Research Topics
Genomes and Genes
| Anil K AgarwalSummaryAffiliation: University of Texas Southwestern Medical Center Country: USA Publications
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Detail Information
Publications
Lysophospholipid acyltransferases: 1-acylglycerol-3-phosphate O-acyltransferases. From discovery to diseaseAnil K Agarwal
Division of Nutrition and Metabolic Diseases, Department of Internal Medicine, Center for Human Nutrition, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA
Curr Opin Lipidol 23:290-302. 2012..In this review, we summarize their biochemical features and discuss their functional role...
Enzymatic activity of the human 1-acylglycerol-3-phosphate-O-acyltransferase isoform 11: upregulated in breast and cervical cancersAnil K Agarwal
Division of Nutrition and Metabolic Diseases, Department of Internal Medicine and Center for Human Nutrition, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390, USA
J Lipid Res 51:2143-52. 2010..Our enzymatic assays strongly suggest that the cDNA previously identified as LPCAT2/lyso platelet-activating factor-acetyltransferase cDNA has AGPAT activity and thus we prefer to identify this clone as AGPAT11 as well...
Functional characterization of human 1-acylglycerol-3-phosphate-O-acyltransferase isoform 9: cloning, tissue distribution, gene structure, and enzymatic activityAnil K Agarwal
Division of Nutrition and Metabolic Diseases, Department of Internal Medicine, Center for Human Nutrition, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75390 USA
J Endocrinol 193:445-57. 2007..Based on the activity and expression pattern of AGPAT9 in the lung and spleen, this novel isoform could be implicated in the biosynthesis of phospholipids and TG in these tissues...- Functional characterization of human 1-acylglycerol-3-phosphate acyltransferase isoform 8: cloning, tissue distribution, gene structure, and enzymatic activityAnil K Agarwal
Division of Nutrition and Metabolic Diseases, Department of Internal Medicine, Center for Human Nutrition, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX 75390, USA
Arch Biochem Biophys 449:64-76. 2006.... - Human 1-acylglycerol-3-phosphate O-acyltransferase isoforms 1 and 2: biochemical characterization and inability to rescue hepatic steatosis in Agpat2(-/-) gene lipodystrophic miceAnil K Agarwal
Division of Nutrition and Metabolic Diseases, University of Texas Southwestern Medical Center at Dallas, Dallas, Texas 75390, USA
J Biol Chem 286:37676-91. 2011..From these studies, we suggest that the role of AGPAT1 or AGPAT2 in liver lipogenesis is minimal and that accumulation of liver fat is primarily a consequence of insulin resistance and loss of adipose tissue in Agpat2(-/-) mice... - Genetic basis of congenital generalized lipodystrophyA K Agarwal
Division of Nutrition and Metabolic Diseases, Department of Internal Medicine, Center for Human Nutrition, University of Texas Southwestern Medical Center, Dallas, 75390, USA
Int J Obes Relat Metab Disord 28:336-9. 2004..Thus, several distinct mechanisms can lead to extreme lack of adipose tissue in humans and cause CGL... - Cortisol metabolism and visceral obesity: role of 11beta-hydroxysteroid dehydrogenase type I enzyme and reduced co-factor NADPHAnil K Agarwal
Division of Nutrition and Metabolic Diseases, Department of Internal Medicine, Center for Human Nutrition, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA
Endocr Res 29:411-8. 2003..In this commentary we explore the possibility that increased intracellular availability of reduced co-factor, NADPH, could exacerbate the enzymatic activity... - Focal segmental glomerulosclerosis in patients with mandibuloacral dysplasia owing to ZMPSTE24 deficiencyAnil K Agarwal
From the Division of Nutrition and Metabolic Diseases, University of Texas Southwestern Medical Center, Dallas, TX 75390 9052, USA
J Investig Med 54:208-13. 2006.... - Atypical progeroid syndrome due to heterozygous missense LMNA mutationsAbhimanyu Garg
Division of Nutrition and Metabolic Diseases, University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Boulevard, Dallas, Texas 75390 8537, USA
J Clin Endocrinol Metab 94:4971-83. 2009..Heterozygous LMNA mutations have also been reported in a small number of patients with a less well-characterized atypical progeroid syndrome (APS)... - Severe mandibuloacral dysplasia-associated lipodystrophy and progeria in a young girl with a novel homozygous Arg527Cys LMNA mutationAnil K Agarwal
