title: Selective increase in monocyte p38 mitogen-activated protein kinase activity in metabolic syndrome.
abstract: OBJECTIVE
  Metabolic syndrome is a common disorder that predisposes to both cardiovascular disease and diabetes. There is paucity of data on cellular signal transduction pathways in metabolic syndrome. This study determined monocyte mitogen-activated protein kinase activity in patients with metabolic syndrome.
  
  
  METHODS
  The p38, extracellular signal-regulated kinase-1/2 and Jun N-terminal kinase-mitogen-activated protein kinase activities were assayed in isolated monocytes from patients with metabolic syndrome and controls (n = 36 per group) and correlated with features of metabolic syndrome, inflammation and oxidative stress biomarkers.
  
  
  RESULTS
  A significant increase in p38 mitogen-activated protein kinase activity was observed in metabolic syndrome even following adjustment for adiposity. There were no significant differences in extracellular signal-regulated kinase-1/2 and Jun N-terminal kinase activities. P38 mitogen-activated protein kinase activity correlated significantly with homeostasis model assessment-estimated insulin resistance and biomarkers of inflammation and oxidative stress.
  
  
  CONCLUSIONS
  We are first to observe a selective increase in monocyte p38 mitogen-activated protein kinase activity in metabolic syndrome and suggest it as a pivotal molecular target for ameliorating insulin resistance and inflammation.
authors.affiliation: Laboratory of Atherosclerosis and Metabolic Research, Department of Pathology and Internal Medicine, University of California Davis Medical Center, Sacramento, CA, USA Veterans Affairs Medical Center, Mather, CA, USA ijialal@ucdavis.edu.
authors.forename: Ishwarlal
authors.initials: I
authors.lastname: Jialal
authors.affiliation: Department of Biostatistics, The University of Texas Southwestern Medical Center, Dallas, TX, USA.
authors.forename: Beverley
authors.initials: B
authors.lastname: Adams-Huet
authors.affiliation: Laboratory of Atherosclerosis and Metabolic Research, Department of Pathology and Internal Medicine, University of California Davis Medical Center, Sacramento, CA, USA.
authors.forename: Roma
authors.initials: R
authors.lastname: Pahwa
mesh_terms: D000328:Adult; D000368:Aged; D002097:C-Reactive Protein / Q000378:metabolism; D016022:Case-Control Studies; D005260:Female; D006801:Humans; D048031:JNK Mitogen-Activated Protein Kinases / Q000378:metabolism; D008297:Male; D024821:Metabolic Syndrome / Q000378:metabolism*; D008875:Middle Aged; D019950:Mitogen-Activated Protein Kinase 1 / Q000378:metabolism; D048052:Mitogen-Activated Protein Kinase 3 / Q000378:metabolism; D009000:Monocytes / Q000378:metabolism*; D010750:Phosphoproteins / Q000378:metabolism; D010766:Phosphorylation; D055815:Young Adult; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism*
chemical_list: D010750:Phosphoproteins; D002097:C-Reactive Protein; D048031:JNK Mitogen-Activated Protein Kinases; C535150:MAPK1 protein, human; D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3; D048051:p38 Mitogen-Activated Protein Kinases
keywords: Mitogen-activated protein kinase; inflammation; metabolic syndrome; monocytes