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 language | English (US) |
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Pages (from-to) | 93-96 |
Number of pages | 4 |
Journal | Diabetes and Vascular Disease Research |
Volume | 13 |
Issue number | 1 |
DOIs | |
State | Published - Jan 1 2016 |
Keywords
- Mitogen-activated protein kinase
- inflammation
- metabolic syndrome
- monocytes
ASJC Scopus subject areas
- Internal Medicine
- Endocrinology, Diabetes and Metabolism
- Cardiology and Cardiovascular Medicine