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Article Dans Une Revue eLife Année : 2015

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

Markus Heine
  • Fonction : Auteur
Laurent Vergnes
  • Fonction : Auteur
Mariëtte Boon
  • Fonction : Auteur
Gert Schaart
  • Fonction : Auteur
Matthijs Kc Hesselink
  • Fonction : Auteur
Karen Reue
  • Fonction : Auteur
Wouter van Marken Lichtenbelt
  • Fonction : Auteur
Gunilla Olivecrona
  • Fonction : Auteur
Patrick Cn Rensen
  • Fonction : Auteur
Joerg Heeren
  • Fonction : Auteur
Sander Kersten
  • Fonction : Auteur

Résumé

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.

Dates et versions

hal-03350294 , version 1 (21-09-2021)

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Citer

Wieneke Dijk, Markus Heine, Laurent Vergnes, Mariëtte Boon, Gert Schaart, et al.. ANGPTL4 mediates shuttling of lipid fuel to brown adipose tissue during sustained cold exposure. eLife, 2015, 4, ⟨10.7554/eLife.08428⟩. ⟨hal-03350294⟩
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