Selective increase in monocyte p38 mitogen-activated protein kinase activity in metabolic syndrome

Ishwarlal Jialal, Beverley Adams-Huet, Roma Pahwa

Research output: Contribution to journalArticle

7 Scopus citations

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. Research design and 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.

Original languageEnglish (US)
Pages (from-to)93-96
Number of pages4
JournalDiabetes and Vascular Disease Research
Volume13
Issue number1
DOIs
Publication statusPublished - Jan 1 2016

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Keywords

  • inflammation
  • metabolic syndrome
  • Mitogen-activated protein kinase
  • monocytes

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Internal Medicine
  • Cardiology and Cardiovascular Medicine

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