Division of Nutrition and Metabolic Diseases, University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Boulevard, Dallas, Texas 75390 8537, USA
J Clin Endocrinol Metab 93:4617-23. 2008..Mandibuloacral dysplasia (MAD) is a rare autosomal recessive progeroid syndrome due to mutations in genes encoding nuclear lamina proteins, lamins A/C (LMNA) or prelamin A processing enzyme, and zinc metalloproteinase (ZMPSTE24)... - Functional characterization of the human 1-acylglycerol-3-phosphate-O-acyltransferase isoform 10/glycerol-3-phosphate acyltransferase isoform 3Suja Sukumaran
Division of Nutrition and Metabolic Diseases, Department of Internal Medicine and Center for Human Nutrition, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA
J Mol Endocrinol 42:469-78. 2009..These observations strongly suggest that the cDNA previously identified as GPAT3 has AGPAT activity and thus we prefer to identify this clone as AGPAT10 as well... - A novel homozygous Ala529Val LMNA mutation in Turkish patients with mandibuloacral dysplasiaAbhimanyu Garg
Division of Nutrition and Metabolic Diseases, Department of Internal Medicine, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75390 9052, USA
J Clin Endocrinol Metab 90:5259-64. 2005.... - Zinc metalloproteinase, ZMPSTE24, is mutated in mandibuloacral dysplasiaAnil K Agarwal
Division of Nutrition and Metabolic Diseases, Department of Internal Medicine, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX 75390, USA
Hum Mol Genet 12:1995-2001. 2003..We conclude that mutations in ZMPSTE24 may cause MAD by affecting prelamin A processing... - AGPAT2 is mutated in congenital generalized lipodystrophy linked to chromosome 9q34Anil K Agarwal
Department of Internal Medicine, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, Texas 75390, USA
Nat Genet 31:21-3. 2002..AGPAT2 mRNA is highly expressed in adipose tissue. We conclude that mutations in AGPAT2 may cause congenital generalized lipodystrophy by inhibiting triacylglycerol synthesis and storage in adipocytes... - Novel subtype of congenital generalized lipodystrophy associated with muscular weakness and cervical spine instabilityVinaya Simha
Division of Nutrition and Metabolic Diseases, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA
Am J Med Genet A 146:2318-26. 2008..The genetic basis of this novel subtype remains to be determined... - Genetic and phenotypic heterogeneity in patients with mandibuloacral dysplasia-associated lipodystrophyVinaya Simha
Division of Nutrition and Metabolic Diseases, Center for Human Nutrition, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA
J Clin Endocrinol Metab 88:2821-4. 2003..e. AGPAT2, Seipin, and PPARG also revealed no substantial alterations. We conclude that MAD is a genetically and phenotypically heterogeneous disorder. Besides LMNA gene, other as yet unmapped loci could be linked to MAD... - Phenotypic heterogeneity in body fat distribution in patients with atypical Werner's syndrome due to heterozygous Arg133Leu lamin A/C mutationKatherine N Jacob
Department of Internal Medicine, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75390-9052, USA
J Clin Endocrinol Metab 90:6699-706. 2005..Furthermore, the severity of metabolic complications seems to correlate with the extent of lipodystrophy... - Enzymatic activities of the human AGPAT isoform 3 and isoform 5: localization of AGPAT5 to mitochondriaSneha S Prasad
Division of Nutrition and Metabolic Diseases, Department of Internal Medicine and Center for Human Nutrition, University of Texas Southwestern Medical Center, Dallas, TX, USA
J Lipid Res 52:451-62. 2011.... - Molecular mechanisms of hepatic steatosis and insulin resistance in the AGPAT2-deficient mouse model of congenital generalized lipodystrophyVíctor A Cortés
Department of Molecular Genetics, University of Texas Southwestern Medical Center at Dallas, Dallas, TX 75390, USA
Cell Metab 9:165-76. 2009..These observations suggest that both dietary fat and hepatic triglyceride biosynthesis via a monoacylglycerol pathway may contribute to hepatic steatosis in Agpat2(-/-) mice... - The lipodystrophy protein seipin is found at endoplasmic reticulum lipid droplet junctions and is important for droplet morphologyKimberly M Szymanski
Department of Pharmacology, University of Texas Southwestern Medical School, Dallas, TX 75390, USA
