The role of adipokines in β-cell failure of type 2 diabetes

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   Figure 1

   Diagrammatic representation of the interrelationship between adipose tissue and the pancreatic β-cell: the 'adipo-insular axis'. Positive regulation may include stimulation of insulin synthesis and secretion and cell proliferation. Negative regulation can involve inhibition of insulin synthesis and secretion and increased cell apoptosis and/or necrosis.
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   Figure 2

   Complex interaction between adipokines in β-cell specific effects. Many adipokines act via post-receptor pathways in the β-cell which intersect in a number of places. In addition insulin itself, the release of which is affected by these adipokines, has autocrine effects on the β-cell. Signalling pathways which are negatively or positively affected by adipokines include one of the main pathways activated in insulin signalling the PI3K pathway as well as pathways such as MAPK/ERK1/2 and AMPK. AC, Adenylyl cyclase; AdipoR, Adiponectin receptor; Akt/PKB, Protein Kinase B; AMPK, AMP-activated protein kinase; ApelinR, Apelin receptor (APJ receptor); DPP-IV, Dipeptidyl peptidase IV; ERK, Extracellular signal-regulated kinases; GLP1, Glucagon-like peptide 1; GLP1-R, GLP1 receptor; InsR, Insulin Receptor; JAK/STAT, Janus Kinase/ Signal Transducer and Activator of Transcription; KATP, ATP-sensitive potassium channel/sulphonylurea receptor; LepR, Leptin receptor; MAPK, Mitogen-activated protein kinases (eg ERK, JNK, p38); NFκB, nuclear factor kappa B; NMN, nicotinamide mononucleotide; PDE-3B, phosphodiesterase-3B; PDX-1, Pancreatic and duodenal homeobox 1; PI3K, phosphatidyl inositol 3 kinase; PKA, protein kinase A (cAMP-dependent protein kinase; PTEN, Phosphatase and tensin homolog; TNFR-1, TNFα-receptor 1

• © 2013 Society for Endocrinology