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Gewählte Publikation:
SHR Neuro Krebs Kardio Lipid Stoffw Microb
Duta-Mare, M; Sachdev, V; Leopold, C; Kolb, D; Vujic, N; Korbelius, M; Hofer, DC; Xia, W; Huber, K; Auer, M; Gottschalk, B; Magnes, C; Graier, WF; Prokesch, A; Radovic, B; Bogner-Strauss, JG; Kratky, D.
Lysosomal acid lipase regulates fatty acid channeling in brown adipose tissue to maintain thermogenesis.
Biochim Biophys Acta. 2018; 1863(4):467-478
Doi: 10.1016/j.bbalip.2018.01.011
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- Führende Autor*innen der Med Uni Graz
- Duta-Mare Madalina-Cristina
- Kratky Dagmar
- Co-Autor*innen der Med Uni Graz
- Auer Martina
- Gottschalk Benjamin
- Graier Wolfgang
- Kolb Dagmar
- Korbelius Melanie
- Leopold Christina
- Prokesch Andreas
- Radovic Branislav
- Sachdev Vinay
- Vujic Nemanja
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- Abstract:
- Lysosomal acid lipase (LAL) is the only known enzyme, which hydrolyzes cholesteryl esters and triacylglycerols in lysosomes of multiple cells and tissues. Here, we explored the role of LAL in brown adipose tissue (BAT). LAL-deficient (Lal-/-) mice exhibit markedly reduced UCP1 expression in BAT, modified BAT morphology with accumulation of lysosomes, and mitochondrial dysfunction, consequently leading to regular hypothermic events in mice kept at room temperature. Cold exposure resulted in reduced lipid uptake into BAT, thereby aggravating dyslipidemia and causing life threatening hypothermia in Lal-/- mice. Linking LAL as a potential regulator of lipoprotein lipase activity, we found Angptl4 mRNA expression upregulated in BAT. Our data demonstrate that LAL is critical for shuttling fatty acids derived from circulating lipoproteins to BAT during cold exposure. We conclude that inhibited lysosomal lipid hydrolysis in BAT leads to impaired thermogenesis in Lal-/- mice. Copyright © 2018 The Author(s). Published by Elsevier B.V. All rights reserved.
- Find related publications in this database (Keywords)
- Brown adipose tissue
- LAL deficiency
- Lysosome
- UCP1
- Thermogenesis
- Dyslipidemia