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      Protein kinases: mechanisms and downstream targets in inflammation mediated obesity and insulin resistance

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          Abstract

          Obesity induced low-grade inflammation (metaflammation) impairs insulin receptor signaling (IRS). This has been implicated in the development of insulin resistance. Insulin signaling in the target tissues is mediated by stress kinases such as p38 mitogen-activated protein kinase (MAPK), c-Jun NH2-terminal kinase (JNK), inhibitor of NF-kB kinase complex beta (IKKβ), AMP activated protein kinase (AMPK), protein kinase C (PKC), Rho associated coiled-coil containing protein kinase (ROCK) and RNA-activated protein kinase (PKR), etc. Most of these kinases phosphorylate several key regulators in glucose homeostasis. The phosphorylation of serine residues in the insulin receptor (IR) and IRS-1 molecule results in diminished enzymatic activity in the phosphatidylinositol 3-kinase (PI3K)/Akt pathway. This has been one of the key mechanisms observed in the tissues that are implicated in insulin resistance especially in Type II Diabetes Mellitus (T2-DM). Identifying the specific protein kinases involved in obesity induced chronic inflammation may help in developing the targeted drug therapies to minimize the insulin resistance. This review is focused on the protein kinases involved in the inflammatory cascade and molecular mechanisms and their downstream targets with special reference to obesity induced T2-DM.

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          Author and article information

          Journal
          0364456
          5915
          Mol Cell Biochem
          Mol. Cell. Biochem.
          Molecular and cellular biochemistry
          0300-8177
          1573-4919
          22 November 2016
          21 November 2016
          February 2017
          01 February 2018
          : 426
          : 1-2
          : 27-45
          Affiliations
          [1 ]Department of Surgery, Creighton University School of Medicine, Omaha, Nebraska, USA
          [2 ]Department of Clinical & Translational Science, Creighton University School of Medicine, Omaha, Nebraska, USA
          Author notes
          [* ]Address for Correspondence: Dr. Kalyana C Nandipati, MBBS, MD., Associate Professor of Surgery, Associate Program Director, Department of Surgery, Department of Clinical & Translational Science, 601 N. 30th Street, Suite # 3700, Creighton University, School of Medicine, Omaha, NE, 68131, USA, Tel: (402) 280 3488 Fax: (402) 280 1421, Kalyana.Nandipati@ 123456alegent.org
          Article
          PMC5291752 PMC5291752 5291752 nihpa831339
          10.1007/s11010-016-2878-8
          5291752
          27868170
          Categories
          Article

          Obesity, Insulin resistance, Inflammation, Protein kinases

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