxidative tissues in response to food intake. During fasting, adipose tissue releases fatty acids into the circulation for uptake by oxidative tissues. After feeding, the flow of fatty acids is reversed and the adipose tissue is replenished. In mice lacking ANGPTL3, the uptake of fatty acids from the circulation into adipose tissue was markedly reduced after refeeding. Triglyceride stores were maintained by increasing glucose uptake and converting it to fatty acids and triglycerides. Thus, ANGPTL3 acts like a hormone that is produced by the liver to coordinate substrate trafficking to peripheral tissues in response to dietary intake.

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  • Disruption of ANGPTL3 primarily affects triglyceride metabolism and lipid partitioning in the fed state despite ANGPTL3 expression itself not being feeding induced.

    “disruption of ANGPTL3 primarily effects triglyceride metabolism and lipid partitioning in the fed state despite the fact that ANGPTL3 expression itself is not feeding induced (72, 106).”

    From Regulation of lipoprotein metabolism by ANGPTL3, ANGPTL4, and ANGPTL8 (2021) · cites this paper as [106]

  • ANGPTL3 deficiency increased TG-derived fatty acid uptake into heart and skeletal muscle, but simultaneously decreased uptake into white adipose tissue.

    “Wang et al. (106) found that ANGPTL3 deficiency did increase TG-derived fatty acid uptake into heart and skeletal muscle, but that ANGPTL3 deficiency simultaneously decreased uptake into white adipose tissue.”

    From Regulation of lipoprotein metabolism by ANGPTL3, ANGPTL4, and ANGPTL8 (2021) · cites this paper as [106]

  • Circulating levels of ANGPTL3 are relatively constant across feeding states.

    “circulating levels of ANGPTL3 are relatively constant across feeding states (72, 106, 115).”

    From Regulation of lipoprotein metabolism by ANGPTL3, ANGPTL4, and ANGPTL8 (2021) · cites this paper as [106]

  • ANGPTL3 null mice have decreased cholesterol and triglyceride levels and increased LPL activity in postheparin plasma.

    “ANGPTL3 null mice have decreased cholesterol and triglyceride levels and increased LPL activity in postheparin plasma (16, 18, 106).”

    From Regulation of lipoprotein metabolism by ANGPTL3, ANGPTL4, and ANGPTL8 (2021) · cites this paper as [106]

  • Mice and humans lacking ANGPTL3 have lower plasma cholesterol levels.

    “In addition to decreased plasma triglycerides, mice and humans lacking ANGPTL3 also have lower plasma cholesterol levels (16, 18, 106, 108, 109, 116–118).”

    From Regulation of lipoprotein metabolism by ANGPTL3, ANGPTL4, and ANGPTL8 (2021) · cites this paper as [106]

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Citations

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Research works printed but not linked: 38

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Metadata

Authors
Wang, Y., McNutt, M. C., Banfi, S., Levin, M. G., Holland, W. L., Gusarova, V., Gromada, J., Cohen, J. C., & Hobbs, H. H.
Affiliations
  • Howard Hughes Medical Institute, University of Texas Southwestern Medical Center, Dallas, TX 75390;
  • Department of Molecular Genetics, University of Texas Southwestern Medical Center, Dallas, TX 75390;
  • Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390;
  • Regeneron Pharmaceuticals, Tarrytown, NY 10591
Venue
Proceedings of the National Academy of Sciences
Publisher
National Academy of Sciences
Published
2015-08-24
Volume
112
Issue
37
Pages
11630-11635
ISSN
  • 0027-8424
  • 1091-6490
DOI
10.1073/pnas.1515374112
Cited by
134
References
5
Language
en
Licence
www.pnas.org/site/misc/userlicense.xhtml (vor)
Funders
HHS | National Institutes of Health (PO1 HL20948)

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