Tissue inflammation and nitric oxide-mediated alterations in cardiovascular function are major determinants of endotoxin-induced insulin resistance.

House LM, Morris RT, Barnes TM, Lantier L, Cyphert TJ, McGuinness OP, Otero YF
Cardiovasc Diabetol. 2015 14: 56

PMID: 25986700 · PMCID: PMC4484635 · DOI:10.1186/s12933-015-0223-2

Endotoxin (i.e. LPS) administration induces a robust inflammatory response with accompanying cardiovascular dysfunction and insulin resistance. Overabundance of nitric oxide (NO) contributes to the vascular dysfunction. However, inflammation itself also induces insulin resistance in skeletal muscle. We sought to investigate whether the cardiovascular dysfunction induced by increased NO availability without inflammatory stress can promote insulin resistance. Additionally, we examined the role of inducible nitric oxide synthase (iNOS or NOS2), the source of the increase in NO availability, in modulating LPS-induced decrease in insulin-stimulated muscle glucose uptake (MGU).

MeSH Terms (25)

Animals Arterial Pressure Cardiac Output Chemokine CCL2 Echocardiography Endothelium-Dependent Relaxing Factors Gene Expression Glucose Glucose Clamp Technique Heart Inflammation Insulin Resistance Interleukin-6 Lipopolysaccharides Mice Mice, Knockout Microspheres Muscle, Skeletal Muscle Cells Nitric Oxide Nitric Oxide Synthase Type II Regional Blood Flow RNA, Messenger Serpin E2 Tumor Necrosis Factor-alpha

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