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  Indian J Med Microbiol
 

Figure 2: Mechanism of insulin resistance. Endocrine, inflammatory, and neuronal pathways link obesity to insulin resistance. Excess extracellular lipid, fatty acyl CoA inhibits the association of insulin receptor substrate 1 with phosphatidyl inositol 3-kinase leading to the activation of serine/threonine kinases. Reduced activity of phosphatidyl inositol 3-kinase and protein kinase B and defects in the pancreatic beta cell can lead to insulin receptor. Obesity is characterized by an increase in the accumulation of inflammatory factors such as tumor necrosis factor-α which inhibit insulin signaling. PTPase 1B negatively regulates insulin action by dephosphorylating the insulin receptor. Loss of cellular mitochondrial activity and reduced number of insulin receptor also play a major role in insulin resistance

Figure 2: Mechanism of insulin resistance. Endocrine, inflammatory, and neuronal pathways link obesity to insulin resistance. Excess extracellular lipid, fatty acyl CoA inhibits the association of insulin receptor substrate 1 with phosphatidyl inositol 3-kinase leading to the activation of serine/threonine kinases. Reduced activity of phosphatidyl inositol 3-kinase and protein kinase B and defects in the pancreatic beta cell can lead to insulin receptor. Obesity is characterized by an increase in the accumulation of inflammatory factors such as tumor necrosis factor-α which inhibit insulin signaling. PTPase 1B negatively regulates insulin action by dephosphorylating the insulin receptor. Loss of cellular mitochondrial activity and reduced number of insulin receptor also play a major role in insulin resistance