Recombinant Mouse Resistin (carrier-free)

Resistin, originally found in the inflammatory zone in humans, is a cysteine-rich secreted peptide hormone. It belongs to a member of the resistin-like molecule family. In rodents, resistin exists in two distinct states in circulating serum, noncovalent coiled-coil trimers and disulfide bond-linked tail-to-tail hexamers. Rodent resistin is mainly secreted by mature adipocytes, and it has been linked to the pathogenesis of obesity-mediated insulin resistance and of type 2 diabetes. Resistin-deficient mice exhibit low glucose levels and reduced hepatic glucose production after fasting, suggesting a role of resistin in the maintenance of blood glucose during fasting. Administration of recombinant resistin to normal mice leads to impairment of glucose tolerance and insulin action. Rodent resistin inhibits adipocyte differentiation, as a feedback regulator of adipogenesis. In addition, resistin stimulates pro-inflammatory cytokines TNF-α and IL-6 via NF-κB activation in rat pancreatic acinar cells.  In humans, resistin is primarily expressed and secreted from peripheral blood mononuclear cells, bone marrow cells and macrophages. Resistin serum levels are associated with insulin resistance, disease severity, clinical complications, and prognosis in patients with chronic liver disease. Human resistin directly aggravates atherosclerosis by stimulating monocytes to induce vascular inflammation.  Human resistin stimulates the pro-inflammatory cytokines TNF-α/IL-12 in macrophages and TNF-α/IL-6 in adipocytes via an NF-κB-dependent pathway. TNF-α induces upregulation of resistin in human macrophages. Resistin promotes neutrophil pro-inflammatory activation, neutrophil extracellular trap formation, and increases the severity of acute lung injury in humanized resistin mice (hRTN+/−/−) (mice that express human resistin but lack murine resistin). Resistin is increased in the circulation of patients with acute respiratory distress syndromes and sepsis.