Review
Copyright ©The Author(s) 2015.
World J Diabetes. May 15, 2015; 6(4): 598-612
Published online May 15, 2015. doi: 10.4239/wjd.v6.i4.598
Figure 1
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Figure 1 Functions of various immune cell types in pathogenesis of type 2 diabetes. IL: Interleukin; MCP-1: Monocyte chemoattractant protein-1; TNF-α: Tumor necrosis factor α.
Figure 2
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Figure 2 Various hormone functions of insulin.
Figure 3
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Figure 3 Target genes activated by NF-κB. TNF-α: Tumor necrosis factor-alpha; IFN-γ: Interferon-gamma; IL: Interleukin; TGF-β: Tumor growth factor-beta; MCP-1: Monocyte chemoattractant protein-1; MIP: Major intrinsic protein; TNFR: Tumor necrosis factor receptor; INFR: Interferon receptor; IL-R: Interleukin receptor; CD: Cluster of differentiation; ICAM: Intracellular cell adhesion molecule; VCAM: Vascular cell adhesion molecule; CCR: Chemokine CC receptor; TLR: Toll-like receptor; Lox: Lysyl oxidase; RAGE: Receptor advanced glycation end product; PAI: Plasminogen inhibitor activator; SAA: Serum amyloid; CRP: C-reactive protein; COX: Cyclo-oxygenase; iNOS: Inducible nitric oxide synthase; VEGF: Vascular endothelial growth factor; IGFBPs: Insulin-like growth factor binding protein; MnSOD: Manganese superoxide dismutase; RelA: Reticuloendotheliosis viral oncogene homolog A; NF-κB: Nuclear factor-kappa B; IKK: Inhibitor Kappa B kinase; IκBα: Inhibitor of NF-κB; TNFAIP3: TNF-α induced protein 3.
Figure 4
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Figure 4 Mechanism of endoplasmic reticulum stress. ER: Endoplasmic-reticulum; ATF6: Activating transcription factor 6; PERK: Double-stranded RNA-activated protein kinase (PKR)-like ER kinase; IRE1: Inositol-requiring kinase 1; IL: Interleukin; MCP: Monocyte chemoattractant protein; TNF-α: Tumor necrosis factor α; JNK: c-Jun NH2-terminal kinase; NF-κB: Nuclear factor κB.
Figure 5
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Figure 5 Activation of inflammasomes in type 2 diabetes (metabolic stress activates multiprotein complex, inflammasome in β-cells that induce caspase-1 to cleave pro-interleukin-1β (pro-IL-1β) into active IL-1β. β-cell-derived IL-1β promote the release of chemokines and recruitment of macrophages that are activated by human islet amyloid polypeptide, leading to deleterious concentrations of IL-1β. FFA: Free fatty acid; IL: Interleukin.