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Preserved insulin receptor activity was supported by Thr-308 phosphorylation of Akt following GPAT1 overexpression in Them2 -/- hepatocytes.
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Silencing of GPAT1 by gpat1 siRNA transfection reduced glucosamine-mediated anti-apoptosis in mouse embryonic stem cells and reduced mammalian target of rapamycin phosphorylation.
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GPAT1, but not GPAT4, is required to incorporate de novo synthesized fatty acids into TAG and to divert them away from oxidation.
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GPAT1 deletion is capable of reducing the number of new T cells produced via alterations in membrane receptor function.
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In the neonatal liver, DNA methylation of the Gpam promoter inhibited recruitment of the lipogenic transcription factor SREBP-1c, whereas in the adult, decreased DNA methylation resulted in active chromatin conformation, allowing recruitment of SREBP-1c.
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It was hypothesized that GPAT isoform GPAT1 might influence liver susceptibility to tumorigenesis. Data show that alterations in the formation of complex lipids catalyzed by Gpat1 reduce susceptibility to DEN-induced liver tumorigenesis.
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Sterol regulatory element binding protein 1 mediated induction of hepatic steatosis in obese mice requires Gpat1.
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Data confirm the role of mitochondrial glycerol-3-phosphate acyltransferase (GPAT) in the synthesis of triacylglycerol, in the fatty acid content of triacylglycerol and cholesterol esters, and in the positioning of specific fatty acids in phospholipids.
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results support the concept that increased hepatic mtGPAT activity associated with obesity positively contributes to lipid disorders by reducing oxidative processes and promoting de novo glycerolipid synthesis.
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mtGPAT1 is essential for normal acyl-CoA metabolism, and that the absence of hepatic mtGPAT1 results in the partitioning of fatty acids away from triacylglycerol synthesis and toward oxidation and ketogenesis
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Increased hepatic mtGPAT activity associated with obesity and insulin resistance MAY contribute to increased TAG biosynthesis and inhibition of fatty acid oxidation, responses that would promote hepatic steatosis and dyslipidemia.
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acute reduction of mtGPAT1 in liver of ob/ob mice reduces TAG synthesis, which points to a role for mtGPAT1 in the correction of obesity and related disorders
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Gpat1-/- liver exhibits increased oxidative stress and sensitivity of the mitochondrial permeability transition pore, and a balanced increase in apoptosis and proliferation.
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GPAT1 contributes significantly to cardiomyocyte triacylglycerol synthesis during lipogenic or high-fat diets and influences the incorporation of 20:4n6 into heart phospholipids.
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a novel link between GPAT-1 and changes in T-lymphocyte function
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Our results indicate differential roles of the two promoters in the regulation of hepatic GPAT1 gene expression in mice.
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Data indicate that a lack of GPAT1 activity affects both innate and adaptive immune mechanisms. Innate mechanisms may be affected by altered membrane composition or host redox status, whereas the adaptive response may require GPAT1 activity itself
