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ANGPTL4 mediates shuttling of lipid fuel to brown adipose tissue during sustained cold exposure
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2015 (English)In: eLIFE, E-ISSN 2050-084X, Vol. 4, e08428Article in journal (Refereed) PublishedText
Abstract [en]

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.

Place, publisher, year, edition, pages
eLife Sciences Publications , 2015. Vol. 4, e08428
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Microbiology in the medical area
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URN: urn:nbn:se:umu:diva-119687DOI: 10.7554/eLife.08428ISI: 000373443000001OAI: oai:DiVA.org:umu-119687DiVA: diva2:922869
Available from: 2016-04-25 Created: 2016-04-25 Last updated: 2016-04-25Bibliographically approved

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