Patents in Targets and Drugs for Insulin Resistance: Correlation with Inflammatory Mediators
Daniel S. de Carvalho, Fernando R. M. da Silva Seixas and Elizabeth P. Sampaio
Affiliation: Av Brasil 4365, Fundacao Oswaldo Cruz - Departamento de Micobacterioses - Laboratorio de Hanseniase. CEP 21045-900 . Rio de Janeiro, Brazil.
Keywords: Insulin, insulin resistance, TNFα, IKK, MAPK, JNK, IRS, Type-2 diabetes, diabetes, SOCS
In the past decade the involvement of inflammatory responses with metabolic disorders became well established, more specifically the insulin resistance, responsible for Type-2 diabetes. The major evidence for insulin resistance is the deactivation of insulin receptors substrates (IRS) trough inflammatory activated pathways and the presence of pro-inflammatory cytokines, especially tumor necrosis factor alpha (TNFα) at adipose tissues. The intracellular regulation of TNFα is mediated by several processes, thus the knowledge about these pathways may provide targets to inhibit TNFα synthesis, such as mitogen activated protein kinases (MAPK) cascades and nuclear factor kappa B (NF-κB) activation pathways. Natural anti-inflammatory pathways can also be activated in order to treat or ameliorate these disorders, such as peroxisome proliferator-activated receptors (PPAR) and suppressors of cytokine signaling (SOCS) families. It is discussed here international bibliography regarding insulin resistance related to inflammation and also patent literature disclosing methods to treat Type-2 diabetes targeting immune systems molecules and pathways.
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