| GPAT1 Activity and Abundant Palmitic Acid Impair Insulin Suppression of Hepatic Glucose Production in Primary Mouse Hepatocytes. | GPAT1 Activity and Abundant Palmitic Acid Impair Insulin Suppression of Hepatic Glucose Production in Primary Mouse Hepatocytes.
Zhang C, Steadman M, Santos HP Jr, Shaikh SR, Xavier RM., | 04/18/2024 |
| GPAT1 Deficiency in Mice Modulates NASH Progression in a Model-Dependent Manner. | GPAT1 Deficiency in Mice Modulates NASH Progression in a Model-Dependent Manner.
Smith KR, Wang W, Miller MR, Boucher M, Reynold JE, Daurio NA, Li D, Hirenallur-Shanthappa D, Ahn Y, Beebe DA, Kelly KL, Ross TT, Bence KK, Wan M., Free PMC Article | 01/26/2024 |
| GPAT Gene Silencing in Muscle Reduces Diacylglycerols Content and Improves Insulin Action in Diet-Induced Insulin Resistance. | GPAT Gene Silencing in Muscle Reduces Diacylglycerols Content and Improves Insulin Action in Diet-Induced Insulin Resistance.
Kojta I, Zabielski P, Roszczyc-Owsiejczuk K, Imierska M, Sokołowska E, Błachnio-Zabielska A., Free PMC Article | 03/6/2021 |
| Preserved insulin receptor activity was supported by Thr-308 phosphorylation of Akt following GPAT1 overexpression in Them2 -/- hepatocytes. | Thioesterase superfamily member 2 promotes hepatic insulin resistance in the setting of glycerol-3-phosphate acyltransferase 1-induced steatosis.
Tillander V, Miniami A, Alves-Bezerra M, Coleman RA, Cohen DE., Free PMC Article | 05/18/2019 |
| Silencing of GPAT1 by gpat1 siRNA transfection reduced glucosamine-mediated anti-apoptosis in mouse embryonic stem cells and reduced mammalian target of rapamycin phosphorylation. | Glycerol-3-phosphate acyltransferase-1 upregulation by O-GlcNAcylation of Sp1 protects against hypoxia-induced mouse embryonic stem cell apoptosis via mTOR activation.
Lee HJ, Ryu JM, Jung YH, Lee KH, Kim DI, Han HJ., Free PMC Article | 12/24/2016 |
| GPAT1, but not GPAT4, is required to incorporate de novo synthesized fatty acids into TAG and to divert them away from oxidation. | Glycerol-3-phosphate acyltransferase (GPAT)-1, but not GPAT4, incorporates newly synthesized fatty acids into triacylglycerol and diminishes fatty acid oxidation.
Wendel AA, Cooper DE, Ilkayeva OR, Muoio DM, Coleman RA., Free PMC Article | 11/30/2013 |
| GPAT1 deletion is capable of reducing the number of new T cells produced via alterations in membrane receptor function. | Glycerol-3-phosphate acyltransferase-1 gene ablation results in altered thymocyte lipid content and reduces thymic T cell production in mice.
Gulvady AA, Murphy EJ, Ciolino HP, Cabrera RM, Jolly CA. | 06/15/2013 |
| 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. | Role of DNA methylation in the regulation of lipogenic glycerol-3-phosphate acyltransferase 1 gene expression in the mouse neonatal liver.
Ehara T, Kamei Y, Takahashi M, Yuan X, Kanai S, Tamura E, Tanaka M, Yamazaki T, Miura S, Ezaki O, Suganami T, Okano M, Ogawa Y., Free PMC Article | 12/29/2012 |
| 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. | Mice deficient in glycerol-3-phosphate acyltransferase-1 have a reduced susceptibility to liver cancer.
Ellis JM, Paul DS, Depetrillo MA, Singh BP, Malarkey DE, Coleman RA., Free PMC Article | 10/20/2012 |
| Sterol regulatory element binding protein 1 mediated induction of hepatic steatosis in obese mice requires Gpat1. | Glycerol-3-phosphate acyltransferase 1 deficiency in ob/ob mice diminishes hepatic steatosis but does not protect against insulin resistance or obesity.
