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Adipose acyl-CoA synthetase-1 directs fatty acids toward beta-oxidation and is required for cold thermogenesis.

Authors: Ellis, Jessica M  Li, Lei O  Wu, Pei-Chi  Koves, Timothy R  Ilkayeva, Olga  Stevens, Robert D  Watkins, Steven M  Muoio, Deborah M  Coleman, Rosalind A 
Citation: Ellis JM, etal., Cell Metab. 2010 Jul 7;12(1):53-64. doi: 10.1016/j.cmet.2010.05.012.
Pubmed: (View Article at PubMed) PMID:20620995
DOI: Full-text: DOI:10.1016/j.cmet.2010.05.012

Long-chain acyl-CoA synthetase-1 (ACSL1) contributes 80% of total ACSL activity in adipose tissue and was believed to be essential for the synthesis of triacylglycerol. We predicted that an adipose-specific knockout of ACSL1 (Acsl1(A-/-)) would be lipodystrophic, but compared to controls, Acsl1(A-/-) mice had 30% greater fat mass when fed a low-fat diet and gained weight normally when fed a high-fat diet. Acsl1(A-/-) adipocytes incorporated [(14)C]oleate into glycerolipids normally, but fatty acid (FA) oxidation rates were 50%-90% lower than in control adipocytes and mitochondria. Acsl1(A-/-) mice were markedly cold intolerant, and beta(3)-adrenergic agonists did not increase oxygen consumption, despite normal adrenergic signaling in brown adipose tissue. The reduced adipose FA oxidation and marked cold intolerance of Acsl1(A-/-) mice indicate that normal activation of FA for oxidation in adipose tissue in vivo requires ACSL1. Thus, ACSL1 has a specific function in directing the metabolic partitioning of FAs toward beta-oxidation in adipocytes.

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RGD ID: 13673874
Created: 2018-06-23
Species: All species
Last Modified: 2018-06-23
Status: ACTIVE



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