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ANGPTL4 mediates shuttling of lipid fuel to brown adipose tissue during sustained cold exposure

Standard

ANGPTL4 mediates shuttling of lipid fuel to brown adipose tissue during sustained cold exposure. / Dijk, Wieneke; Heine, Markus; Vergnes, Laurent; Boon, Mariëtte R; Schaart, Gert; Hesselink, Matthijs Kc; Reue, Karen; van Marken Lichtenbelt, Wouter D; Olivecrona, Gunilla; Rensen, Patrick Cn; Heeren, Joerg; Kersten, Sander.

in: ELIFE, Jahrgang 4, 17.10.2015.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Dijk, W, Heine, M, Vergnes, L, Boon, MR, Schaart, G, Hesselink, MK, Reue, K, van Marken Lichtenbelt, WD, Olivecrona, G, Rensen, PC, Heeren, J & Kersten, S 2015, 'ANGPTL4 mediates shuttling of lipid fuel to brown adipose tissue during sustained cold exposure', ELIFE, Jg. 4. https://doi.org/10.7554/eLife.08428

APA

Dijk, W., Heine, M., Vergnes, L., Boon, M. R., Schaart, G., Hesselink, M. K., Reue, K., van Marken Lichtenbelt, W. D., Olivecrona, G., Rensen, P. C., Heeren, J., & Kersten, S. (2015). ANGPTL4 mediates shuttling of lipid fuel to brown adipose tissue during sustained cold exposure. ELIFE, 4. https://doi.org/10.7554/eLife.08428

Vancouver

Dijk W, Heine M, Vergnes L, Boon MR, Schaart G, Hesselink MK et al. ANGPTL4 mediates shuttling of lipid fuel to brown adipose tissue during sustained cold exposure. ELIFE. 2015 Okt 17;4. https://doi.org/10.7554/eLife.08428

Bibtex

@article{ab95ef50928f4f21a141c3b1a27c6185,
title = "ANGPTL4 mediates shuttling of lipid fuel to brown adipose tissue during sustained cold exposure",
abstract = "Brown adipose tissue (BAT) activation via cold exposure is increasingly scrutinized as a potential approach to ameliorate cardio-metabolic risk. Transition to cold temperatures requires changes in the partitioning of energy substrates, re-routing fatty acids to BAT to fuel non-shivering thermogenesis. However, the mechanisms behind the redistribution of energy substrates to BAT remain largely unknown. Angiopoietin-like 4 (ANGPTL4), a protein that inhibits lipoprotein lipase (LPL) activity, is highly expressed in BAT. Here, we demonstrate that ANGPTL4 is part of a shuttling mechanism that directs fatty acids derived from circulating triglyceride-rich lipoproteins to BAT during cold. Specifically, we show that cold markedly down-regulates ANGPTL4 in BAT, likely via activation of AMPK, enhancing LPL activity and uptake of plasma triglyceride-derived fatty acids. In contrast, cold up-regulates ANGPTL4 in WAT, abolishing a cold-induced increase in LPL activity. Together, our data indicate that ANGPTL4 is an important regulator of plasma lipid partitioning during sustained cold.",
author = "Wieneke Dijk and Markus Heine and Laurent Vergnes and Boon, {Mari{\"e}tte R} and Gert Schaart and Hesselink, {Matthijs Kc} and Karen Reue and {van Marken Lichtenbelt}, {Wouter D} and Gunilla Olivecrona and Rensen, {Patrick Cn} and Joerg Heeren and Sander Kersten",
year = "2015",
month = oct,
day = "17",
doi = "10.7554/eLife.08428",
language = "English",
volume = "4",
journal = "ELIFE",
issn = "2050-084X",
publisher = "eLife Sciences Publications",

}

RIS

TY - JOUR

T1 - ANGPTL4 mediates shuttling of lipid fuel to brown adipose tissue during sustained cold exposure

AU - Dijk, Wieneke

AU - Heine, Markus

AU - Vergnes, Laurent

AU - Boon, Mariëtte R

AU - Schaart, Gert

AU - Hesselink, Matthijs Kc

AU - Reue, Karen

AU - van Marken Lichtenbelt, Wouter D

AU - Olivecrona, Gunilla

AU - Rensen, Patrick Cn

AU - Heeren, Joerg

AU - Kersten, Sander

PY - 2015/10/17

Y1 - 2015/10/17

N2 - Brown adipose tissue (BAT) activation via cold exposure is increasingly scrutinized as a potential approach to ameliorate cardio-metabolic risk. Transition to cold temperatures requires changes in the partitioning of energy substrates, re-routing fatty acids to BAT to fuel non-shivering thermogenesis. However, the mechanisms behind the redistribution of energy substrates to BAT remain largely unknown. Angiopoietin-like 4 (ANGPTL4), a protein that inhibits lipoprotein lipase (LPL) activity, is highly expressed in BAT. Here, we demonstrate that ANGPTL4 is part of a shuttling mechanism that directs fatty acids derived from circulating triglyceride-rich lipoproteins to BAT during cold. Specifically, we show that cold markedly down-regulates ANGPTL4 in BAT, likely via activation of AMPK, enhancing LPL activity and uptake of plasma triglyceride-derived fatty acids. In contrast, cold up-regulates ANGPTL4 in WAT, abolishing a cold-induced increase in LPL activity. Together, our data indicate that ANGPTL4 is an important regulator of plasma lipid partitioning during sustained cold.

AB - Brown adipose tissue (BAT) activation via cold exposure is increasingly scrutinized as a potential approach to ameliorate cardio-metabolic risk. Transition to cold temperatures requires changes in the partitioning of energy substrates, re-routing fatty acids to BAT to fuel non-shivering thermogenesis. However, the mechanisms behind the redistribution of energy substrates to BAT remain largely unknown. Angiopoietin-like 4 (ANGPTL4), a protein that inhibits lipoprotein lipase (LPL) activity, is highly expressed in BAT. Here, we demonstrate that ANGPTL4 is part of a shuttling mechanism that directs fatty acids derived from circulating triglyceride-rich lipoproteins to BAT during cold. Specifically, we show that cold markedly down-regulates ANGPTL4 in BAT, likely via activation of AMPK, enhancing LPL activity and uptake of plasma triglyceride-derived fatty acids. In contrast, cold up-regulates ANGPTL4 in WAT, abolishing a cold-induced increase in LPL activity. Together, our data indicate that ANGPTL4 is an important regulator of plasma lipid partitioning during sustained cold.

U2 - 10.7554/eLife.08428

DO - 10.7554/eLife.08428

M3 - SCORING: Journal article

C2 - 26476336

VL - 4

JO - ELIFE

JF - ELIFE

SN - 2050-084X

ER -