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ACSL1-mediated metabolic trapping of exogenous LCFA accelerates LCFA uptake rates, albeit to a lesser extent in females, which distinctly affects LCFA trafficking to acyl intermediates but not triglyceride storage or mitochondrial oxidation and is affected by female sex hormones.
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Data (including data from studies in cell line from knockout mice) suggest high incorporation of long-chain fatty acids, partly mediated by Acsl1, plays role in supply of octanoic acid for ghrelin acylation/lipoylation in ghrelin-producing cells.
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Acyl-CoA synthetase 1 deficiency alters cardiolipin species and impairs mitochondrial function
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ACSL1 is a programmable mediator of insulin sensitivity and cellular lipid content.
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long-chain acyl-CoA synthetase isoform 1 (ACSL1) deficiency in the heart activated mTORC1, thereby inhibiting autophagy and increasing the number of damaged mitochondria.
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Acsl1(M-/-) mice were more insulin sensitive, and, during an overnight fast, their respiratory exchange ratio was higher, indicating greater glucose use and during endurance exercise, Acsl1(M-/-) mice ran only 48% as far as controls.
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These data indicate that Acsl1-deficiency causes diastolic dysfunction and that mTOR activation is linked to the development of cardiac hypertrophy in Acsl1(H-/-) mice.
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Data indicate that the expression levels of ACSL1 and its metabolite triglyceride levels were remarkably increased in hepatitis B virus X protein (HBx)-induced liver cancer tissues from the HBx transgenic mice model.
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Increases understanding of the role of ACSL1 in monocytes/macrophages in inflammation and diabetes-accelerated atherosclerosis offers hope for new treatment to combat diabetic vascular disease[review]
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Acyl-CoA synthetase 1 is induced by Gram-negative bacteria and lipopolysaccharide and is required for phospholipid turnover in stimulated macrophages
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Endothelial ACSL1 is not required for inflammatory and apoptotic effects of a saturated fatty acid-rich environment.
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the reduced ABCA1 and cholesterol efflux in macrophages subjected to conditions of diabetes and elevated fatty load may, at least in part, be mediated by ACSL1
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Acsl1 knockdown stimulated expression of lipogenic genes.
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ACSL1 plays a critical role by promoting the inflammatory phenotype of macrophages associated with type 1 diabetes
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Acsl1 is required for heart fatty acid oxidation. Heart-specific Acsl1 deficiency causes cardiac hypertrophy.
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Acsl1(A-/-) adipocytes incorporated [(14)C]oleate into glycerolipids normally, but fatty acid oxidation rates were 50%-90% lower than in control adipocytes and mitochondria.
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O-GlcNAc interrupts a known interaction between Sp1 and sterol regulatory element binding protein 2 (SREBP2), thereby inhibiting expression of the gene encoding acetyl-CoA synthetase 1, which is involved in lipid synthesis.
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Normoleptinemic control ACS-transgenic mice developed severe dilated cardiomyopathy with thickened left ventricular walls and profound impairment of systolic function on echocardiogram
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Together, our findings suggest that a constitutive interaction between FATP1 and ACSL1 contributes to the efficient cellular uptake of LCFAs in adipocytes through vectorial acylation.
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primary role of ACSL1 in adipocytes not in control of lipid influx, as previously considered, but in lipid efflux and fatty acid-induced insulin resistance