Proc Natl Acad Sci U S A 104:20890-5. 2007..The genes identified in our screen should be of value in understanding the pathway of lipid droplet biogenesis and maintenance and the cause of some lipodystrophies... - Genetic basis of lipodystrophies and management of metabolic complicationsAnil K Agarwal
Division of Nutrition and Metabolic Diseases, Department of Internal Medicine and the Center for Human Nutrition, The University of Texas Southwestern Medical Center at Dallas, Dallas, Texas 75390-9052, USA
Annu Rev Med 57:297-311. 2006..Additional loci remain to be discovered. We discuss features of autosomal recessive and dominant types of lipodystrophies and therapeutic interventions available for these patients... - Phenotypic and genetic heterogeneity in congenital generalized lipodystrophyAnil K Agarwal
Department of Internal Medicine, Division of Nutrition and Metabolic Diseases and Center for Human Nutrition, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA
J Clin Endocrinol Metab 88:4840-7. 2003..We conclude that besides AGPAT2 and BSCL2, there may be additional loci for CGL. The genetic heterogeneity in CGL patients is accompanied by phenotypic heterogeneity... - Lipodystrophies: disorders of adipose tissue biologyAbhimanyu Garg
Division of Nutrition and Metabolic Diseases, Department of Internal Medicine, Center for Human Nutrition, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX 75390, USA
Biochim Biophys Acta 1791:507-13. 2009..PPARgamma and AKT2 play important role in adipogenesis and lipid synthesis. In this review, we discuss and speculate about the contribution of various lipodystrophy genes and their products in the lipid droplet formation... - A homozygous mutation in the lamin A/C gene associated with a novel syndrome of arthropathy, tendinous calcinosis, and progeroid featuresHilde Van Esch
Division of Nutrition and Metabolic Diseases, Department of Internal Medicine, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9052, USA
J Clin Endocrinol Metab 91:517-21. 2006..Thus, arthropathy with tendinous calcifications can be added to the growing list of disorders associated with LMNA mutations... - Mislocalization of prelamin A Tyr646Phe mutant to the nuclear pore complex in human embryonic kidney 293 cellsYong Pan
Department of Internal Medicine and Center for Human Nutrition, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390, USA
Biochem Biophys Res Commun 355:78-84. 2007..The toxicity of prenylated prelamin A may be due to its association and/or accumulation at the nuclear pore complex which could be partially reversed by farnesyl transferase inhibitors... - Risk factors for diabetes in familial partial lipodystrophy, Dunnigan varietyWasim A Haque
Division of Nutrition and Metabolic Diseases, Center for Human Nutrition, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas 75390, USA
Diabetes Care 26:1350-5. 2003..CONCLUSIONS: We conclude that increased adiposity as reflected by excess subcutaneous fat accumulation in the chin region and parity may predispose women with FPLD to develop diabetes... - Congenital generalized lipodystrophy, type 4 (CGL4) associated with myopathy due to novel PTRF mutationsSavitha Shastry
Division of Nutrition and Metabolic Diseases, Department of Internal Medicine, Center for Human Nutrition, University of Texas Southwestern Medical Center at Dallas, Dallas, Texas, USA
Am J Med Genet A 152:2245-53. 2010..It is unclear how mutations in PTRF, which plays an essential role in formation of caveolae, affect a wide variety of tissues resulting in a variable phenotype... - Enzymatic activity of naturally occurring 1-acylglycerol-3-phosphate-O-acyltransferase 2 mutants associated with congenital generalized lipodystrophyWasim Haque
Division of Nutrition and Metabolic Diseases, Department of Internal Medicine, Center for Human Nutrition, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX 75390, USA
Biochem Biophys Res Commun 327:446-53. 2005..We suggest that reduction in AGPAT2 enzymatic activity underlies the loss of adipose tissue in CGL. Our observations reveal an important role of various carboxy-terminal residues in determining the enzymatic activity of AGPAT2... - Genetic disorders of adipose tissue development, differentiation, and deathAnil K Agarwal
Division of Nutrition and Metabolic Diseases, Department of Internal Medicine and the Center for Human Nutrition, University of Texas Southwestern Medical Center at Dallas, Dallas, Texas 75390-9052, USA
