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Updated: Apr 1, 2026
Quantification of Monocyte Chemotactic Activity In Vivo and Characterization of Blood Monocyte Derived Macrophages
Published on: August 12, 2019
Selective increase in monocyte p38 mitogen-activated protein kinase activity in metabolic syndrome
Ishwarlal Jialal1, Beverley Adams-Huet2, Roma Pahwa3
1Laboratory 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.
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.