Wendel AA, Li LO, Li Y, Cline GW, Shulman GI, Coleman RA., Free PMC Article | 08/16/2010 |
| 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 | Glycerol-3-phosphate acyltransferase 1 is essential for the immune response to infection with coxsackievirus B3 in mice.
Karlsson EA, Wang S, Shi Q, Coleman RA, Beck MA., Free PMC Article | 01/21/2010 |
| Our results indicate differential roles of the two promoters in the regulation of hepatic GPAT1 gene expression in mice. | Identification of cis-acting promoter sequences required for expression of the glycerol-3-phosphate acyltransferase 1 gene in mice.
Yoshida M, Harada N, Yamamoto H, Taketani Y, Nakagawa T, Yin Y, Hattori A, Zenitani T, Hara S, Yonemoto H, Nakamura A, Nakano M, Mawatari K, Teshigawara K, Arai H, Hosaka T, Takahashi A, Yoshimoto K, Nakaya Y. | 01/21/2010 |
| a novel link between GPAT-1 and changes in T-lymphocyte function | Glycerol-3-phosphate acyltransferase-1 regulates murine T-lymphocyte proliferation and cytokine production.
Collison LW, Murphy EJ, Jolly CA., Free PMC Article | 01/21/2010 |
| GPAT1 contributes significantly to cardiomyocyte triacylglycerol synthesis during lipogenic or high-fat diets and influences the incorporation of 20:4n6 into heart phospholipids. | Mice deficient in mitochondrial glycerol-3-phosphate acyltransferase-1 have diminished myocardial triacylglycerol accumulation during lipogenic diet and altered phospholipid fatty acid composition.
Lewin TM, de Jong H, Schwerbrock NJ, Hammond LE, Watkins SM, Combs TP, Coleman RA., Free PMC Article | 01/21/2010 |
| 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. | Mitochondrial glycerol-3-phosphate acyltransferase-deficient mice have reduced weight and liver triacylglycerol content and altered glycerolipid fatty acid composition.
Hammond LE, Gallagher PA, Wang S, Hiller S, Kluckman KD, Posey-Marcos EL, Maeda N, Coleman RA., Free PMC Article | 01/21/2010 |
| 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. | Overexpression of mitochondrial GPAT in rat hepatocytes leads to decreased fatty acid oxidation and increased glycerolipid biosynthesis.
Lindén D, William-Olsson L, Rhedin M, Asztély AK, Clapham JC, Schreyer S. | 01/21/2010 |
| 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. | Liver-directed overexpression of mitochondrial glycerol-3-phosphate acyltransferase results in hepatic steatosis, increased triacylglycerol secretion and reduced fatty acid oxidation.
Lindén D, William-Olsson L, Ahnmark A, Ekroos K, Hallberg C, Sjögren HP, Becker B, Svensson L, Clapham JC, Oscarsson J, Schreyer S. | 01/21/2010 |
| Gpat1-/- liver exhibits increased oxidative stress and sensitivity of the mitochondrial permeability transition pore, and a balanced increase in apoptosis and proliferation. | Increased oxidative stress is associated with balanced increases in hepatocyte apoptosis and proliferation in glycerol-3-phosphate acyltransferase-1 deficient mice.
Hammond LE, Albright CD, He L, Rusyn I, Watkins SM, Doughman SD, Lemasters JJ, Coleman RA., Free PMC Article | 01/21/2010 |
| 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 | Mitochondrial glycerol-3-phosphate acyltransferase-1 is essential in liver for the metabolism of excess acyl-CoAs.
Hammond LE, Neschen S, Romanelli AJ, Cline GW, Ilkayeva OR, Shulman GI, Muoio DM, Coleman RA. | 01/21/2010 |
| 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 | Hepatic knockdown of mitochondrial GPAT1 in ob/ob mice improves metabolic profile.
Xu H, Wilcox D, Nguyen P, Voorbach M, Suhar T, Morgan SJ, An WF, Ge L, Green J, Wu Z, Gimeno RE, Reilly R, Jacobson PB, Collins CA, Landschulz K, Surowy T. | 01/21/2010 |