Annu Rev Genomics Hum Genet 7:175-99. 2006..In this review, we focus on the molecular basis of inherited lipodystrophies as they relate to adipocyte biology and their associated phenotypic manifestations... - PSMB8 encoding the β5i proteasome subunit is mutated in joint contractures, muscle atrophy, microcytic anemia, and panniculitis-induced lipodystrophy syndromeAnil K Agarwal
Department of Internal Medicine, Center for Human Nutrition, University of Texas Southwestern Medical Center, Dallas, 75390, USA
Am J Hum Genet 87:866-72. 2010..We conclude that mutations in PSMB8 cause JMP syndrome, most probably by affecting MHC class I antigen processing... - Congenital generalized lipodystrophy: significance of triglyceride biosynthetic pathwaysAnil K Agarwal
Division of Nutrition and Metabolic Diseases, Department of Internal Medicine, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX 75390, USA
Trends Endocrinol Metab 14:214-21. 2003..Here, we discuss the significance of these in energy storage, in addition to the normal functioning of cell membranes... - Cofactors, redox state, and directional preferences of hydroxysteroid dehydrogenasesDaniel P Sherbet
Division of Endocrinology and Metabolism, Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390 8857, United States
Mol Cell Endocrinol 265:83-8. 2007.... - Increased expression and activity of 11beta-HSD-1 in diabetic islets and prevention with troglitazoneLaurence Duplomb
Gifford Laboratories, Center for Diabetes Research, Department of Internal Medicine, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390, USA
Biochem Biophys Res Commun 313:594-9. 2004..We conclude that 11beta-HSD-1 expression and activity are increased in islets of diabetic, but not prediabetic ZDF rats, and that TGZ prevents both the increase in 11beta-HSD-1 and the diabetes... - Usual ACE inhibitor therapy in CKD patients is associated with lower plasma aldosterone levels than usual angiotensin receptor blocker therapyNabil Haddad
Department of Internal Medicine, The Ohio State University, Columbus, Ohio 43210, USA
Kidney Blood Press Res 30:299-305. 2007..This study tested whether ACE inhibitor (I) therapy achieves lower plasma (p) ALDO levels than angiotensin receptor blocker (ARB) therapy when they are used under usual clinical conditions in chronic kidney disease (CKD) patients... - A novel heterozygous mutation in peroxisome proliferator-activated receptor-gamma gene in a patient with familial partial lipodystrophyAnil K Agarwal
Department of Internal Medicine, Division of Nutrition and Metabolic Diseases and Center for Human Nutrition, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA
J Clin Endocrinol Metab 87:408-11. 2002..None of the four unaffected family members harbored the mutation. We conclude that heterozygous, R425C, mutation in PPARG could be the molecular basis for one of the familial partial lipodystrophy phenotypes... - Seipin: a mysterious proteinAnil K Agarwal
Division of Nutrition and Metabolic Diseases, the Department of Internal Medicine and the Center for Human Nutrition, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390, USA
Trends Mol Med 10:440-4. 2004 - Proposed pathogenesis of idiopathic loin pain-hematuria syndromeDan N Spetie
Department of Internal Medicine, The Ohio State University, Columbus, OH 43210, USA
Am J Kidney Dis 47:419-27. 2006..Primary LPHS pain may be initiated by obstructing RBC casts and perhaps microcrystals in those with a history of urolithiasis. Nevertheless, other factors are needed to explain the severe pain in patients with primary LPHS... - Minireview: cellular redox state regulates hydroxysteroid dehydrogenase activity and intracellular hormone potencyAnil K Agarwal
Division of Endocrinology and Metabolism, Department of Internal Medicine, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75390-8857, USA
Endocrinology 146:2531-8. 2005..We will review the evidence linking cofactor handling and HSD activity, speculate on additional ways that intracellular metabolism can alter HSD activity and, thus, hormone potency, and discuss fruitful avenues of further investigation... - A homozygous ZMPSTE24 null mutation in combination with a heterozygous mutation in the LMNA gene causes Hutchinson-Gilford progeria syndrome (HGPS): insights into the pathophysiology of HGPSJonas Denecke
Department of Pediatrics, University Hospital of Munster, Munster, Germany
Hum Mutat 27:524-31. 2006..The mutations of our patient indicate that farnesylated prelamin A is the deleterious agent leading to the HGPS phenotype, which gives further insights into the pathophysiology of the disorder...